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1. Takeuchi I, Tagawa H, Tsujikawa A, Nakagawa M, Katayama-Suguro M, Guo Y, Seto M: The potential of copy number gains and losses, detected by array-based comparative genomic hybridization, for computational differential diagnosis of B-cell lymphomas and genetic regions involved in lymphomagenesis. Haematologica; 2009 Jan;94(1):61-9
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  • [Title] The potential of copy number gains and losses, detected by array-based comparative genomic hybridization, for computational differential diagnosis of B-cell lymphomas and genetic regions involved in lymphomagenesis.
  • BACKGROUND: The differentiation of biologically and clinically different malignant lymphoma diseases or subtypes is crucial because it leads to better prognostication and therapeutic decision-making.
  • Attempts have been made at subtype classification for diagnosing lymphomas on the basis of gene-expression profiling.
  • Although array-based comparative genomic hybridization (array CGH) has identified a characteristic genomic alteration pattern for each disease entity, it has not been clear whether each patient with certain genomic alterations can be classified by array CGH data.
  • DESIGN AND METHODS: Data on copy number gains and losses for 46 diffuse large B-cell lymphomas and 29 mantle cell lymphomas were used.
  • The gene expressions of the diffuse large B-cell lymphomas cases were profiled and hierarchical clustering revealed that 28 of them were of the activated B-cell type and 18 were of the germinal center-B-cell type.
  • Using these data, we developed a computer algorithm to classify lymphoma diseases or subtypes on the basis of copy number gains and losses.
  • RESULTS: The method correctly classified 88% of the diffuse large B-cell lymphomas and mantle cell lymphomas, and 83% of the activated B-cell and germinal center-B-cell subtypes.
  • These results demonstrate that copy number gains and losses detected by array CGH can be used for classifying lymphomas into biologically and clinically distinct diseases or subtypes.
  • CONCLUSIONS: Our computer algorithm based on array CGH data successfully classified diffuse large B-cell lymphomas and mantle cell lymphomas and activated B-cell and germinal center-B-cell subtypes with high accuracy.
  • An important finding is that the regions automatically identified by the computer algorithm were located in the critical regions that are likely to be involved in the development of lymphoma.
  • [MeSH-major] Cell Transformation, Neoplastic / genetics. Gene Dosage / genetics. Lymphoma, Large B-Cell, Diffuse / diagnosis. Lymphoma, Large B-Cell, Diffuse / genetics
  • [MeSH-minor] Comparative Genomic Hybridization. Computers. Diagnosis, Differential. Humans. Lymphoma, Mantle-Cell / classification. Lymphoma, Mantle-Cell / genetics. Oligonucleotide Array Sequence Analysis

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  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2431-42 [16760443.001]
  • [Cites] Blood. 2006 Jun 1;107(11):4500-7 [16484591.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Aug;46(8):784-90 [17492756.001]
  • [Cites] Nat Rev Cancer. 2007 Oct;7(10):750-62 [17891190.001]
  • [Cites] Haematologica. 2008 May;93(5):688-96 [18367485.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15149-54 [11742071.001]
  • [Cites] Cancer Res. 2002 Feb 15;62(4):957-60 [11861363.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Cancer Cell. 2003 Feb;3(2):185-97 [12620412.001]
  • [Cites] Blood. 2003 Jun 1;101(11):4539-46 [12560219.001]
  • [Cites] Cancer Res. 2003 Jun 1;63(11):2872-80 [12782593.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] Nat Rev Cancer. 2004 Apr;4(4):309-14 [15057290.001]
  • [Cites] Cancer Res. 2004 May 1;64(9):3087-95 [15126345.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5948-55 [15342373.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Oncogene. 2005 Feb 17;24(8):1348-58 [15608680.001]
  • [Cites] Blood. 2005 Jun 1;105(11):4445-54 [15718413.001]
  • [Cites] Blood. 2005 Sep 1;106(5):1770-7 [15886317.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):247-55 [16049916.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2352-7 [16461462.001]
  • [Cites] J Clin Oncol. 2007 Apr 1;25(10):1216-22 [17296973.001]
  • (PMID = 19029149.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC2625430
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2. Jardin F, Ruminy P, Kerckaert JP, Parmentier F, Picquenot JM, Quief S, Villenet C, Buchonnet G, Tosi M, Frebourg T, Bastard C, Tilly H: Detection of somatic quantitative genetic alterations by multiplex polymerase chain reaction for the prediction of outcome in diffuse large B-cell lymphomas. Haematologica; 2008 Apr;93(4):543-50
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  • [Title] Detection of somatic quantitative genetic alterations by multiplex polymerase chain reaction for the prediction of outcome in diffuse large B-cell lymphomas.
  • BACKGROUND: Genomic gains and losses play a crucial role in the development of diffuse large B-cell lymphomas.
  • We developed a polymerase chain reaction assay to provide information regarding gains or losses of relevant genes and prognosis in diffuse large B-cell lymphomas.
  • The biological and clinical relevance of this assay were assessed.
  • In 77 cases of diffuse large B-cell lymphomas, gains of MYC, CDKN1B, c-REL and BCL2 were detected in 12%, 40%, 27% and 29%, respectively.
  • The prognostic value of a single QMPSF assay including TP53, MYC, CDKN2A, SIM1 and CDKN1B was predictive of the outcome independently of the germinal center B-cell like/non-germinal center B-cell like subtype or the International Prognostic Index.
  • CONCLUSIONS: QMPSF is a reliable and flexible method for detecting somatic quantitative genetic alterations in diffuse large B-cell lymphomas and could be integrated in future prognostic predictive models.
  • [MeSH-major] Gene Dosage. Lymphoma, Large B-Cell, Diffuse / genetics. Neoplasm Proteins / genetics. Polymerase Chain Reaction / methods
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chromosome Aberrations. Combined Modality Therapy. Female. Gene Amplification. Gene Deletion. Genes, Tumor Suppressor. Hematopoietic Stem Cell Transplantation. Humans. Male. Middle Aged. Nucleic Acid Hybridization. Prognosis. Proto-Oncogenes. Rituximab. Treatment Outcome

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  • (PMID = 18287131.001).
  • [ISSN] 1592-8721
  • [Journal-full-title] Haematologica
  • [ISO-abbreviation] Haematologica
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Neoplasm Proteins; 4F4X42SYQ6 / Rituximab
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3. Field KA, Charoenthongtrakul S, Bishop JM, Refaeli Y: Farnesyl transferase inhibitors induce extended remissions in transgenic mice with mature B cell lymphomas. Mol Cancer; 2008 May 19;7:39
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  • [Title] Farnesyl transferase inhibitors induce extended remissions in transgenic mice with mature B cell lymphomas.
  • BACKGROUND: We have used a mouse model based on overexpression of c-Myc in B cells genetically engineered to be self-reactive to test the hypothesis that farnesyl transferase inhibitors (FTIs) can effectively treat mature B cell lymphomas.
  • FTIs are undergoing clinical trials to treat both lymphoid and non-lymphoid malignancies and we wished to obtain evidence to support the inclusion of B cell lymphomas in future trials.
  • RESULTS: We report that two FTIs, L-744,832 and SCH66336, blocked the growth of mature B cell lymphoma cells in vitro and in vivo.
  • The FTI treatment affected the proliferation and survival of the transformed B cells to a greater extent than naïve B cells stimulated with antigen.
  • In syngeneic mice transplanted with the transgenic lymphoma cells, L-744,832 treatment prevented the growth of the tumor cells and the morbidity associated with the resulting lymphoma progression.
  • Tumors that arose from transplantation of the lymphoma cells regressed with as little as three days of treatment with L-744,832 or SCH66336.
  • Treatment of these established lymphomas with L-744,832 for seven days led to long-term remission of the disease in approximately 25% of animals.
  • CONCLUSION: FTI treatment can block the proliferation and survival of self-reactive transformed B cells that overexpress Myc.
  • In mice transplanted with mature B cell lymphomas, we found that FTI treatment led to regression of disease.
  • FTIs warrant further consideration as therapeutic agents for mature B cell lymphomas and other lymphoid tumors.

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  • [Cites] Blood. 2001 Mar 1;97(5):1399-403 [11222386.001]
  • [Cites] PLoS Biol. 2008 Jun 24;6(6):e152 [18578569.001]
  • [Cites] Neuro Oncol. 2000 Jul;2(3):151-8 [11302335.001]
  • [Cites] Methods Enzymol. 2001;333:306-18 [11400347.001]
  • [Cites] Curr Med Chem. 2001 Oct;8(12):1419-36 [11562275.001]
  • [Cites] Cell Mol Life Sci. 2001 Oct;58(11):1636-49 [11706990.001]
  • [Cites] Curr Treat Options Oncol. 2002 Aug;3(4):291-305 [12074766.001]
  • [Cites] Ann Oncol. 2002 Jul;13(7):1067-71 [12176785.001]
  • [Cites] Eur J Cancer. 2002 Sep;38(13):1685-700 [12175684.001]
  • [Cites] Mol Cancer Ther. 2002 Jun;1(8):575-83 [12479217.001]
  • [Cites] Int Immunopharmacol. 2003 Apr;3(4):475-83 [12689653.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5656-68 [14522880.001]
  • [Cites] Clin Cancer Res. 2003 Nov 15;9(15):5735-48 [14654559.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2968-76 [15131032.001]
  • [Cites] Br J Haematol. 2004 Oct;127(1):3-11 [15384972.001]
  • [Cites] Nature. 1985 Dec 12-18;318(6046):533-8 [3906410.001]
  • [Cites] Nature. 1988 Aug 25;334(6184):676-82 [3261841.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9268-72 [3057505.001]
  • [Cites] J Exp Med. 1989 Jan 1;169(1):255-68 [2462608.001]
  • [Cites] J Clin Oncol. 1991 Jun;9(6):941-6 [1709685.001]
  • [Cites] Blood. 1991 Aug 1;78(3):581-5 [1859876.001]
  • [Cites] Nature. 1991 Oct 24;353(6346):765-9 [1944535.001]
  • [Cites] Methods Enzymol. 1995;255:378-86 [8524123.001]
  • [Cites] Cancer Res. 1995 Nov 15;55(22):5302-9 [7585592.001]
  • [Cites] Nat Med. 1995 Aug;1(8):792-7 [7585182.001]
  • [Cites] Biochim Biophys Acta. 1997 Aug 8;1333(1):F51-71 [9294018.001]
  • [Cites] Mol Cell Biol. 1998 Jan;18(1):85-92 [9418856.001]
  • [Cites] Cancer Res. 1998 Mar 15;58(6):1253-9 [9515813.001]
  • [Cites] Oncogene. 1998 Sep 17;17(11 Reviews):1439-45 [9779989.001]
  • [Cites] J Clin Invest. 1998 Oct 15;102(8):1515-25 [9788964.001]
  • [Cites] Cancer Res. 1998 Nov 1;58(21):4947-56 [9810004.001]
  • [Cites] Int J Immunopharmacol. 1998 Nov;20(11):643-60 [9848396.001]
  • [Cites] Clin Cancer Res. 1999 Jan;5(1):35-42 [9918200.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2469-76 [10498620.001]
  • [Cites] Invest New Drugs. 2005 Jan;23(1):21-9 [15528977.001]
  • [Cites] Blood. 2005 Mar 1;105(5):2135-7 [15522957.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1306-15 [15735016.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4097-102 [15753301.001]
  • [Cites] J Biol Chem. 2005 Apr 1;280(13):12766-73 [15687498.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):251-62 [15803153.001]
  • [Cites] Oncogene. 1999 Dec 9;18(52):7514-26 [10602510.001]
  • [Cites] Cancer Res. 2000 Apr 1;60(7):1871-7 [10766174.001]
  • [Cites] Cancer Res. 2000 May 15;60(10):2680-8 [10825141.001]
  • [Cites] Cancer Chemother Pharmacol. 2000;46(1):79-83 [10912583.001]
  • [Cites] J Biol Chem. 2000 Sep 29;275(39):30451-7 [10852915.001]
  • [Cites] J Exp Med. 2000 Oct 16;192(8):1183-90 [11034608.001]
  • [Cites] J Clin Oncol. 2001 Feb 15;19(4):1167-75 [11181683.001]
  • [Cites] Blood. 2005 Nov 15;106(10):3532-7 [16051737.001]
  • [Cites] Nat Rev Immunol. 2006 May;6(5):358-70 [16639429.001]
  • [Cites] Annu Rev Med. 2007;58:329-46 [16987079.001]
  • [Cites] Blood Rev. 2007 Jul;21(4):173-82 [17293017.001]
  • [Cites] Blood. 2007 Sep 15;110(6):1982-8 [17545504.001]
  • [Cites] Curr Opin Pediatr. 2008 Feb;20(1):17-22 [18197034.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1404-12 [11222387.001]
  • (PMID = 18489761.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA44338
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / L 744832; 0 / Piperidines; 0 / Pyridines; 193275-84-2 / lonafarnib; AE28F7PNPL / Methionine; EC 2.5.1.29 / Farnesyltranstransferase
  • [Other-IDs] NLM/ PMC2409375
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4. Zamò A, Malpeli G, Scarpa A, Doglioni C, Chilosi M, Menestrina F: Expression of TP73L is a helpful diagnostic marker of primary mediastinal large B-cell lymphomas. Mod Pathol; 2005 Nov;18(11):1448-53
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  • [Title] Expression of TP73L is a helpful diagnostic marker of primary mediastinal large B-cell lymphomas.
  • Primary mediastinal large B-cell lymphoma is a well-defined lymphoma entity whose molecular pathogenesis is incompletely understood and also lacking well-established diagnostic markers.
  • Recently, the presence of overlapping features between classical Hodgkin's lymphoma and primary mediastinal large B-cell lymphoma was highlighted by gene expression profiling as well as morphological studies.
  • We investigated the expression of TP73L (commonly known as p63) isoforms in primary mediastinal large B-cell lymphoma at both protein and mRNA level, and demonstrated the exclusive presence of transactivating (TA) isoforms in all cases.
  • We also demonstrated that TP73L is expressed in a subset of germinal center B-cells, as well as in some diffuse large B-cell lymphomas, but it is never present in classical Hodgkin lymphoma.
  • Nodular lymphocyte predominant Hodgkin's lymphoma also showed TP73L positivity by immunohistochemistry.
  • Isoform analysis by real-time PCR showed that TA-TP73Lalpha is the most represented in primary mediastinal large B-cell lymphoma, but TA-TP73Lgamma is the most differentially expressed in comparison to both germinal center B-cells and diffuse large B-cell lymphomas.
  • TP73L expression proved a useful diagnostic marker of primary mediastinal large B-cell lymphoma, and gave new insights in to the molecular pathways playing a role in this lymphoma.
  • [MeSH-major] Hodgkin Disease / diagnosis. Lymphoma, B-Cell / diagnosis. Lymphoma, Large B-Cell, Diffuse / diagnosis. Mediastinal Neoplasms / diagnosis. Phosphoproteins / biosynthesis. Trans-Activators / biosynthesis
  • [MeSH-minor] Biomarkers, Tumor / analysis. DNA-Binding Proteins. Diagnosis, Differential. Gene Expression. Gene Expression Profiling. Genes, Tumor Suppressor. Humans. Immunohistochemistry. Protein Isoforms / biosynthesis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors. Tumor Suppressor Proteins

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  • [Copyright] Modern Pathology (2005) 18, 1448-1453. doi:10.1038/modpathol.3800440; published online 13 May 2005.
  • (PMID = 15920542.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
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5. Iskander K, Barrios RJ, Jaiswal AK: NRH:quinone oxidoreductase 2-deficient mice are highly susceptible to radiation-induced B-cell lymphomas. Clin Cancer Res; 2009 Mar 1;15(5):1534-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NRH:quinone oxidoreductase 2-deficient mice are highly susceptible to radiation-induced B-cell lymphomas.
  • Present studies investigated in vivo role of NQO2 in prevention of myeloproliferative disease and lymphomas.
  • EXPERIMENTAL DESIGN: Wild-type and NQO2-null mice were exposed to 0, 1, and 3 Gy gamma-radiation.
  • One year later, the mice were analyzed for the development of myeloproliferative disease and lymphomas.
  • Immunohistochemistry analysis determined the B- and T-cell origin of lymphomas.
  • The mice were also sacrificed at 6 and 48 h after radiation exposure and bone marrow was collected and analyzed for p53, Bax, and B-cell apoptosis.
  • Bone marrow cells were cultured and the rate of degradation of p53 was analyzed.
  • RESULTS: Seventy-two percent NQO2-null mice showed development of B-cell lymphomas in multiple tissues compared with 11% in wild-type mice exposed to 3 Gy gamma-radiation.
  • In contrast, only 22% NQO2-null mice showed myeloproliferation compared with none in wild-type mice.
  • Further analysis revealed that bone marrow from NQO2-null mice contained lower levels of p53 compared with wild-type mice due to rapid degradation of p53.
  • In addition, the exposure to radiation resulted in lower induction of p53 and Bax and decreased B-cell apoptosis in NQO2-null mice.
  • CONCLUSION: NQO2-null mice are highly susceptible to develop radiation-induced B-cell lymphomas.
  • The lack of significant induction of p53 and Bax and decrease in B-cell apoptosis presumably contributed to the development of lymphomas.
  • NQO2 functions as endogenous factor in prevention against radiation-induced B-cell lymphomas.

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  • [Cites] Cancer Res. 2000 Aug 1;60(15):4179-86 [10945627.001]
  • [Cites] Biochemistry. 1999 Aug 3;38(31):9881-6 [10433694.001]
  • [Cites] Chem Biol Interact. 2000 Dec 1;129(1-2):77-97 [11154736.001]
  • [Cites] J Natl Cancer Inst. 2001 Aug 1;93(15):1166-70 [11481389.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Nov 9;288(4):887-92 [11688992.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):3099-104 [11867746.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3030-6 [12036909.001]
  • [Cites] J Biol Chem. 2002 Nov 29;277(48):46131-9 [12351651.001]
  • [Cites] Tissue Antigens. 2003 Dec;62(6):483-91 [14617031.001]
  • [Cites] Methods Enzymol. 2004;378:221-38 [15038972.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):5925-8 [15342368.001]
  • [Cites] Free Radic Biol Med. 2004 Oct 15;37(8):1231-43 [15451063.001]
  • [Cites] Mutat Res. 1986 Apr;164(2):91-9 [3754306.001]
  • [Cites] Nat Genet. 1994 Sep;8(1):66-9 [7987394.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 4;94(5):1669-74 [9050836.001]
  • [Cites] Pharmacogenetics. 1999 Jun;9(3):413-8 [10471077.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2054-8 [15781611.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12513-8 [16113082.001]
  • [Cites] Free Radic Biol Med. 2006 May 15;40(10):1843-56 [16678022.001]
  • [Cites] J Biol Chem. 2006 Oct 13;281(41):30917-24 [16905546.001]
  • [Cites] Cancer Res. 2007 Jun 1;67(11):5380-8 [17545619.001]
  • [Cites] EMBO Rep. 2008 Jun;9(6):576-81 [18388957.001]
  • [Cites] Cancer Res. 2008 Oct 1;68(19):7915-22 [18829548.001]
  • [Cites] Arch Biochem Biophys. 1997 Nov 15;347(2):221-8 [9367528.001]
  • [Cites] J Biol Chem. 1998 Mar 27;273(13):7382-9 [9516435.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):5913-5 [11085502.001]
  • (PMID = 19223498.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA081057-08; United States / NIEHS NIH HHS / ES / R01 ES07943; United States / NCI NIH HHS / CA / R01 CA81057; United States / NIEHS NIH HHS / ES / ES007943-12; United States / NIEHS NIH HHS / ES / R01 ES007943; United States / NCI NIH HHS / CA / R01 CA081057; United States / NIEHS NIH HHS / ES / R01 ES007943-12; United States / NCI NIH HHS / CA / R01 CA081057-08
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bax protein, mouse; 0 / Tumor Suppressor Protein p53; 0 / bcl-2-Associated X Protein; EC 1.6.99.- / NRH - quinone oxidoreductase2; EC 1.6.99.- / Quinone Reductases
  • [Other-IDs] NLM/ NIHMS297132; NLM/ PMC3118578
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6. Amria S, Cameron C, Stuart R, Haque A: Defects in HLA class II antigen presentation in B-cell lymphomas. Leuk Lymphoma; 2008 Feb;49(2):353-5
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  • [Title] Defects in HLA class II antigen presentation in B-cell lymphomas.
  • [MeSH-major] Histocompatibility Antigens Class II. Lymphoma, B-Cell / immunology

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  • (PMID = 18231926.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Histocompatibility Antigens Class II
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7. Fan G, Molstad M, Braziel RM, Standley M, Huang J, Rodgers W, Nagalla S: Proteomic profiling of mature CD10+ B-cell lymphomas. Am J Clin Pathol; 2005 Dec;124(6):920-9
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  • [Title] Proteomic profiling of mature CD10+ B-cell lymphomas.
  • Proteomic profiling with protein-chip technology has been used successfully to discover biomarkers with potential clinical usefulness in several cancer types.
  • Little proteomic study has been done in B-cell lymphomas.
  • We determined whether the expression of a set of proteins by protein-chip technology coupled with new informatics tools could be used to build a model to molecularly classify B-cell lymphoma subgroups.
  • We used surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to analyze 18 CD10+ B-cell lymphomas, including 6 grade 1 (G1) follicular lymphomas (FLs), 7 grade 3 (G3) FLs, and 5 Burkitt lymphomas.
  • By using SAX2 ProteinChip arrays (Ciphergen Biosystems, Fremont, CA), we found a unique protein expression profile for each type of lesion.
  • Two-way hierarchical clustering analysis of these protein expression profiles differentiated reactive follicular hyperplasia, FL, and Burkitt lymphoma, with 5 major clusters of differentially expressed protein peaks.
  • To our knowledge, this is the first proteomic study using protein-chip technology for molecular classification of B-cell lymphoma subtypes with clinical samples.
  • [MeSH-major] Biomarkers, Tumor / analysis. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology. Neprilysin / metabolism. Protein Array Analysis

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  • (PMID = 16416742.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Histones; EC 3.4.24.11 / Neprilysin
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8. Catherwood MA, Venkatraman L: Follicular origin of a subset of CD5(+) diffuse large B-cell lymphomas. Am J Clin Pathol; 2006 Jun;125(6):954-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Follicular origin of a subset of CD5(+) diffuse large B-cell lymphomas.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Follicular / pathology. Lymphoma, Large B-Cell, Diffuse / pathology

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  • [CommentOn] Am J Clin Pathol. 2005 Aug;124(2):182-90 [16040287.001]
  • (PMID = 16761357.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / Biomarkers, Tumor
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9. Yang W, Listinsky CM: Aggressive B-cell lymphomas. Adv Exp Med Biol; 2005;563:125-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aggressive B-cell lymphomas.
  • [MeSH-major] Lymphoma, B-Cell / classification. Lymphoma, B-Cell / pathology
  • [MeSH-minor] Burkitt Lymphoma / pathology. Diagnosis, Differential. Humans. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / pathology. Mediastinal Neoplasms / pathology

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  • (PMID = 16433128.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 24
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10. Ortonne N: [Primary centrofollicular B-cell lymphomas]. Ann Dermatol Venereol; 2007 Aug-Sep;134(8-9):701-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary centrofollicular B-cell lymphomas].
  • [Transliterated title] Lymphomes B centrofolliculaires cutanés primitifs.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Lymphoma, Follicular / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] B-Lymphocytes / pathology. Biomarkers, Tumor / analysis. Cell Nucleolus / ultrastructure. Diagnosis, Differential. Humans. Immunohistochemistry. Molecular Biology

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  • (PMID = 17925703.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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11. Juszczyński P, Nowak J, Warzocha K: Host immune response in B-cell lymphomas: friend or foe? Arch Immunol Ther Exp (Warsz); 2008 Jul-Aug;56(4):245-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Host immune response in B-cell lymphomas: friend or foe?
  • The interaction of B-cell malignancies with the host immune system is a dynamic and bilateral process.
  • Certain lymphomas more commonly arise within a background of autoimmunity or chronic infection.
  • Initiation of these tumors is commonly reliant on antigenic stimulation and/or T-cell help.
  • Data obtained by studying gene-targeted animals and human lymphomas that support the critical role of the immune response in the initiation, progression, and immunoediting of lymphoid malignancies are summarized here.
  • A thorough understanding of this interaction will lead to the identification of more rational treatment targets and improved immunotherapies in B-cell lymphomas.
  • [MeSH-major] B-Lymphocytes / immunology. Immunologic Surveillance. Inflammation / immunology. Lymphoma, B-Cell / immunology. Tumor Escape
  • [MeSH-minor] Animals. CD4-Positive T-Lymphocytes / immunology. CD4-Positive T-Lymphocytes / metabolism. Cytokines / immunology. Cytokines / metabolism. Histocompatibility Antigens / immunology. Histocompatibility Antigens / metabolism. Humans. Killer Cells, Natural / immunology. Killer Cells, Natural / metabolism

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  • (PMID = 18726146.001).
  • [ISSN] 0004-069X
  • [Journal-full-title] Archivum immunologiae et therapiae experimentalis
  • [ISO-abbreviation] Arch. Immunol. Ther. Exp. (Warsz.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Cytokines; 0 / Histocompatibility Antigens
  • [Number-of-references] 103
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12. Marmey B, Boix C, Barbaroux JB, Dieu-Nosjean MC, Diebold J, Audouin J, Fridman WH, Mueller CG, Molina TJ: CD14 and CD169 expression in human lymph nodes and spleen: specific expansion of CD14+CD169- monocyte-derived cells in diffuse large B-cell lymphomas. Hum Pathol; 2006 Jan;37(1):68-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD14 and CD169 expression in human lymph nodes and spleen: specific expansion of CD14+CD169- monocyte-derived cells in diffuse large B-cell lymphomas.
  • The mononuclear phagocyte system of human lymphoid tissue comprises macrophages and dendritic cells (DCs).
  • The heterogeneity of the non-DC mononuclear phagocyte population in human lymphoid tissue has been little addressed.
  • Here, we studied the expression of 2 monocyte-derived markers, CD14 and CD169 (sialoadhesin), in reactive human lymphoid tissue as well as in a series of 51 B-cell lymphomas by immunohistochemistry on paraffin-embedded tissue.
  • We confirmed that lymph node sinusoidal monocyte-derived cells were the only population staining for CD169.
  • Although most sinusoidal histiocytes also expressed CD14, monocyte-derived cells with phagocytosis such as erythrophagocytosis, anthracosis, or tingible bodies macrophage lacked CD14 and CD169.
  • Among B-cell lymphomas, splenic marginal zone lymphoma was the only one associated with an expansion of the CD14(+)CD169(+) cells in the cords.
  • With respect to nodal B-cell lymphomas, CD14(+) cells were rare among B-chronic lymphocytic leukemia, follicular lymphoma (FL), mantle cell lymphoma (MCL).
  • However, strikingly, we found a strong expansion of CD14(+)CD169(-) cells in numerous diffuse large B-cell lymphomas (DLBCLs), except in cases associated with numerous mitoses, apoptotic bodies, and tingible bodies macrophages.
  • When cultivated in granulocyte/macrophage colony stimulating factor/interleukin 4, DLBCL purified CD14(+) cells differentiate into plasmacytoid cells, expressing DC-specific intercellular adhesion molecule 3-grabbing nonintegrin, suggesting dendritic cell differentiation potential.
  • [MeSH-major] Antigens, CD14 / metabolism. Lymph Nodes / metabolism. Lymphoma, B-Cell / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism. Membrane Glycoproteins / metabolism. Monocytes / metabolism. Receptors, Immunologic / metabolism. Spleen / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Cell Separation. Dendritic Cells / metabolism. Dendritic Cells / pathology. Flow Cytometry. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. Lymphadenitis / metabolism. Lymphadenitis / pathology. Sialic Acid Binding Ig-like Lectin 1

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  • (PMID = 16360418.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD14; 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic; 0 / SIGLEC1 protein, human; 0 / Sialic Acid Binding Ig-like Lectin 1
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13. Tari A, Asaoku H, Kashiwado K, Yoshino T, Kitadai Y, Tanaka S, Fujihara M: Predictive value of endoscopy and endoscopic ultrasonography for regression of gastric diffuse large B-cell lymphomas after Helicobacter pylori eradication. Dig Endosc; 2009 Oct;21(4):219-27
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Predictive value of endoscopy and endoscopic ultrasonography for regression of gastric diffuse large B-cell lymphomas after Helicobacter pylori eradication.
  • BACKGROUND: Some gastric diffuse large B-cell lymphomas have been reported to regress completely after the successful eradication of Helicobacter pylori.
  • The aim of this study was to investigate the clinical characteristics of gastric diffuse large B-cell lymphomas without any detectable mucosa-associated lymphoid tissue (MALT) lymphoma that went into complete remission after successful H. pylori eradication.
  • PATIENTS AND METHODS: We examined the effect of H. pylori eradication in 15 H. pylori-positive gastric diffuse large B-cell lymphoma patients without any evidence of an associated MALT lymphoma (clinical stage I by the Lugano classification) by endoscopic examination including biopsies, endoscopic ultrasonography, computed tomography, and bone marrow aspiration.
  • RESULTS: H. pylori eradication was successful in all the patients and complete remission was achieved in four patients whose clinical stage was I.
  • CONCLUSION: In gastric diffuse large B-cell lymphomas without a concomitant MALT lymphoma but associated with H. pylori infection, only superficial cases and lesions limited to the shallow portion of the submucosa regressed completely after successful H. pylori eradication.
  • The endoscopic appearance and the rating of the depth of invasion by endosonography are both valuable for predicting the efficacy of H. pylori eradication in treating gastric diffuse large B-cell lymphomas.
  • [MeSH-major] Endoscopy. Endosonography. Helicobacter Infections / drug therapy. Helicobacter pylori. Lymphoma, Large B-Cell, Diffuse / diagnosis. Stomach Neoplasms / diagnosis

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  • (PMID = 19961519.001).
  • [ISSN] 1443-1661
  • [Journal-full-title] Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society
  • [ISO-abbreviation] Dig Endosc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents
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14. Saleh MN, Pitot H, Maleski J, Leopold L, Forero A: Extended phase I trial of the oral pan-Bcl-2 inhibitor AT-101 by multiple dosing schedules in patients with advanced cancers. J Clin Oncol; 2009 May 20;27(15_suppl):e14537

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extended phase I trial of the oral pan-Bcl-2 inhibitor AT-101 by multiple dosing schedules in patients with advanced cancers.
  • : e14537 Background: Over-expression of Bcl-2 family proteins is common in human cancers.
  • Initial trials of the oral, pan-Bcl-2 inhibitor AT-101 showed acute dose limiting toxicity of Gr 3-4 AST/ALT (MTD 40 mg/d) and ileus with prolonged dosing daily (QD) for 21/28 days per cycle (Saleh, NCI/EORTC, 2005; James, ASCO, 2006 and Saleh, ASCO, 2007).
  • Stable disease was reported in 13/37 (35%) pts.
  • One pt with NSCLC continues on study with stable disease for 33 cycles and 2 additional pts were on study with stable disease for 18 and 9 cycles.

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  • (PMID = 27963553.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Johnston PB, LaPlant B, Kurtin P, Habermann T, Moore D, Nabbout N, Nikcevich D, Rowland K, Witzig T: Salvage chemotherapy with rituximab, oxaliplatin, cytosine arabinoside, and dexamethasone (ROAD) in patients with relapsed CD20+ aggressive B-cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8556

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Salvage chemotherapy with rituximab, oxaliplatin, cytosine arabinoside, and dexamethasone (ROAD) in patients with relapsed CD20+ aggressive B-cell lymphoma.
  • : 8556 Background: In the original PARMA trial it was demonstrated that salvage chemotherapy with DHAP followed by autologous bone marrow transplant resulted in increased overall survival over salvage chemotherapy with DHAP alone in patients with aggressive lymphomas.
  • Patients were considered for autologous stem cell transplantation after 2 cycles if eligible.
  • Eligible histologies included diffuse large B cell lymphoma, mantle cell lymphoma and transformed lymphoma in first relapse.
  • 31 patients experienced grade III/IV hematologic toxicity and 22 patients had grade III/IV non-hematologic toxicity, primarily febrile neutropenia.
  • One patient developed grade III nephrotoxicity due to disease progression.
  • CONCLUSIONS: ROAD is a safe and effective salvage chemotherapy regimen for relapsed aggressive lymphoma, including as a preparatory regimen prior to stem cell transplant.

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  • (PMID = 27960991.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Micallef IN, Maurer MJ, Nikcevich DA, Cannon MW, Schaefer EW, Moore DF, Kurtin P, Witzig TE: Final results of NCCTG N0489: Epratuzumab and rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy (ER-CHOP) in patients with previously untreated diffuse large B-cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8508

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Final results of NCCTG N0489: Epratuzumab and rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy (ER-CHOP) in patients with previously untreated diffuse large B-cell lymphoma.
  • : 8508 Background: A prior pilot study of epratuzumab (Immunomedics) and rituximab in combination with CHOP chemotherapy (ER-CHOP) in untreated patients with diffuse large B-cell lymphoma demonstrated feasibility and safety.

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  • (PMID = 27960859.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Barth TF, Barth CA, Kestler HA, Michl P, Weniger MA, Buchholz M, Möller P, Gress T: Transcriptional profiling suggests that secondary and primary large B-cell lymphomas of the gastrointestinal (GI) tract are blastic variants of GI marginal zone lymphoma. J Pathol; 2007 Feb;211(3):305-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transcriptional profiling suggests that secondary and primary large B-cell lymphomas of the gastrointestinal (GI) tract are blastic variants of GI marginal zone lymphoma.
  • The pathogenetic relationship of marginal zone B-cell lymphoma (MALT lymphoma) of the gastrointestinal (GI) tract and eventually co-existing aggressive B-cell lymphoma and primary aggressive B-cell lymphoma remains to be elucidated.
  • The RNA of laser-microdissected cells was isolated and amplified from small and/or large cell compartments of eight MALT lymphomas (small cell lymphoma, SCL), 14 GI diffuse large B-cell lymphomas (large cell lymphoma, LCL), and ten GI B-cell lymphomas with composite small and large cell compartments (ComL) and expression analyses were performed using cDNA arrays.
  • Hierarchical cluster analysis clearly separated SCL and LCL and the small and large cell compartments of ComL.
  • Likewise, cluster analysis with all samples of SCL, LCL, and ComL yielded two main 'small cell' and 'large cell' branches.
  • Furthermore, 60 genes were differentially expressed between SCL and LCL, and 82 genes between the small and large cell components of ComL; 26 genes were discriminators in both settings.
  • Collectively, the data strongly suggest that both secondary and primary aggressive B-cell lymphomas of the GI tract are blastic marginal zone lymphomas.
  • [MeSH-major] Gastrointestinal Neoplasms / genetics. Gene Expression Profiling. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Oligonucleotide Array Sequence Analysis. Transcription, Genetic
  • [MeSH-minor] Genetic Markers. Humans. Immunohistochemistry / methods. In Situ Hybridization, Fluorescence. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Copyright 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
  • (PMID = 17152084.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
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18. Hernandez-Ilizaliturri FJ, Khubchandani S, Olejniczak SH, Hoskin P, Czuczman MS: Strategies to overcoming rituximab-chemotherapy resistance by targeting the autophagy pathway using bortezomib in combination with the Bcl-2 inhibitor obatoclax in non-Hodgkin's lymphomas (NHL). J Clin Oncol; 2009 May 20;27(15_suppl):8543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Strategies to overcoming rituximab-chemotherapy resistance by targeting the autophagy pathway using bortezomib in combination with the Bcl-2 inhibitor obatoclax in non-Hodgkin's lymphomas (NHL).
  • : 8543 We found that repeated rituximab exposure leads to deregulation of Bcl-2 proteins and concomitant chemotherapy resistance.
  • We demonstrated that obatoclax (O), a potent Bcl-2 inhibitor, enhanced the anti-tumor activity of rituximab or chemotherapy agents.
  • The proteasome is known to regulate Bcl-2 family members expression.
  • In the current work we study the interactions between bortezomib (B) and O against B-cell NHL.
  • Studies were conducted in rituximab sensitive (RSCL) and resistant cell lines (RRCL), as well as in malignant B-cells derived from patients with NHL (n = 20).
  • Cells were exposed in vitro to escalating doses of O with/without B.
  • Cell death was determined by the Cell glow luminescent assay and DNA synthesis by [<sup>3</sup>H]-Thymidine incorporation.
  • O or B monotherapy induced time- and dose-dependent cell death of all cells tested.
  • In vitro exposure of RRCL, RSCL and lymphoma specimens to O and B resulted in significant synergistic activity.
  • In vitro exposure of NHL cells to O lead to p53 degradation and Noxa or PUMA induction; while exposure to B resulted in Bax upregulation and Mcl-1 downregulation.
  • Inhibition of caspase activity did not affect the ability of O or B to kill NHL cells.
  • Induction of autophagy was detected by LC3 conversion and EM not only in RSCL or RRCL but also in patient-derived tumor cells.
  • Additionally, cell death induced by O could be inhibited by knock-down of Beclin-1 or p53.

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  • (PMID = 27960960.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Morales D, Beltran B, Hurtado de Mendoza F, Riva L, Quiñones P: Analysis of prognostic factors in patients with EBV positive diffuse large B cell lymphoma of the elderly. J Clin Oncol; 2009 May 20;27(15_suppl):e19542

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of prognostic factors in patients with EBV positive diffuse large B cell lymphoma of the elderly.
  • : e19542 Background: EBV positive diffuse large B cell lymphoma of the elderly is a new entity included in the Fourth edition of WHO Classification.
  • AIM: The goal of this study was to evaluate clinical characteristics and survival of EBV positive diffuse large B cell lymphoma of the elderly from Peruvian patients.
  • METHODS: Between January 2002 and June 2008, eleven patients with EBV positive diffuse large B cell lymphoma of the elderly were included in the analysis.
  • All cases were positive to the presence of EBV encoded RNA (EBER) by CISH and CD20 and/or Pax-5 expression by immunohistochemistry.Clinical data were reviewed retrospectively and patient's biopsies were analyzed for the immunohistochemical expression of BCL6, CD10, CD30 and MUM-1/IRF4 by tissue microarray (TMA) technique..
  • Extranodal disease occurred in 6/11 (54%) patients: pleura (n=2), suprarenal gland (n=1), stomach (n=1), cecum (n=1), bone (1), skin (1) and bone marrow (n=1).
  • Ten cases (83%) were of the Non-GC and 1 case was GC.
  • Complete response (n=2), partial response (n=0) and progressive disease (n=3).
  • CONCLUSIONS: EBV positive diffuse large B cell lymphoma of the elderly was related to high IPI, poor ECOG, frequent extranodal disease, poor response to treatment and very short survival.
  • It is the first report of this entity in a non-Asian population.

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  • (PMID = 27960995.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Roberts AW, Wilson W, Gandhi L, O'Connor OA, Rudin CM, Brown JR, Xiong H, Chiu Y, Enschede S, Krivoshik AP: Ongoing phase I studies of ABT-263: Mitigating Bcl-X&lt;sub&gt;L&lt;/sub&gt; induced thrombocytopenia with lead-in and continuous dosing. J Clin Oncol; 2009 May 20;27(15_suppl):3505

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ongoing phase I studies of ABT-263: Mitigating Bcl-X<sub>L</sub> induced thrombocytopenia with lead-in and continuous dosing.
  • : 3505 Background: ABT-263, a novel, oral BH3 mimetic, potently inhibits multiple antiapoptotic Bcl-2 family proteins.
  • Ongoing phase 1 studies of ABT-263 show anti-tumor activity in CLL and some lymphomas (Wilson W et al, ASH. 2008).
  • However, thrombocytopenia (TCP) due to on-target Bcl-X<sub>L</sub> inhibition-induced platelet apoptosis is also observed.

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  • (PMID = 27961281.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Jeevangi N, Joshi A, Shah M, Kannan S, Gupta S, Nair R, Khattry N: Results of autologous transplants for lymphomas from a tertiary cancer center in India. J Clin Oncol; 2009 May 20;27(15_suppl):7106

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results of autologous transplants for lymphomas from a tertiary cancer center in India.
  • : 7106 Background: Autologous stem cell transplanation is the standard of care for patients of relapsed and refractory non-Hodgkin's lymphoma (NHL) and Hodgkin's lymphoma (HL).
  • We report the results of transplants in lymphomas from our center and role of possible prognostic factors.
  • Seventy eight percent of patients received peripheral blood stem cells (PBSC), 8% bone marrow (BM) and 14% both PBSC and BM.
  • Prognostic factors evaluated for progression free survival (PFS) were serum albumin level and body mass index (BMI) at the time of transplant, stage at diagnosis and source of stem cells, while for over all survival (OS), status of disease at transplant was also included.
  • RESULTS: The median time to transplant was 2.25 years from the time of diagnosis.
  • At the time of transplant, thirty two percent were in complete remission (CR), 50% in partial remission (PR) and 18% had refractory disease (RD).
  • The best disease response rate was 86% (CR+PR) in patients evaluable for response.
  • CONCLUSIONS: These data provide the first published report of outcomes of autologous transplants in lymphomas from India.
  • Our data suggests that serum albumin level at the time of transplant and stem cell source are important prognostic factors for PFS and OS.

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  • (PMID = 27961648.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Ehinger M, Linderoth J, Christensson B, Sander B, Cavallin-Ståhl E: A subset of CD5- diffuse large B-cell lymphomas expresses nuclear cyclin D1 with aberrations at the CCND1 locus. Am J Clin Pathol; 2008 Apr;129(4):630-8
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  • [Title] A subset of CD5- diffuse large B-cell lymphomas expresses nuclear cyclin D1 with aberrations at the CCND1 locus.
  • In 231 diffuse large B-cell lymphomas, the expression of cyclin D1 and CD5 was evaluated.
  • In another case, the telomeric probe signal for cyclin D1 was lost in most tumor cells, and in a small proportion of the cells, there were fluorescence signals indicative of the t(11;14).
  • All cases but 1 were positive for bcl-6 or MUM1, disfavoring the possibility of misdiagnosed blastoid variants of CD5- mantle cell lymphomas.
  • Thus, contrary to the current view, there seems to exist a certain number of cyclin D1+ and CD5- diffuse large B-cell lymphomas, some of which have structural aberrations at the CCND1 locus, including the t(11;14).
  • [MeSH-major] Antigens, CD5 / metabolism. Cell Nucleus / metabolism. Chromosome Aberrations. Cyclins / metabolism. Lymphoma, Large B-Cell, Diffuse / metabolism
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Count. Cyclin D. DNA, Neoplasm / analysis. DNA-Binding Proteins / metabolism. Female. Fluorescent Antibody Technique, Direct. Humans. Immunoenzyme Techniques. In Situ Hybridization, Fluorescence. Interferon Regulatory Factors / metabolism. Male. Middle Aged

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  • (PMID = 18343791.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD5; 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / Cyclin D; 0 / Cyclins; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / interferon regulatory factor-4
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23. Maza S, Gellrich S, Assaf C, Beyer M, Spilker L, Orawa H, Munz DL, Sterry W, Steinhoff M: Yttrium-90 ibritumomab tiuxetan radioimmunotherapy in primary cutaneous B-cell lymphomas: first results of a prospective, monocentre study. Leuk Lymphoma; 2008 Sep;49(9):1702-9
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  • [Title] Yttrium-90 ibritumomab tiuxetan radioimmunotherapy in primary cutaneous B-cell lymphomas: first results of a prospective, monocentre study.
  • Radioimmunotherapy with Yttrium-90 ((90)Y) ibritumomab tiuxetan (IT) has been shown to be effective in systemic B-cell lymphomas.
  • We conducted a pilot study to evaluate the outcome and assess complications of (90)Y IT therapy in patients with primary cutaneous B-cell lymphomas (PCBCL).
  • Radioimmunotherapy with (90)Y IT is an effective treatment in relapsed primary cutaneous follicle centre lymphomas and diffuse large B-cell lymphoma leg-type.
  • Further investigations in controlled randomised clinical trials evaluating the role of (90)Y IT versus rituximab in PCBCL are needed.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Lymphoma, B-Cell / radiotherapy. Radioimmunotherapy / methods. Skin Neoplasms / radiotherapy. Yttrium Radioisotopes / therapeutic use
  • [MeSH-minor] Aged. Aged, 80 and over. Disease-Free Survival. Female. Humans. Male. Middle Aged. Pilot Projects. Remission Induction. Salvage Therapy. Treatment Outcome

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  • (PMID = 18661405.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Yttrium Radioisotopes; 0 / ibritumomab tiuxetan
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24. Zintzaras E, Bai M, Douligeris C, Kowald A, Kanavaros P: A tree-based decision rule for identifying profile groups of cases without predefined classes: application in diffuse large B-cell lymphomas. Comput Biol Med; 2007 May;37(5):637-41
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  • [Title] A tree-based decision rule for identifying profile groups of cases without predefined classes: application in diffuse large B-cell lymphomas.
  • The technique was applied for the identification of low and high proliferation profile groups of diffuse large B-cell lymphomas according to the immunohistochemical expression levels of proliferation proteins.
  • The methodology was applied to the histology data from 79 cases of diffuse large B-cell lymphomas.
  • [MeSH-major] Decision Trees. Lymphoma, B-Cell / classification. Lymphoma, Large B-Cell, Diffuse / classification

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  • (PMID = 16895724.001).
  • [ISSN] 0010-4825
  • [Journal-full-title] Computers in biology and medicine
  • [ISO-abbreviation] Comput. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin A; 0 / Cyclin B; 0 / Ki-67 Antigen
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25. Soufla G, Baritaki S, Sifakis S, Zafiropulos A, Spandidos DA: Transcriptional inactivation of p53, Bax, Bcl-2 and Mdm2 correlates with malignant transformation of the uterine cervix. Int J Biol Markers; 2005 Jan - Mar;20(1):18-27
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  • [Title] Transcriptional inactivation of p53, Bax, Bcl-2 and Mdm2 correlates with malignant transformation of the uterine cervix.
  • : Deregulation of the apoptotic machinery plays a major role in cell death, cellular transformation and cancer. p53, Bcl-2, Bcl-XL, Bax and Mdm2 mRNA expression patterns were evaluated in tissue samples with cervical intraepithelial neoplasia (CIN) and cervical cancer compared to those of normal cervical tissues, and correlated with the underlying cervical lesions.
  • Transcript levels of the above genes were assessed by RT-PCR analysis in a total of 44 cervical specimens. p53, Bcl-2, Bax and Mdm2 transcript levels were significantly different in the normal, CIN and cancer specimen groups (p=0.003, p=0.009, p=0.040 and p=0.001, respectively).
  • Specifically, p53, Bax and Bcl-2 exhibited substantially lower transcript levels in CIN lesions compared to controls, whereas Bax mRNA levels showed a significant decrease in cancer compared to normal specimens.
  • High-grade squamous intraepithelial lesions exhibited lower p53 and Bcl-2 mRNA levels than controls (p=0.002, p=0.016).
  • Coexpression analysis revealed more correlations between the above apoptosis-related molecules in normal tissues compared to CIN or cancer specimens. p53 showed significant coexpression with Bax, Bcl-2 and Mdm2 (p=0.040, p=0.013 and p=0.015, respectively) in normal cervical specimens.
  • Bax and Bcl-XL mRNA expression was negatively correlated.
  • Mdm2 transcriptional levels correlated significantly with those of Bax, Bcl-XL and Bcl-2.
  • Our findings show that p53, Bax, Bcl-2 and Mdm2 mRNA expression levels correlate with the malignant transformation of the uterine cervix. mRNA coexpression patterns of the members of the pro- and anti-apoptotic family examined in cervical carcinogenesis were found to be disrupted in CIN and cancer, as already demonstrated at the protein level. (Int J Biol Markers 2005; 20: 18-27).

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  • (PMID = 28207100.001).
  • [ISSN] 1724-6008
  • [Journal-full-title] The International journal of biological markers
  • [ISO-abbreviation] Int. J. Biol. Markers
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
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26. Fiveash JB, Chowdhary SA, Peereboom D Jr, Mikkelsen T, Nabors LB, Lesser GJ, Rosenfeld MR, Ye X, Grossman SA: NABTT-0702: A phase II study of R-(-)-gossypol (AT-101) in recurrent glioblastoma multiforme (GBM). J Clin Oncol; 2009 May 20;27(15_suppl):2010

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  • : 2010 Background: R-(-)-gossypol (AT-101) is an oral bcl-2 family protein inhibitor (Bcl-2, Bcl-X<sub>L</sub>, Mcl-1, Bcl-W) and potent inducer of proapoptotic proteins.
  • A prior study of racemic gossypol demonstrated objective responses in patients with malignant glioma.
  • METHODS: Fifty-six patients with recurrent GBM were enrolled in this multi-institution phase II clinical trial through the NABTT CNS consortium designed to detect a 33% increase in overall survival (OS, primary endpoint) from 5 to 6.65 months with Power/Alpha 80%/0.01.
  • Seven patients (16%) had stable disease as the best response.

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  • (PMID = 27964593.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Pitot HC, Mould D, Maleski J, Leopold L: Analysis of a phase I pharmacokinetic (PK)/food effect study of AT-101 in patients with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):2557

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  • : 2557 Background: AT-101 is an oral, pan-Bcl-2 inhibitor (Bcl-2, Bcl-XL, Bcl-W, Mcl-1).
  • Overexpression of Bcl-2 family proteins is common in human cancers.

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  • (PMID = 27961871.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Goteri G, Ranaldi R, Simonetti O, Capretti R, Menzo S, Stramazzotti D, Morichetti D, Offidani AM, Rupoli S, Leoni P: Clinicopathological features of primary cutaneous B-cell lymphomas from an academic regional hospital in central Italy: no evidence of Borrelia burgdorferi association. Leuk Lymphoma; 2007 Nov;48(11):2184-8
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  • [Title] Clinicopathological features of primary cutaneous B-cell lymphomas from an academic regional hospital in central Italy: no evidence of Borrelia burgdorferi association.
  • We reviewed the clinico-pathological features of 73 primary cutaneous B-cell lymphomas (PCBCLs), diagnosed in 10 years in Marche region in central Italy, which included 16 marginal zone lymphomas (MZL), 33 follicle centre lymphomas (FCL) and 24 diffuse large B cell lymphomas (DLBCL).
  • Differences in age, sex, location site, response to therapy, disease recurrence and 5-year disease-specific survival were observed among the 3 histological groups.
  • [MeSH-major] Borrelia burgdorferi / isolation & purification. Lymphoma, B-Cell / etiology. Lymphoma, B-Cell / microbiology. Skin Neoplasms / etiology. Skin Neoplasms / microbiology

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  • (PMID = 17926178.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Bacterial
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29. Tzankov A, Heiss S, Ebner S, Sterlacci W, Schaefer G, Augustin F, Fiegl M, Dirnhofer S: Angiogenesis in nodal B cell lymphomas: a high throughput study. J Clin Pathol; 2007 May;60(5):476-82
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  • [Title] Angiogenesis in nodal B cell lymphomas: a high throughput study.
  • AIM: To assess the biological significance of vascular endothelial growth factor (VEGF) A, VEGF receptor (Flk-1) and cyclooxygenase 2 (COX2) expression with respect to microvessel density (MVD), proliferative activity (Ki-67), expression of p53 and clinical presentation in a large cohort of nodal B cell lymphomas.
  • METHODS: An immunohistochemical and morphometric study was performed on a validated tissue microarray containing 271 B cell lymphoma specimens, 197 of which included follow-up data.
  • Strong VEGF expression was observed in only 20 diffuse large B cell lymphomas (DLBCLs).
  • Flk-1 and COX2 were expressed in 53 and 21 cases, respectively, mainly in DLBCLs, follicular lymphoma (FL) grade 3 and mantle cell lymphomas (MCLs), in a low proportion of cells.
  • MVD decreased in the following order: DLBCLs, FLs, MCLs and small lymphocytic lymphomas/chronic lymphocytic leukaemia (SLL/CLLs).
  • The analysed angiogenesis parameters did not correlate with clinical parameters or survival.
  • CONCLUSIONS: Angiogenesis plays a differential role in various B cell lymphomas.
  • Aggressive lymphomas express the potential molecular therapeutic targets VEGF and COX2, and have higher MVD.
  • In a few low proliferation-fraction lymphomas, Flk-1 might have a role in proliferative advantage.
  • Therapeutic strategies aimed at angiogenesis should take into account lymphoma heterogeneity.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Lymphoma, B-Cell / metabolism. Neovascularization, Pathologic / metabolism
  • [MeSH-minor] Aged. Cell Proliferation. Cyclooxygenase 2 / metabolism. Female. Humans. Immunoenzyme Techniques. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Mantle-Cell / metabolism. Lymphoma, Mantle-Cell / pathology. Male. Microcirculation / pathology. Middle Aged. Neoplasm Proteins / metabolism. Survival Analysis. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism

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  • [Cites] Leuk Lymphoma. 2003 Dec;44(12):2089-93 [14959852.001]
  • [Cites] Cancer. 2004 Mar 15;100(6):1186-9 [15022285.001]
  • [Cites] Semin Oncol. 2004 Apr;31(2 Suppl 7):2-11 [15179620.001]
  • [Cites] World J Gastroenterol. 2004 Jul 1;10(13):1862-6 [15222024.001]
  • [Cites] N Engl J Med. 2004 Jul 15;351(3):250-9 [15254283.001]
  • [Cites] Leuk Lymphoma. 2004 Jul;45(7):1395-9 [15359639.001]
  • [Cites] Lab Invest. 2004 Nov;84(11):1512-9 [15311211.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2893-902 [15238424.001]
  • [Cites] EMBO J. 1990 May;9(5):1595-602 [1691710.001]
  • [Cites] Anticancer Res. 1990 Mar-Apr;10(2A):401-6 [1693265.001]
  • [Cites] Am J Pathol. 1995 Jul;147(1):9-19 [7541613.001]
  • [Cites] Cell. 1996 Dec 27;87(7):1153-5 [8980221.001]
  • [Cites] J Pathol. 1997 Sep;183(1):44-50 [9370946.001]
  • [Cites] Am J Respir Cell Mol Biol. 1997 Dec;17(6):748-56 [9409562.001]
  • [Cites] Cancer Res. 1999 Feb 1;59(3):728-33 [9973224.001]
  • [Cites] Br J Cancer. 1999 Feb;79(5-6):965-70 [10070898.001]
  • [Cites] J Biol Chem. 1999 Apr 16;274(16):10911-5 [10196169.001]
  • [Cites] J Pathol. 1998 Nov;186(3):313-8 [10211122.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):154-61 [15671540.001]
  • [Cites] Blood. 2005 Feb 15;105(4):1383-95 [15471951.001]
  • [Cites] Folia Histochem Cytobiol. 2004;42(4):241-3 [15704651.001]
  • [Cites] Ann Hematol. 2005 Aug;84(8):510-6 [15834569.001]
  • [Cites] Exp Gerontol. 2005 Aug-Sep;40(8-9):737-44 [16125349.001]
  • [Cites] Curr Opin Oncol. 2005 Nov;17(6):611-6 [16224242.001]
  • [Cites] Eur J Haematol. 2005 Dec;75(6):485-91 [16313260.001]
  • [Cites] Eur J Haematol. 2006 Jan;76(1):42-50 [16343270.001]
  • [Cites] J Clin Pathol. 2006 Jan;59(1):48-55 [16394280.001]
  • [Cites] Leuk Lymphoma. 2009 May;50(5):728-35 [19373598.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2002 Dec;10(4):316-21 [12607599.001]
  • [Cites] Ann Diagn Pathol. 2003 Feb;7(1):1-8 [12616467.001]
  • [Cites] Blood. 2000 Jul 1;96(1):282-7 [10891463.001]
  • [Cites] Blood. 2000 Dec 1;96(12):3712-8 [11090051.001]
  • [Cites] Med Oncol. 2000 Nov;17(4):314-8 [11114711.001]
  • [Cites] APMIS. 2001 Jan;109(1):66-72 [11297195.001]
  • [Cites] Leuk Lymphoma. 2000 Dec;40(1-2):157-66 [11426617.001]
  • [Cites] Histopathology. 2002 Mar;40(3):253-60 [11895491.001]
  • [Cites] J Histochem Cytochem. 2002 Apr;50(4):533-40 [11897806.001]
  • [Cites] Histopathology. 2002 Oct;41(4):322-30 [12383214.001]
  • [Cites] Anticancer Res. 2002 Sep-Oct;22(5):2899-901 [12530014.001]
  • [Cites] Br J Cancer. 2003 Feb 24;88(4):553-9 [12592369.001]
  • [Cites] Cancer. 2003 Jun 1;97(11):2767-75 [12767089.001]
  • [Cites] Leuk Res. 2004 Feb;28(2):179-90 [14654083.001]
  • (PMID = 16790692.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC1994554
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30. Adams H, Tzankov A, d'Hondt S, Jundt G, Dirnhofer S, Went P: Primary diffuse large B-cell lymphomas of the bone: prognostic relevance of protein expression and clinical factors. Hum Pathol; 2008 Sep;39(9):1323-30
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  • [Title] Primary diffuse large B-cell lymphomas of the bone: prognostic relevance of protein expression and clinical factors.
  • Diffuse large B-cell lymphomas can be considered primary bone tumors if they are monostotic or polyostotic, affecting multiple skeletal sites without visceral or lymph node involvement.
  • They are rarely considered as extranodal lymphomas or as bone tumors, respectively.
  • To elucidate the prognostic relevance of clinicopathologic characteristics in such disease, we collected a cohort of primary diffuse large B-cell lymphomas of the bone and retrospectively investigated 33 patients.
  • Disease stage was I and II in 30 and IV in 3 patients.
  • Clinical factors favoring a good prognosis were age younger than 53 and administration of chemotherapy.
  • Of the phenotypic markers analyzed (CD10, CD44s, CD138, Bcl-2, Bcl-6, MUM1, and Ki-67), MUM1 expression in more than 10% of the tumor cells and CD10 expression in less than 55% as well as a nongerminal center signature substantiated adverse outcome in a univariate model.
  • [MeSH-major] Bone Neoplasms / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Adult. Aged, 80 and over. Child, Preschool. Cohort Studies. Female. Gene Expression. Gene Rearrangement, B-Lymphocyte. Humans. In Situ Hybridization, Fluorescence. Interferon Regulatory Factors / biosynthesis. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Prognosis. Proto-Oncogene Proteins c-bcl-2 / genetics. Retrospective Studies. Survival Analysis

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  • (PMID = 18614198.001).
  • [ISSN] 1532-8392
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / interferon regulatory factor-4
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31. de la Fouchardière A, Balme B, Chouvet B, Perrot H, Thomas L, Claudy A, Felman P, Salles G, Coiffier B, Berger F: [Pathological and clinical correlations in primary cutaneous B-cell lymphomas: a series of 44 cases]. Ann Pathol; 2005 Feb;25(1):8-17
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  • [Title] [Pathological and clinical correlations in primary cutaneous B-cell lymphomas: a series of 44 cases].
  • [Transliterated title] Lymphomes B cutanés primitifs: corrélations anatomo-cliniques dans une série de 44 cas.
  • AIMS: histological and clinical relationship study of 44 cases of primary cutaneous B cell lymphoma, classified according to WHO classification.
  • MATERIALS AND METHODS: histological, immunological and molecular analysis was correlated with clinical data.
  • RESULTS: 33 cases (75%) were marginal zone B-cell lymphomas (MZL), with head and trunk predominance (median age = 54 years).
  • 9 (20%) diffuse large B-cell lymphomas (DLBCL) appeared as a unique nodule, with female predominance (median age = 74 years) and 4 lymphoma-related deaths which seemed age-related (> 70 years) with only one lower limb localization.
  • 2 (5%) WHO grade 3 follicular lymphomas (FL) had an heterogeneous phenotype, with head localization, cutaneous relapses and good outcome.
  • CONCLUSIONS: MZL, the predominant type, has a good prognosis, although transformation can occur, needing a more aggressive treatment.
  • DLBCL, observed in older patients, has clinical and histological prognostic factors identical to extra-cutaneous lymphomas.
  • [MeSH-major] Lymphoma, B-Cell / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. DNA, Neoplasm / analysis. Fatal Outcome. Female. Humans. Immunohistochemistry. Immunophenotyping. Lymphoma, Follicular / genetics. Lymphoma, Follicular / pathology. Lymphoma, Follicular / therapy. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large B-Cell, Diffuse / therapy. Male. Middle Aged. Neoplasm Recurrence, Local. Polymerase Chain Reaction. Radiotherapy. Remission Induction. Surgical Procedures, Operative

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  • (PMID = 15981927.001).
  • [ISSN] 0242-6498
  • [Journal-full-title] Annales de pathologie
  • [ISO-abbreviation] Ann Pathol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm
  • [Number-of-references] 33
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32. Sevilla DW, Weeden EM, Alexander S, Murty VV, Alobeid B, Bhagat G: Nodular pattern of bone marrow infiltration: frequent finding in immunosuppression-related EBV-associated large B-cell lymphomas. Virchows Arch; 2009 Oct;455(4):323-36
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  • [Title] Nodular pattern of bone marrow infiltration: frequent finding in immunosuppression-related EBV-associated large B-cell lymphomas.
  • Different patterns of bone marrow (BM) infiltration by diffuse large B cell lymphomas (DLBCL) have been described.
  • A pure nodular pattern is uncommon, and the pathologic features, as well as the clinical correlates of DLBCL manifesting this pattern in the BM have not been well characterized.
  • We evaluated BM biopsies involved by large B cell lymphomas diagnosed at our institute over an 11-year period to assess the morphology, phenotype, cytogenetic abnormalities, and clinical features of cases associated with a nodular pattern.
  • The majority of EBV+ DLBCL associated with a nodular pattern had distinctive morphologic features (polymorphic cellular infiltrate and pleomorphic cytology), and CD30 expression was more commonly observed in this group (P = 0.0163).
  • Our study indicates a much higher predilection for EBV+ DLBCL to involve the marrow in a nodular pattern compared to EBV- cases and highlights similarities in the morphologic pattern of BM involvement by previously recognized subsets of immunodeficiency-related EBV + lymphomas and the newer entity of "EBV+ DLBCL of the elderly. "
  • [MeSH-major] Bone Marrow / pathology. Herpesvirus 4, Human / isolation & purification. Lymphoma, Large B-Cell, Diffuse / pathology

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  • [Cites] Clin Cancer Res. 2007 Sep 1;13(17):5124-32 [17785567.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Virchows Arch. 2005 Dec;447(6):920-37 [16231177.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1163-72 [1694234.001]
  • [Cites] Am J Surg Pathol. 2003 Jan;27(1):16-26 [12502924.001]
  • [Cites] J Exp Med. 2006 Feb 20;203(2):311-7 [16492805.001]
  • [Cites] Am J Surg Pathol. 2002 Nov;26(11):1458-66 [12409722.001]
  • [Cites] J Clin Exp Hematop. 2006 Mar;46(1):1-4 [17058802.001]
  • [Cites] J Korean Med Sci. 2008 Apr;23(2):185-92 [18436998.001]
  • [Cites] Jpn J Cancer Res. 2000 Dec;91(12):1233-40 [11123421.001]
  • [Cites] J Pathol. 1995 Mar;175(3):263-71 [7745495.001]
  • [Cites] Cancer Genet Cytogenet. 2002 Jan 15;132(2):125-32 [11850073.001]
  • [Cites] Am J Surg Pathol. 2003 Mar;27(3):293-302 [12604885.001]
  • [Cites] J Clin Pathol. 1992 Sep;45(9):745-50 [1401199.001]
  • [Cites] Am J Surg Pathol. 1996 Oct;20(10):1279-87 [8827036.001]
  • [Cites] Korean J Lab Med. 2007 Dec;27(6):383-7 [18160826.001]
  • [Cites] Am J Clin Pathol. 1994 Mar;101(3):305-11 [8135186.001]
  • [Cites] Mech Ageing Dev. 2003 Apr;124(4):477-85 [12714256.001]
  • [Cites] Cancer. 2002 Jun 15;94(12):3083-8 [12115338.001]
  • [Cites] Am J Surg Pathol. 2003 Jul;27(7):903-11 [12826882.001]
  • [Cites] Leuk Lymphoma. 2006 Aug;47(8):1667-9 [16966281.001]
  • [Cites] Cancer Sci. 2008 Jun;99(6):1085-91 [18429953.001]
  • [Cites] Am J Pathol. 1993 Oct;143(4):1072-85 [8214003.001]
  • [Cites] Cancer. 1982 Mar 1;49(5):888-97 [6977408.001]
  • [Cites] Am J Hematol. 2007 Oct;82(10):893-7 [17573693.001]
  • [Cites] Blood. 2007 Aug 1;110(3):972-8 [17400912.001]
  • [Cites] Blood. 2007 Mar 15;109(6):2571-8 [17119113.001]
  • [Cites] Arch Pathol Lab Med. 2007 May;131(5):742-7 [17488159.001]
  • [Cites] Leukemia. 2007 Jul;21(7):1532-44 [17495977.001]
  • [Cites] Eur J Haematol. 2004 Sep;73(3):149-55 [15287910.001]
  • [Cites] Am J Pathol. 1997 Feb;150(2):543-62 [9033270.001]
  • [Cites] Br J Haematol. 1988 Jun;69(2):229-37 [3291929.001]
  • [Cites] Am J Surg Pathol. 2005 Nov;29(11):1411-21 [16224207.001]
  • [Cites] Am J Hematol. 1996 May;52(1):21-8 [8638607.001]
  • [Cites] J Pathol. 1999 Jun;188(2):133-8 [10398155.001]
  • [Cites] Haematologica. 2006 Oct;91(10):1313-20 [17018379.001]
  • [Cites] Leukemia. 2003 Dec;17(12):2257-317 [14671650.001]
  • [Cites] Nat Rev Immunol. 2009 Jan;9(1):57-62 [19104499.001]
  • [Cites] N Engl J Med. 2000 Aug 17;343(7):481-92 [10944566.001]
  • [Cites] Hematol Oncol Clin North Am. 1988 Dec;2(4):617-35 [3065322.001]
  • [Cites] Cancer Sci. 2006 Feb;97(2):163-6 [16441428.001]
  • [Cites] Neuropathology. 2008 Dec;28(6):640-4 [18410281.001]
  • [Cites] Am J Clin Pathol. 1997 Nov;108(5):570-8 [9353097.001]
  • [Cites] Lab Invest. 2001 Apr;81(4):429-37 [11304562.001]
  • [Cites] Eur J Haematol. 2006 Jun;76(6):473-80 [16529599.001]
  • [Cites] Hematol Oncol. 2008 Dec;26(4):199-211 [18457340.001]
  • [Cites] Am J Transplant. 2008 May;8(5):1016-24 [18312608.001]
  • [Cites] Am J Surg Pathol. 2005 Dec;29(12):1549-57 [16327427.001]
  • (PMID = 19806362.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antigens, CD30
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33. Takeyama K, Monti S, Manis JP, Dal Cin P, Getz G, Beroukhim R, Dutt S, Aster JC, Alt FW, Golub TR, Shipp MA: Integrative analysis reveals 53BP1 copy loss and decreased expression in a subset of human diffuse large B-cell lymphomas. Oncogene; 2008 Jan 10;27(3):318-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Integrative analysis reveals 53BP1 copy loss and decreased expression in a subset of human diffuse large B-cell lymphomas.
  • By combining high-density single nucleotide polymorphism (HD SNP) array data and gene expression profiles, we found 9 of 63 newly diagnosed human diffuse large B-cell lymphomas (DLBCLs) with single copy loss of the chromosome 15q15 region including the 53BP1 locus; these nine tumors also had significantly lower levels of 53BP1 transcripts.

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  • (PMID = 17637749.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA122833-01A1; United States / NCI NIH HHS / CA / K08 CA122833-01A1; United States / NCI NIH HHS / CA / P01 CA092625; United States / NCI NIH HHS / CA / K08 CA122833; United States / NCI NIH HHS / CA / P01 CA92625
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / TP53BP1 protein, human
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34. Ruzinova MB, Caron T, Rodig SJ: Altered subcellular localization of c-Myc protein identifies aggressive B-cell lymphomas harboring a c-MYC translocation. Am J Surg Pathol; 2010 Jun;34(6):882-91
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  • [Title] Altered subcellular localization of c-Myc protein identifies aggressive B-cell lymphomas harboring a c-MYC translocation.
  • Nearly 100% of Burkitt lymphomas (BLs) and 5% to 8% of diffuse large B-cell lymphomas (DLBCLs) harbor a balanced translocation involving c-MYC.
  • Although characteristic morphologic and immunophenotypic features can identify BL in most cases, tumors with atypical features are often encountered in clinical practice.
  • Furthermore, no morphologic or immunophenotypic finding can predict an underlying c-MYC translocation in DLBCL with certainty.
  • Here we report on a novel monoclonal antibody recognizing the c-myc protein in formalin-fixed, paraffin-embedded tissue which we used to evaluate a spectrum of aggressive B-cell lymphomas by standard immunohistochemistry.
  • Cases consisted of 17 BLs (15 cases with confirmed c-MYC translocation), 19 DLBCLs without a c-MYC translocation, 5 DLBCLs with a c-MYC translocation, and 2 B-cell lymphomas, unclassifiable, with features intermediate between DLBCL and BL (intermediate DBLCL/BL, one case with c-MYC translocation and one case without a c-MYC translocation).
  • We observed c-myc expression in the tumor cells of all cases regardless of c-MYC status.
  • Among BLs, c-myc protein primarily localized to the nucleus of tumor cells in 15 of 17 cases (88%) and equally localized to the nucleus and cytoplasm of tumor cells in 2 of 17 cases (12%).
  • In contrast, among DLBCLs lacking a c-MYC translocation the c-myc protein primarily localized to the cytoplasm of the tumor cells in 18 of 19 cases (95%) and equally localized to the nucleus and cytoplasm in the tumor cells in 1 of 19 cases (5%).
  • Among DLBCLs with a c-MYC translocation and intermediate DBLCL/BLs, the c-myc protein primarily localized to the nucleus, or equally localized to the nucleus and cytoplasm of the tumor cells in 4 of 5 cases (80%) and 2 of 2 cases (100%), respectively.
  • Taken together, we find that a primarily nuclear or mixed nuclear and cytoplasmic staining pattern for c-myc in an aggressive B-cell lymphoma is highly predictive of a c-MYC translocation (positive-predictive value=0.92, negative-predictive value=0.95, P<0.0001).
  • Thus this novel immunohistochemsitry test is a useful tool for identifying aggressive B-cell lymphomas likely to harbor a c-MYC rearrangement and thus warrant genetic testing.
  • [MeSH-major] Antibodies, Monoclonal. Burkitt Lymphoma / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Proto-Oncogene Proteins c-myc / genetics. Proto-Oncogene Proteins c-myc / metabolism
  • [MeSH-minor] Cell Nucleus / metabolism. Cytoplasm / metabolism. Genes, myc. Humans. Immunohistochemistry / methods. Observer Variation. Translocation, Genetic

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  • (PMID = 20442643.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-myc
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35. Refaeli Y, Young RM, Turner BC, Duda J, Field KA, Bishop JM: The B cell antigen receptor and overexpression of MYC can cooperate in the genesis of B cell lymphomas. PLoS Biol; 2008 Jun 24;6(6):e152
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  • [Title] The B cell antigen receptor and overexpression of MYC can cooperate in the genesis of B cell lymphomas.
  • A variety of circumstantial evidence from humans has implicated the B cell antigen receptor (BCR) in the genesis of B cell lymphomas.
  • The tumors that arose in the presence of constitutive BCR differed from those initiated by MYC alone and resembled chronic B cell lymphocytic leukemia/lymphoma (B-CLL), whereas those that arose in response to antigen stimulation resembled large B-cell lymphomas, particularly Burkitt lymphoma (BL).
  • First, in reconstruction experiments, stimulation of B cells by an autoantigen in the presence of overexpressed MYC gave rise to BL-like tumors that were, in turn, dependent on both MYC and the antigen for survival and proliferation.
  • Second, genetic disruption of the pathway that mediates signaling from the BCR promptly killed cells of the BL-like tumors as well as the tumors resembling B-CLL.
  • The mouse models described here should be useful in exploring further the pathogenesis of lymphomas, and in preclinical testing of new therapeutics.
  • [MeSH-major] Genes, myc. Lymphoma, B-Cell / etiology. Receptors, Antigen, B-Cell / physiology
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Lineage. Mice. Transgenes

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  • [Cites] Int J Cancer. 1970 Jul 15;6(1):1-9 [4319231.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10209-13 [10954754.001]
  • [Cites] Cancer Cell. 2003 Nov;4(5):343-8 [14667501.001]
  • [Cites] Blood. 1959 Oct;14:1151-8 [13813891.001]
  • [Cites] Int J Cancer. 1985 Apr 15;35(4):435-41 [2985508.001]
  • [Cites] Nat Med. 2002 Feb;8(2):128-35 [11821896.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 13;101(28):10380-5 [15240889.001]
  • [Cites] J Immunol. 2003 Jun 15;170(12):5851-60 [12794110.001]
  • [Cites] J Immunol. 2001 Nov 1;167(9):5136-42 [11673525.001]
  • [Cites] Semin Cancer Biol. 2006 Aug;16(4):313-7 [16935001.001]
  • [Cites] Mol Med. 1995 Jul;1(5):495-505 [8529116.001]
  • [Cites] Mol Cell. 1999 Aug;4(2):199-207 [10488335.001]
  • [Cites] Nat Genet. 1997 Jun;16(2):161-70 [9171827.001]
  • [Cites] J Immunol. 2000 Mar 1;164(5):2533-41 [10679091.001]
  • [Cites] Ann N Y Acad Sci. 1993 Aug 12;690:34-41 [8368749.001]
  • [Cites] Blood. 2000 Nov 15;96(10):3578-84 [11071657.001]
  • [Cites] Semin Hematol. 2001 Oct;38(4 Suppl 10):22-6 [11694948.001]
  • [Cites] J Clin Oncol. 2000 Nov 1;18(21):3707-21 [11054444.001]
  • [Cites] Cell. 1986 Oct 10;47(1):11-8 [3093082.001]
  • [Cites] Pediatr Hematol Oncol. 2001 Oct-Nov;18(7):427-42 [11594706.001]
  • [Cites] J Immunol. 2005 Jan 1;174(1):205-14 [15611242.001]
  • [Cites] Nature. 1992 Mar 26;356(6367):314-7 [1372394.001]
  • [Cites] J Biol Chem. 1999 Jun 25;274(26):18470-6 [10373455.001]
  • [Cites] EMBO J. 1983;2(12):2375-83 [6321164.001]
  • [Cites] Nature. 1999 Jul 29;400(6743):468-72 [10440378.001]
  • [Cites] Clin Immunol Immunopathol. 1992 Jun;63(3):205-13 [1535838.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Sep 27;91(20):9302-6 [7937760.001]
  • [Cites] J Exp Med. 2004 Jun 7;199(11):1523-32 [15173209.001]
  • [Cites] Oncology (Williston Park). 1989 Nov;3(11):41-53; discussion 53-4, 56, 59-60 [2578020.001]
  • [Cites] Ann Oncol. 1997;8 Suppl 2:11-6 [9209633.001]
  • [Cites] Clin Immunol Immunopathol. 1996 Sep;80(3 Pt 2):S40-5 [8811062.001]
  • [Cites] Mol Med. 1995 Sep;1(6):647-58 [8529131.001]
  • [Cites] Cell. 2000 Jan 7;100(1):57-70 [10647931.001]
  • [Cites] J Exp Med. 2003 Jun 16;197(12):1677-87 [12796466.001]
  • [Cites] Nature. 1988 Dec 1;336(6198):446-50 [3143076.001]
  • [Cites] Nat Genet. 2000 Jan;24(1):57-60 [10615128.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4097-102 [15753301.001]
  • [Cites] Am J Pathol. 1995 Nov;147(5):1398-407 [7485402.001]
  • [Cites] Cancer Cell. 2005 May;7(5):445-55 [15894265.001]
  • [Cites] Nature. 2000 Feb 10;403(6770):672-6 [10688206.001]
  • [Cites] Cell. 1979 May;17(1):65-75 [222476.001]
  • [Cites] Proc R Soc Med. 1971 Sep;64(9):909-10 [4329792.001]
  • [Cites] Blood. 1998 Jun 1;91(11):4292-9 [9596678.001]
  • [Cites] Curr Opin Investig Drugs. 2006 Nov;7(11):1002-7 [17117589.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3940-4 [10097142.001]
  • [Cites] Oncol Rep. 2001 Jan-Feb;8(1):77-81 [11115573.001]
  • [Cites] Nat Biotechnol. 2004 Mar;22(3):326-30 [14758366.001]
  • [Cites] J Cell Biochem. 1995 Dec;59(4):463-72 [8749716.001]
  • [Cites] Oncogene. 2002 May 13;21(21):3414-21 [12032779.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3249-62 [11751631.001]
  • [Cites] Blood. 2000 Mar 1;95(5):1797-803 [10688840.001]
  • [Cites] J Immunol. 1997 Dec 1;159(11):5318-28 [9548471.001]
  • [Cites] Jpn J Cancer Res. 1992 Mar;83(3):269-73 [1582889.001]
  • [Cites] Nature. 1991 Oct 24;353(6346):765-9 [1944535.001]
  • [Cites] Histopathology. 2005 Mar;46(3):241-55 [15720410.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1073-83 [9323135.001]
  • [Cites] Nature. 1988 Aug 25;334(6184):676-82 [3261841.001]
  • [Cites] Leuk Lymphoma. 2000 Dec;40(1-2):119-22 [11426612.001]
  • [Cites] Cell. 2002 May 3;109(3):335-46 [12015983.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Dec;79(24):7824-7 [6961453.001]
  • [Cites] N Engl J Med. 1984 Jul 5;311(1):20-7 [6427612.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14392-7 [12381789.001]
  • [Cites] Nature. 1968 Nov 2;220(5166):504-6 [4301061.001]
  • [Cites] J Biol Chem. 1999 Apr 2;274(14):9812-20 [10092671.001]
  • [Cites] Leuk Lymphoma. 1998 Jul;30(3-4):257-67 [9713958.001]
  • [Cites] Blood. 1995 Apr 15;85(8):2176-81 [7718888.001]
  • [Cites] Immunol Lett. 2008 Mar 15;116(2):184-94 [18194817.001]
  • [Cites] J Exp Med. 2002 Oct 7;196(7):999-1005 [12370261.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):251-62 [15803153.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]
  • [Cites] Int J Cancer. 1976 Sep 15;18(3):310-6 [783053.001]
  • [Cites] Blood. 2003 Nov 1;102(9):3333-9 [12855567.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8724-8 [7568005.001]
  • [Cites] Nature. 1991 Aug 8;352(6335):532-6 [1830923.001]
  • [Cites] J Virol. 1998 Nov;72(11):8463-71 [9765382.001]
  • [Cites] Autoimmunity. 1992;13(3):215-24 [1472633.001]
  • [Cites] J Exp Med. 2001 Dec 3;194(11):1583-96 [11733573.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Aug;85(16):6047-51 [3261863.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):108-12 [18066064.001]
  • [Cites] Ann Intern Med. 1978 Dec;89(6):888-92 [102228.001]
  • [Cites] J Virol. 2000 Nov;74(21):10223-8 [11024153.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3745-9 [11739181.001]
  • [Cites] Clin Exp Immunol. 1983 Nov;54(2):387-96 [6317239.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5595-610 [11607812.001]
  • [Cites] Oncogene. 1998 Sep 17;17(11 Reviews):1353-64 [9779983.001]
  • [Cites] Ann Oncol. 2000 Dec;11(12):1571-7 [11205465.001]
  • [Cites] Cell. 2004 Jun 11;117(6):787-800 [15186779.001]
  • [Cites] Cell. 1997 Sep 19;90(6):971-3 [9323124.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Mar 15;90(6):2189-93 [8460122.001]
  • [Cites] Oncogene. 1999 Sep 20;18(38):5268-77 [10498879.001]
  • [Cites] Cytometry. 1996 Feb 1;23(2):131-9 [8742172.001]
  • [Cites] Science. 1976 Oct 1;194(4260):23-8 [959840.001]
  • [Cites] J Exp Med. 2000 Oct 16;192(8):1183-90 [11034608.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11713-8 [16864779.001]
  • [Cites] Blood. 2002 Jul 1;100(1):246-58 [12070034.001]
  • [Cites] Curr Top Microbiol Immunol. 2004;279:169-97 [14560958.001]
  • [Cites] J Exp Med. 2007 Mar 19;204(3):633-43 [17353367.001]
  • [Cites] Br Med J (Clin Res Ed). 1981 Jun 20;282(6281):2023-7 [6788179.001]
  • [Cites] Microbiol Immunol. 1997;41(11):891-4 [9444332.001]
  • [Cites] N Engl J Med. 1980 Jun 5;302(23):1293-7 [6245364.001]
  • (PMID = 18578569.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA117802; United States / NCI NIH HHS / CA / T32 CA009043; United States / NCI NIH HHS / CA / CA-117802
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Receptors, Antigen, B-Cell
  • [Other-IDs] NLM/ PMC2435152
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36. Ludes-Meyers JH, Kil H, Nuñez MI, Conti CJ, Parker-Thornburg J, Bedford MT, Aldaz CM: WWOX hypomorphic mice display a higher incidence of B-cell lymphomas and develop testicular atrophy. Genes Chromosomes Cancer; 2007 Dec;46(12):1129-36
SciCrunch. Marmoset Gene list: Data: Gene Annotation .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] WWOX hypomorphic mice display a higher incidence of B-cell lymphomas and develop testicular atrophy.
  • WWOX tumor suppressor activity was suggested by re-expressing WWOX in breast, ovarian, and lung tumor cell lines leading to tumor growth inhibition in vivo.
  • Testes from Wwox(gt/gt) males had high numbers of atrophic seminiferous tubules and reduced fertility when compared with wild-type counterparts.
  • We observed that the Wwox(gt/gt) mice had a significantly shorter lifespan, and female hypomorphs had a higher incidence of spontaneous B-cell lymphomas.
  • Importantly, our observation that Wwox hypomorphs had an increased incidence of B-cell lymphomas supports a role of Wwox as a tumor suppressor.
  • [MeSH-major] Lymphoma, B-Cell / genetics. Oxidoreductases / genetics. Testis / pathology
  • [MeSH-minor] Animals. Atrophy. Cell Line, Tumor. Embryo, Mammalian / metabolism. Female. Gene Expression Regulation, Neoplastic. Male. Mice. Mice, Knockout. Mice, Transgenic. Models, Animal

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • [Cites] Nature. 2006 Mar 9;440(7081):242-5 [16525476.001]
  • [Cites] Mol Cancer Res. 2003 Nov;1(13):940-7 [14638866.001]
  • [Cites] Oncogene. 2005 Feb 24;24(9):1625-33 [15674328.001]
  • [Cites] Carcinogenesis. 2005 Mar;26(3):689-99 [15618236.001]
  • [Cites] Breast Cancer Res Treat. 2005 Jan;89(2):99-105 [15692750.001]
  • [Cites] Dev Dyn. 1998 Jun;212(2):171-80 [9626493.001]
  • [Cites] Mamm Genome. 1997 Jun;8(6):390-3 [9166580.001]
  • [Cites] Br J Cancer. 2004 Aug 16;91(4):753-9 [15266310.001]
  • [Cites] Cytogenet Genome Res. 2003;100(1-4):101-10 [14526170.001]
  • [Cites] Genes Chromosomes Cancer. 2002 Jun;34(2):154-67 [11979549.001]
  • [Cites] Blood. 2002 Mar 1;99(5):1745-57 [11861292.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8068-73 [11719429.001]
  • [Cites] Genomics. 2000 Oct 1;69(1):37-46 [11013073.001]
  • [Cites] BMC Cancer. 2005;5:64 [15982416.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8629-33 [14695174.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4401-6 [15070730.001]
  • [Cites] Cancer. 2004 Apr 15;100(8):1605-14 [15073846.001]
  • [Cites] Int J Hematol. 2004 Apr;79(3):238-42 [15168591.001]
  • [Cites] Oncogene. 2004 Jun 24;23(29):5049-55 [15064722.001]
  • [Cites] Blood. 2006 Sep 1;108(5):1733-43 [16705090.001]
  • [Cites] J Mol Histol. 2006 May;37(3-4):115-25 [16941225.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):3949-54 [17360458.001]
  • [Cites] Cancer Res. 2000 Apr 15;60(8):2140-5 [10786676.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11417-22 [11572989.001]
  • [Cites] Oncogene. 2001 Jul 19;20(32):4298-304 [11466610.001]
  • (PMID = 17823927.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102444-01; United States / NCI NIH HHS / CA / R01 CA102444-06A1; United States / NCI NIH HHS / CA / R01 CA102444-04; United States / NCI NIH HHS / CA / R01 CA102444-05; United States / NCI NIH HHS / CA / R01 CA102444-07; United States / NCI NIH HHS / CA / R01 CA102444; United States / NCI NIH HHS / CA / R01 CA102444-03; United States / NCI NIH HHS / CA / R01 CA102444-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 1.- / Oxidoreductases; EC 1.- / Wwox protein, mouse
  • [Other-IDs] NLM/ NIHMS222061; NLM/ PMC4143238
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37. Jaskó R, Horváth E, Szilágyi A, Altorjay A: [Dilemmas associated with the surgical treatment of cutaneous B cell lymphomas]. Orv Hetil; 2007 Sep 9;148(36):1713-6
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  • [Title] [Dilemmas associated with the surgical treatment of cutaneous B cell lymphomas].
  • [Transliterated title] A cutan B-sejtes lymphomák sebészi kezelésének dilemmái.
  • INTRODUCTION: Cutaneous lymphomas belong to the group of non-Hodgkin lymphomas.
  • However, in case of an in-time diagnose and adequate treatment the prognosis of the disease is fairly good.
  • Nevertheless, a thorny path leads to the correct diagnosis as several dermatological diseases cause problems in differential diagnostics.
  • The postoperative biopsy verified cutaneous B-cell lymphoma.
  • DISCUSSION: The cutaneous B-cell lymphomas are such forms of non-Hodgkin lymphomas, where the malignant proliferation appears primarily in the skin, and in 6 months after the diagnosis extracutaneous manifestation cannot be detected.
  • Several cases can be found in the literature, which show long interval between the manifestation of the symptoms and the setting of the diagnosis.
  • This calls the attention to the significance of difficulties in the differential diagnosis.
  • During the treatment of cutaneous lymphomas the type, the cutaneous extension, and the extracutaneous manifestation of the disease must be defined.
  • On the basis of findings in this case and in the literature, a surgical treatment--beyond determining the correct diagnosis--could be a therapeutic alternative in the treatment of cutaneous B-cell lymphomas.
  • [MeSH-major] Lymphoma, T-Cell, Cutaneous / diagnosis. Lymphoma, T-Cell, Cutaneous / surgery. Skin Neoplasms / diagnosis. Skin Neoplasms / surgery
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Female. Humans. Middle Aged

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  • (PMID = 17766223.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Hungary
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38. Martinez A, Pittaluga S, Rudelius M, Davies-Hill T, Sebasigari D, Fountaine TJ, Hewitt S, Jaffe ES, Raffeld M: Expression of the interferon regulatory factor 8/ICSBP-1 in human reactive lymphoid tissues and B-cell lymphomas: a novel germinal center marker. Am J Surg Pathol; 2008 Aug;32(8):1190-200
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  • [Title] Expression of the interferon regulatory factor 8/ICSBP-1 in human reactive lymphoid tissues and B-cell lymphomas: a novel germinal center marker.
  • To assess the role of interferon regulatory factor (IRF) 8 in B-cell development and lymphomagenesis, we studied its expression in reactive lymphoid tissues, its relationship to other B-cell transcription factors, and its expression in a series of 232 B-cell tumors and 30 cell lines representing a variety of B-cell developmental stages.
  • We found that although IRF8 was detectable in most reactive B-cells, its expression levels differed with developmental stage.
  • Germinal center B cells contained the highest levels of IRF8, with lower levels seen in mantle and marginal zone B cells and none in plasma cells.
  • IRF8 was coexpressed with PAX-5, Pu.1, and B-cell lymphoma (BCL)-6, and similar to BCL-6, was absent from the small population of IRF4-positive germinal center B cells thought to be committed to postgerminal center developmental programs.
  • Similarly, IRF8 was most strongly expressed in lymphomas of germinal center origin with lower levels present in mantle cell lymphomas, chronic lymphocytic leukemia, and marginal zone lymphomas, and no expression observed in plasmacytic/plasmablastic neoplasms.
  • The reciprocal expression pattern with IRF4 in reactive tissues was generally maintained in lymphomas with some exceptions.
  • These results suggest an important role for IRF8 during germinal center B-cell development and in related lymphomas, and provide a new diagnostic marker helpful in distinguishing B-cell non-Hodgkin lymphoma subtypes.
  • [MeSH-major] B-Lymphocytes / metabolism. Biomarkers, Tumor / metabolism. Germinal Center / metabolism. Interferon Regulatory Factors / metabolism. Lymphoma, B-Cell / metabolism
  • [MeSH-minor] B-Cell-Specific Activator Protein / metabolism. Cell Line, Tumor. DNA-Binding Proteins / metabolism. Diagnosis, Differential. Humans. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Lymphoma, B-Cell, Marginal Zone / metabolism. Lymphoma, Mantle-Cell / metabolism. Palatine Tonsil / chemistry. Plasma Cells / metabolism. Proto-Oncogene Proteins / metabolism. Trans-Activators / metabolism

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  • (PMID = 18580679.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / B-Cell-Specific Activator Protein; 0 / BCL6 protein, human; 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Interferon Regulatory Factors; 0 / PAX5 protein, human; 0 / Proto-Oncogene Proteins; 0 / Trans-Activators; 0 / interferon regulatory factor-4; 0 / interferon regulatory factor-8; 0 / proto-oncogene protein Spi-1
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39. Lwin T, Hazlehurst LA, Dessureault S, Lai R, Bai W, Sotomayor E, Moscinski LC, Dalton WS, Tao J: Cell adhesion induces p27Kip1-associated cell-cycle arrest through down-regulation of the SCFSkp2 ubiquitin ligase pathway in mantle-cell and other non-Hodgkin B-cell lymphomas. Blood; 2007 Sep 1;110(5):1631-8
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  • [Title] Cell adhesion induces p27Kip1-associated cell-cycle arrest through down-regulation of the SCFSkp2 ubiquitin ligase pathway in mantle-cell and other non-Hodgkin B-cell lymphomas.
  • Mounting evidence suggests that dynamic interactions between a tumor and its microenvironment play a critical role in tumor development, cell-cycle progression, and response to therapy.
  • In this study, we used mantle cell lymphoma (MCL) as a model to characterize the mechanisms by which stroma regulate cell-cycle progression.
  • We demonstrated that adhesion of MCL and other non-Hodgkin lymphoma (NHL) cells to bone marrow stromal cells resulted in a reversible G(1) arrest associated with elevated p27(Kip1) and p21 (WAF1) proteins.
  • Furthermore, we found cell adhesion up-regulated Cdh1 (an activating subunit of anaphase-promoting complex [APC] ubiquitin ligase), and reduction of Cdh1 by siRNA induced Skp2 accumulation and hence p27(Kip1) degradation, thus implicating Cdh1 as an upstream effector of the Skp2/p27(Kip1) signaling pathway.
  • Overall, this report, for the first time, demonstrates that cell-cell contact controls the tumor cell cycle via ubiquitin-proteasome proteolytic pathways in MCL and other NHLs.
  • The understanding of this novel molecular pathway may prove valuable in designing new therapeutic approaches for modifying tumor cell growth and response to therapy.

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  • [Cites] Nat Cell Biol. 1999 Aug;1(4):193-9 [10559916.001]
  • [Cites] Science. 1995 Aug 4;269(5224):682-5 [7624798.001]
  • [Cites] Leuk Lymphoma. 2000 Jun;38(1-2):71-81 [10811449.001]
  • [Cites] Oncogene. 2000 Sep 7;19(38):4319-27 [10980607.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Apr 13;282(4):853-60 [11352628.001]
  • [Cites] Genes Dev. 1995 Aug 1;9(15):1831-45 [7649471.001]
  • [Cites] J Cell Biol. 1996 Apr;133(2):391-403 [8609171.001]
  • [Cites] Curr Biol. 1996 Apr 1;6(4):455-66 [8723350.001]
  • [Cites] Curr Opin Cell Biol. 1997 Dec;9(6):800-6 [9425344.001]
  • [Cites] Curr Top Microbiol Immunol. 1998;227:57-103 [9479826.001]
  • [Cites] Bioessays. 1998 Dec;20(12):1020-9 [10048302.001]
  • [Cites] Semin Hematol. 1999 Apr;36(2):115-27 [10319380.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):9124-9 [10430906.001]
  • [Cites] Blood. 2005 Jul 15;106(2):698-705 [15802532.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):369-81 [16633365.001]
  • [Cites] J Biol Chem. 2006 Aug 4;281(31):22100-7 [16754685.001]
  • [Cites] J Cell Biol. 2001 Jun 25;153(7):1381-90 [11425869.001]
  • [Cites] Leuk Lymphoma. 2002 Jan;43(1):19-27 [11908727.001]
  • [Cites] Mol Cell. 2002 May;9(5):923-5 [12049727.001]
  • [Cites] Semin Diagn Pathol. 2003 Aug;20(3):196-210 [14552431.001]
  • [Cites] J Biol Chem. 2003 Nov 28;278(48):48030-40 [14506229.001]
  • [Cites] Nature. 2004 Mar 11;428(6979):190-3 [15014502.001]
  • [Cites] Nature. 2004 Mar 11;428(6979):194-8 [15014503.001]
  • [Cites] Blood. 2004 May 1;103(9):3503-10 [14670925.001]
  • [Cites] Genes Dev. 1994 Jan;8(1):9-22 [8288131.001]
  • [Cites] Blood. 2000 Feb 1;95(3):846-54 [10648395.001]
  • (PMID = 17502456.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA076292; United States / NCI NIH HHS / CA / P01 CA76292
  • [Publication-type] Clinical Trial; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CDH1 protein, human; 0 / CDKN1A protein, human; 0 / CDKN1B protein, human; 0 / Cadherins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Intracellular Signaling Peptides and Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering; 0 / S-Phase Kinase-Associated Proteins; 0 / Ubiquitin; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes
  • [Other-IDs] NLM/ PMC1975846
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40. Klapper W, Stoecklein H, Zeynalova S, Ott G, Kosari F, Rosenwald A, Loeffler M, Trümper L, Pfreundschuh M, Siebert R, German High-Grade Non-Hodgkin's Lymphoma Study Group: Structural aberrations affecting the MYC locus indicate a poor prognosis independent of clinical risk factors in diffuse large B-cell lymphomas treated within randomized trials of the German High-Grade Non-Hodgkin's Lymphoma Study Group (DSHNHL). Leukemia; 2008 Dec;22(12):2226-9
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  • [Title] Structural aberrations affecting the MYC locus indicate a poor prognosis independent of clinical risk factors in diffuse large B-cell lymphomas treated within randomized trials of the German High-Grade Non-Hodgkin's Lymphoma Study Group (DSHNHL).
  • Recent retrospective studies of heterogeneously treated patients have suggested that chromosomal aberrations of the MYC gene locus indicate an unfavorable prognosis in diffuse large B-cell lymphoma (DLBCL).
  • Here, we investigated the prognostic impact of MYC aberrations analyzed by interphase fluorescence in situ hybridization in 177 patients with de novo DLBCL treated within the two prospective, randomized trials non-Hodgkin's lymphoma NHL-B1 and NHL-B2.
  • In a Cox model adjusted for the international prognostic index, the presence of a MYC gene rearrangement was the strongest statistically independent predictor of OS (relative risk 3.4, P=0.004) and EFS (relative risk 2.5, P=0.015), and this also held true when the cell-of-origin signature detected by immunohistochemistry was included in the model.
  • [MeSH-major] Chromosome Aberrations. Gene Expression Regulation, Neoplastic. Genes, myc / genetics. Lymphoma, Large B-Cell, Diffuse
  • [MeSH-minor] Adult. Aged. Disease-Free Survival. Female. Germany / epidemiology. Humans. Immunohistochemistry. Kaplan-Meier Estimate. Male. Middle Aged. Oligonucleotide Array Sequence Analysis. Predictive Value of Tests. Prognosis. Proportional Hazards Models. Randomized Controlled Trials as Topic. Retrospective Studies. Risk Factors. Young Adult

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  • (PMID = 18754028.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
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41. Nagel S, Hirschmann P, Dirnhofer S, Günthert U, Tzankov A: Coexpression of CD44 variant isoforms and receptor for hyaluronic acid-mediated motility (RHAMM, CD168) is an International Prognostic Index and C-MYC gene status-independent predictor of poor outcome in diffuse large B-cell lymphomas. Exp Hematol; 2010 Jan;38(1):38-45
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  • [Title] Coexpression of CD44 variant isoforms and receptor for hyaluronic acid-mediated motility (RHAMM, CD168) is an International Prognostic Index and C-MYC gene status-independent predictor of poor outcome in diffuse large B-cell lymphomas.
  • We have previously shown that CD44v6 expression in diffuse large B-cell lymphoma (DLBCL) correlates with advanced disease stage and is predominantly detected in non-germinal center B-cell-like DLBCL subtypes.
  • CD44v-RHAMM coexpression was most prevalent in non-germinal center DLBCL cases and usually coincided with expression of osteopontin.
  • [MeSH-major] Antigens, CD44 / genetics. Extracellular Matrix Proteins / genetics. Genes, myc. Lymphoma, Large B-Cell, Diffuse / pathology

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  • (PMID = 19857547.001).
  • [ISSN] 1873-2399
  • [Journal-full-title] Experimental hematology
  • [ISO-abbreviation] Exp. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD44; 0 / Extracellular Matrix Proteins; 0 / hyaluronan-mediated motility receptor
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42. Birgersdotter A, Baumforth KR, Wei W, Murray PG, Sjöberg J, Björkholm M, Porwit A, Ernberg I: Connective tissue growth factor is expressed in malignant cells of Hodgkin lymphoma but not in other mature B-cell lymphomas. Am J Clin Pathol; 2010 Feb;133(2):271-80
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  • [Title] Connective tissue growth factor is expressed in malignant cells of Hodgkin lymphoma but not in other mature B-cell lymphomas.
  • Microarray analysis of 44 classical Hodgkin lymphoma (cHL) samples showed higher CTGF messenger RNA expression in the nodular sclerosis (NS) than in the mixed cellularity (MC) subtype.
  • When analyzed by immunohistochemical analysis, Hodgkin-Reed-Sternberg (H-RS) cells and macrophages in 23 cHLs and "popcorn" cells in 2 nodular lymphocyte predominant Hodgkin lymphomas showed expression of CTGF protein correlating with the extent of fibrosis.
  • Malignant cells in 32 samples of various non-Hodgkin lymphomas were negative for CTGF.
  • A staining pattern of stromal cells similar to that of NS cHL was seen in anaplastic large cell lymphoma.
  • Macrophages stained positively in Burkitt lymphomas and in some mantle cell lymphomas.
  • The high occurrence of fibrosis in cHL may be related to CTGF expression by malignant H-RS cells.
  • [MeSH-major] Connective Tissue Growth Factor / metabolism. Hodgkin Disease / metabolism. Lymphoma, B-Cell / metabolism
  • [MeSH-minor] Biomarkers, Tumor / analysis. Gene Expression Profiling. Humans. RNA, Messenger / metabolism. Reed-Sternberg Cells / metabolism

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  • (PMID = 20093237.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger; 139568-91-5 / Connective Tissue Growth Factor
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43. Kasprzak A, Spachacz R, Wachowiak J, Stefańska K, Kaczmarek E, Zabel M: Tissue expression of interleukin 2 (IL-2) and IL-2 receptor (IL-2R(alpha)/CD25) in non-Hodgkin B-cell lymphomas in children: correlations with clinical data. J Pediatr Hematol Oncol; 2010 Aug;32(6):462-71
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  • [Title] Tissue expression of interleukin 2 (IL-2) and IL-2 receptor (IL-2R(alpha)/CD25) in non-Hodgkin B-cell lymphomas in children: correlations with clinical data.
  • SUMMARY: The study aimed at analysis of tissue expression of interleukin 2 (IL-2) and subunit alpha of its receptor (IL-22R(alpha)/CD25) in B-cell non-Hodgkin lymphomas (B-cell NHLs) in children as related to selected clinical data.
  • The studies were performed on an archival tissue material originating from children with B-cell NHLs (n=26) using avidin-biotin-peroxidase complex method and in-situ hybridization with biotinylated tyramine amplification signal (ImmunoMax technique).
  • As compared with non-neoplastic lesions, in B-cell NHLs a significantly higher expression was noted of both IL-2 and IL-22R(alpha).
  • In children with B-cell NHLs, frequency of IL-2 detection was 62%, and that of IL-22R(alpha), 46%.
  • Using hybridocytochemistry, presence of mRNA for IL-2 could be detected, but not mRNA for IL-22R(alpha) in children with B-cell NHLs.
  • A significant direct relationship was demonstrated between expressions of IL-2 and IL-22R(alpha) in children with B-cell NHLs.
  • No significant relationships could be detected between expression of IL-2 and/or IL-22R(alpha) on one hand and histopathologic diagnosis, tumor location, age, or sex in B-cell NHLs on the other.
  • The new element in the results involved demonstration of significant differences in shorter survival of children with B-cell NHLs, as related to cellular expression of IL-2 and IL-22R(alpha) (CD25).
  • The positive relationship between tissue expression of IL-22R(alpha) and the shorter survival of children with B-cell NHLs should prompt further investigations to identify other risk factors in patients with this type of tumors in children.
  • [MeSH-major] Biomarkers, Tumor / analysis. Interleukin-2 / biosynthesis. Interleukin-2 Receptor alpha Subunit / biosynthesis. Lymphoma, B-Cell / metabolism

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  • (PMID = 20562654.001).
  • [ISSN] 1536-3678
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interleukin-2; 0 / Interleukin-2 Receptor alpha Subunit
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44. Bertrand P, Maingonnat C, Picquenot JM, Dastugue N, Penther D, Ysebaert L, Maisonneuve C, Tilly H, Bastard C: Characterization of three t(3;8)(q27;q24) translocations from diffuse large B-cell lymphomas. Leukemia; 2008 May;22(5):1064-7
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  • [Title] Characterization of three t(3;8)(q27;q24) translocations from diffuse large B-cell lymphomas.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / genetics. Proto-Oncogene Proteins c-bcl-6 / genetics. Proto-Oncogene Proteins c-myc / genetics. Translocation, Genetic

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  • (PMID = 17989722.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-6; 0 / Proto-Oncogene Proteins c-myc
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45. Haralambieva E, Adam P, Ventura R, Katzenberger T, Kalla J, Höller S, Hartmann M, Rosenwald A, Greiner A, Muller-Hermelink HK, Banham AH, Ott G: Genetic rearrangement of FOXP1 is predominantly detected in a subset of diffuse large B-cell lymphomas with extranodal presentation. Leukemia; 2006 Jul;20(7):1300-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetic rearrangement of FOXP1 is predominantly detected in a subset of diffuse large B-cell lymphomas with extranodal presentation.
  • [MeSH-major] Forkhead Transcription Factors / genetics. Gene Rearrangement, B-Lymphocyte / genetics. Lymphoma, B-Cell / genetics. Lymphoma, B-Cell / pathology. Repressor Proteins / genetics

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  • [CommentOn] Leukemia. 2005 Apr;19(4):652-8 [15703784.001]
  • (PMID = 16673020.001).
  • [ISSN] 0887-6924
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FOXP1 protein, human; 0 / Forkhead Transcription Factors; 0 / Repressor Proteins
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46. Nagel I, Bug S, Tönnies H, Ammerpohl O, Richter J, Vater I, Callet-Bauchu E, Calasanz MJ, Martinez-Climent JA, Bastard C, Salido M, Schroers E, Martin-Subero JI, Gesk S, Harder L, Majid A, Dyer MJ, Siebert R: Biallelic inactivation of TRAF3 in a subset of B-cell lymphomas with interstitial del(14)(q24.1q32.33). Leukemia; 2009 Nov;23(11):2153-5
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  • [Title] Biallelic inactivation of TRAF3 in a subset of B-cell lymphomas with interstitial del(14)(q24.1q32.33).
  • [MeSH-major] Chromosome Deletion. Chromosomes, Human, Pair 14. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Lymphoma, B-Cell / genetics. TNF Receptor-Associated Factor 3 / genetics

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  • (PMID = 19693093.001).
  • [ISSN] 1476-5551
  • [Journal-full-title] Leukemia
  • [ISO-abbreviation] Leukemia
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U132670597
  • [Publication-type] Letter; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / TNF Receptor-Associated Factor 3; 0 / TRAF3 protein, human
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47. Golling P, Cozzio A, Dummer R, French L, Kempf W: Primary cutaneous B-cell lymphomas - clinicopathological, prognostic and therapeutic characterisation of 54 cases according to the WHO-EORTC classification and the ISCL/EORTC TNM classification system for primary cutaneous lymphomas other than mycosis fungoides and Sezary syndrome. Leuk Lymphoma; 2008 Jun;49(6):1094-103
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  • [Title] Primary cutaneous B-cell lymphomas - clinicopathological, prognostic and therapeutic characterisation of 54 cases according to the WHO-EORTC classification and the ISCL/EORTC TNM classification system for primary cutaneous lymphomas other than mycosis fungoides and Sezary syndrome.
  • Clinical, prognostic and therapeutic features of 54 primary cutaneous marginal zone B-cell lymphoma (pcMZL), follicle centre lymphoma (pcFCL) and diffuse large B-cell lymphoma, leg type (pcDLBL) were analysed applying the WHO-EORTC classification for cutaneous lymphomas and the new TNM staging scheme of the International Society of Cutaneous Lymphomas.
  • Three of 7 patients (43%) with pcDLBL died due to lymphoma.
  • The new TNM staging system is easily applicable for disease documentation, but our relatively small number of patients in each T stage does not allow the assessment of its prognostic value.
  • [MeSH-major] Lymphoma, B-Cell / classification. Mycosis Fungoides / classification. Sezary Syndrome / classification. Skin Neoplasms / classification. World Health Organization
  • [MeSH-minor] Adolescent. Adult. Aged. Female. Humans. Lymphoma, B-Cell, Marginal Zone / pathology. Lymphoma, B-Cell, Marginal Zone / therapy. Lymphoma, Follicular / pathology. Lymphoma, Follicular / therapy. Lymphoma, Large B-Cell, Diffuse / pathology. Lymphoma, Large B-Cell, Diffuse / therapy. Male. Middle Aged. Neoplasm Staging. Prognosis


48. Guyot A, Ortonne N, Valeyrie-Allanore L, Bagot M: Combined treatment with rituximab and anthracycline-containing chemotherapy for primary cutaneous large B-cell lymphomas, leg type, in elderly patients. Arch Dermatol; 2010 Jan;146(1):89-91
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  • [Title] Combined treatment with rituximab and anthracycline-containing chemotherapy for primary cutaneous large B-cell lymphomas, leg type, in elderly patients.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, Large B-Cell, Diffuse / drug therapy

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  • (PMID = 20083704.001).
  • [ISSN] 1538-3652
  • [Journal-full-title] Archives of dermatology
  • [ISO-abbreviation] Arch Dermatol
  • [Language] eng
  • [Publication-type] Comparative Study; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab; 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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49. Babbo AM, Chokshi M, Rademaker A, Mittal B: The use of single-fraction radiation therapy in cutaneous T-cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19505

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The use of single-fraction radiation therapy in cutaneous T-cell lymphoma.
  • : e19505 Background: Primary cutaneous lymphomas occur in 0.5 to 1 per 100,000 people every year in developed countries.
  • Cutaneous T-cell lymphomas are responsive to radiation therapy, and local radiation therapy, total skin electron beam therapy, phototherapy (with UVB or PUVA), chemotherapy agents (nitrogen mustards, BCNU), retinoids, and steroids have all been used with varying degrees of success.
  • METHODS: This is a retrospective review of all cases of histology-proven cutaneous T-cell lymphoma treated with single-fraction radiation therapy at Northwestern Memorial Hospital in the Department of Radiation Oncology since 1990.
  • We reviewed the charts of 67 patients with cutaneous T-cell lymphoma, of which 40 patients and a total of 130 sites of disease received single-fraction radiation therapy and had available follow-up data.
  • CONCLUSIONS: This review of the experience at our institution since 1990 shows single-fraction radiation therapy to be an effective treatment for cutaneous T-cell lymphoma, with high response rates and very low relapse rates.

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  • (PMID = 27960872.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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50. Tam W, Gomez M, Nie K: Significance of PRDM1beta expression as a prognostic marker in diffuse large B-cell lymphomas. Blood; 2008 Feb 15;111(4):2488-9; author reply 2489-90
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  • [Title] Significance of PRDM1beta expression as a prognostic marker in diffuse large B-cell lymphomas.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Repressor Proteins / genetics. Transcription Factors / genetics

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  • [CommentOn] Blood. 2007 Jul 1;110(1):339-44 [17379744.001]
  • (PMID = 18263789.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Repressor Proteins; 0 / Transcription Factors; 138415-26-6 / PRDM1 protein, human
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51. Frankel AE, Woo J, Zuckero SL, Mankin AA, Grable M, Mitchell K, Lee Y, Neville DM: CD3 immunotoxin therapy of cutaneous T cell lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19511

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD3 immunotoxin therapy of cutaneous T cell lymphoma.
  • : e19511 Background: T cell lymphomas represent 12% of lymphoma cases in the U.S.
  • Cytotoxic chemotherapies, radiation therapies, monoclonal antibodies, transcription modulators and topical therapies yield remissions, but over half of patients relapse and die with progressive disease.
  • One class of T cell directed agents are immunotoxins composed of protein synthesis inactivating peptide toxins covalently linked to antibodies or hormone ligands.
  • We prepared a clinical batch of drug and obtained FDA approval for a phase I trial (IND#100712).
  • CTCAEv3.0 toxicity grading, blood samples counts, chemistries, CMV/EBV PCR, PK, immune response and flow cytometry, and disease assessments by CT scans, skin mapping and bone marrow biopsies were done.
  • Circulating T regulatory cells doubled.
  • CONCLUSIONS: This novel immunotoxin has dramatic clinical activity even at the lowest dose in CTCL patients and merits applications at higher doses in CTCL and other CD3+ T cell leukemia/lymphoma patients.
  • The lymphodepletion with recovery of T regulatory cells suggests the drug may be beneficial for immunosuppression of T cell autoimmune disorders.

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  • (PMID = 27960968.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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52. Schmitz N, Ziepert M, Nickelsen M, Wolf SP, Truemper L, Loeffler M, Ho A, Metzner B, Rosenwald A, Pfreundschuh M: Mature T-/NK-cell lymphomas: Prognostic factors and treatment outcome of patients treated on studies of the German High-Grade Lymphoma Study Group (DSHNHL). J Clin Oncol; 2009 May 20;27(15_suppl):8564

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mature T-/NK-cell lymphomas: Prognostic factors and treatment outcome of patients treated on studies of the German High-Grade Lymphoma Study Group (DSHNHL).
  • : 8564 Background: T-cell lymphomas represent a heterogeneous group of malignancies difficult to diagnose and to treat.
  • METHODS: Between 1993 and 2006 we treated 329 pts with ALK-positive ALCL (73 pts), ALK-negative ALCL (108 pts), PTCL, NOS (68 pts), AITL (28 pts), NK-/T-cell lymphoma (18 pts), and rare T-cell lymphomas on prospective studies.
  • In younger pts (ALK-positive ALCL were excluded) and good-risk disease (LDH <= N) there was a trend for better EFS after the addition of E to CHOP (EFS 63% vs. 48%, p = 0.065).
  • The MegaCHOEP protocol (Schmitz et al., CANCER 2006) failed to improve treatment results for younger pts with poor-risk disease (EFS at 3 yrs: 25.9%, 95% CI: 10.4-41.4); the prospective study comparing MegaCHOEP with CHOEP-14 was stopped for pts with T-cell lymphoma.

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  • (PMID = 27961019.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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53. Gellrich S, Muche JM, Wilks A, Jasch KC, Voit C, Fischer T, Audring H, Sterry W: Systemic eight-cycle anti-CD20 monoclonal antibody (rituximab) therapy in primary cutaneous B-cell lymphomas--an applicational observation. Br J Dermatol; 2005 Jul;153(1):167-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Systemic eight-cycle anti-CD20 monoclonal antibody (rituximab) therapy in primary cutaneous B-cell lymphomas--an applicational observation.
  • BACKGROUND: Primary cutaneous B-cell lymphomas (PCBCLs) are characterized by restriction to the skin and a variable but mostly favourable prognosis.
  • Since 1997 the recombinant, chimeric anti-CD20 antibody rituximab has been used in patients suffering from non-Hodgkin's B-cell lymphomas.
  • Different studies have shown that the effectiveness and safety in the treatment of patients with low-grade follicular lymphoma is comparable to or even higher than the standard CHOP chemotherapy.
  • PATIENTS/METHODS: Ten patients with PCBCL [eight with follicle centre cell lymphoma (FCCL), one with marginal zone lymphoma (MZL) and one with diffuse large B-cell lymphoma of the leg (DLBCL)] were treated by intravenous application of a chimeric antibody against the CD20 transmembrane antigen (rituximab) with a dosage of eight cycles, 375 mg m(-2) body surface, weekly.
  • RESULTS: The treatment regimen resulted in clinical overall response in 9 of 10 patients, in particular there were seven complete responses (70%) plus two partial responses (20%).
  • As expected the B-cell count in peripheral blood was depressed in all patients after infusion.
  • CONCLUSIONS: Intravenous therapy with eight cycles of the anti-CD20 antibody rituximab is a non-toxic and effective treatment for a subset of patients with PCBCL (relapsed, aggressive entity, old patients, multiple lesions) with a long DR.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoma, B-Cell / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / immunology. Disease Progression. Disease-Free Survival. Drug Administration Schedule. Drug Evaluation. Humans. Male. Middle Aged. Rituximab. Treatment Outcome

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  • (PMID = 16029344.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 28
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54. Kubota T, Moritani S, Yoshino T, Nagai H, Terasaki H: Correlation of autoantibodies and CD5+ B cells in ocular adnexal marginal zone B cell lymphomas. J Clin Pathol; 2010 Jan;63(1):79-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Correlation of autoantibodies and CD5+ B cells in ocular adnexal marginal zone B cell lymphomas.
  • AIM: To determine the clinicopathological properties of ocular adnexal marginal zone B cell lymphomas (MZBLs) with CD5+ B cells.
  • RESULTS: Two elderly female patients were found to have ocular adnexal MZBLs with CD5+ B cells; flow cytometry analysis suggested that one of these MZBLs had CD5+ B cell clonal proliferation.
  • The levels of anti-single stranded (SS)-DNA and anti-SS-A/Ro antibodies in these two patients were significantly higher than those in controls that were matched for age, gender and disease (2/2 versus 0/14; p = 0.008) and controls without MZBL (2/2 versus 0/30; p = 0.002).
  • In addition, another patient with ocular adnexal reactive lymphoid hyperplasia with CD5+ B cells also had anti-SS-DNA antibodies.
  • CONCLUSION: Patients with ocular adnexal MZBLs with CD5+ B cells may have a background of systemic conditions with CD5+ B-cell-related autoantibodies.
  • [MeSH-major] Antigens, CD5 / blood. Autoantibodies / blood. B-Lymphocyte Subsets / immunology. Lymphoma, B-Cell, Marginal Zone / immunology. Orbital Neoplasms / immunology
  • [MeSH-minor] Aged. Aged, 80 and over. Antibodies, Antinuclear / blood. Autoimmunity. Case-Control Studies. Cell Proliferation. DNA, Single-Stranded / immunology. Female. Humans. Middle Aged

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  • (PMID = 20026703.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Antinuclear; 0 / Antigens, CD5; 0 / Autoantibodies; 0 / DNA, Single-Stranded
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55. Carpenter RD, Andrei M, Aina OH, Lau EY, Lightstone FC, Liu R, Lam KS, Kurth MJ: Selectively targeting T- and B-cell lymphomas: a benzothiazole antagonist of alpha4beta1 integrin. J Med Chem; 2009 Jan 8;52(1):14-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selectively targeting T- and B-cell lymphomas: a benzothiazole antagonist of alpha4beta1 integrin.
  • Integrin alpha(4)beta(1), a heterodimeric cell surface receptor, is believed to have a low-affinity conformation in resting normal lymphocytes and an activated high-affinity conformation in cancerous cells, specifically T- and B-cell lymphomas.
  • The results presented herein utilized heterocyclic and solid-phase chemistry, cell adhesion assay, and in vivo optical imaging using the cyanine dye Cy5.5 conjugate.

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  • [Cites] J Org Chem. 2007 Jan 5;72(1):284-7 [17194113.001]
  • [Cites] J Med Chem. 2007 Nov 15;50(23):5863-7 [17948981.001]
  • [Cites] Nat Chem Biol. 2006 Jul;2(7):381-9 [16767086.001]
  • [Cites] Dev Biol. 2006 May 1;293(1):165-77 [16529735.001]
  • [Cites] Pharmacol Res. 2006 Jan;53(1):75-9 [16221551.001]
  • [Cites] Curr Opin Chem Biol. 1998 Aug;2(4):453-7 [9736917.001]
  • [Cites] Curr Top Microbiol Immunol. 1998;231:125-41 [9479864.001]
  • [Cites] Blood. 1996 Jun 1;87(11):4780-8 [8639849.001]
  • [Cites] FASEB J. 1994 Sep;8(12):929-38 [7522194.001]
  • [Cites] Anal Biochem. 1970 Apr;34(2):595-8 [5443684.001]
  • [Cites] J Cell Biochem. 2003 Apr 1;88(5):1038-47 [12616540.001]
  • [Cites] Med Res Rev. 2002 Mar;22(2):146-67 [11857637.001]
  • [Cites] Jpn J Pharmacol. 2002 Jan;88(1):69-76 [11855680.001]
  • [Cites] J Med Chem. 2001 Dec 20;44(26):4696-703 [11741487.001]
  • [Cites] J Comb Chem. 2006 Nov-Dec;8(6):907-14 [17096580.001]
  • (PMID = 19072684.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01-GM076151; United States / NIGMS NIH HHS / GM / P41 GM076151; United States / NIGMS NIH HHS / GM / P41 GM076151-02; United States / NCI NIH HHS / CA / U19 CA113298; United States / NIGMS NIH HHS / GM / P41 GM076151-03; United States / NCI NIH HHS / CA / U19CA113298; United States / Howard Hughes Medical Institute / / ; United States / NIGMS NIH HHS / GM / P41 GM076151-01; United States / NIGMS NIH HHS / GM / P41 GM089153
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzothiazoles; 0 / Integrin alpha4beta1; 0 / Sesquiterpenes; 50656-66-1 / molephantin; G5BW2593EP / benzothiazole
  • [Other-IDs] NLM/ NIHMS91260; NLM/ PMC3164867
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56. Nomura K, Kanda-Akano Y, Shimizu D, Okuda T, Yoshida N, Matsumoto Y, Nishida K, Taki T, Yokota S, Horiike S, Taniwaki M: An additional segment at 1p36 derived from der(18)t(14;18) in patients with diffuse large B-cell lymphomas transformed from follicular lymphoma. Ann Hematol; 2005 Jul;84(7):474-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] An additional segment at 1p36 derived from der(18)t(14;18) in patients with diffuse large B-cell lymphomas transformed from follicular lymphoma.
  • The particular translocation in follicular lymphomas (FLs) is a t(14;18)(q32;q21), recombining the immunoglobulin heavy chain (IgH) gene on chromosome 14 with the B-cell leukemia/lymphoma 2 (BCL2) gene on chromosome 18.
  • Some low-grade FLs are aggressively transformed into diffuse large B-cell lymphomas, presumably by acquisition of secondary chromosomal changes, including chromosomal band 1p36.
  • Because it is difficult to identify the origin of add(1)(p36) even on high-resolution G-banding analysis, we used spectral karyotyping (SKY) and double-color fluorescence in situ hybridization (DC-FISH) to define the t(14;18) and the extra band at 1p36 in two cases of diffuse large B-cell lymphoma (DLBCL).
  • [MeSH-major] Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 18 / genetics. Lymphoma, B-Cell / genetics. Oncogene Proteins, Fusion / genetics. Translocation, Genetic
  • [MeSH-minor] Chromosome Banding / methods. Chromosome Painting / methods. Female. Humans. Immunoglobulin Heavy Chains / genetics. Karyotyping / methods. Male. Proto-Oncogene Proteins c-bcl-2 / genetics

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  • (PMID = 15700138.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Immunoglobulin Heavy Chains; 0 / Oncogene Proteins, Fusion; 0 / Proto-Oncogene Proteins c-bcl-2
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57. Ott G, Balague-Ponz O, de Leval L, de Jong D, Hasserjian RP, Elenitoba-Johnson KS: Commentary on the WHO classification of tumors of lymphoid tissues (2008): indolent B cell lymphomas. J Hematop; 2009 Jul;2(2):77-81
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  • [Title] Commentary on the WHO classification of tumors of lymphoid tissues (2008): indolent B cell lymphomas.
  • The 4th edition of the World Health Organization classification of tumors of hematopoietic and lymphoid tissues introduces many new items to the classification scheme of the so-called indolent B cell lymphomas.
  • New proposed entities, such as splenic B cell lymphoma/leukemia, unclassifiable, splenic diffuse red pulp small B cell lymphoma, hairy cell leukemia variant, pediatric follicular lymphoma, and pediatric marginal zone lymphoma have been coined, and some definitions of established diseases, such as chronic lymphocytic leukemia or Waldenström's macroglobulinemia have been revised.
  • One aspect of major importance is the recent description of small clonal B cell populations, in part with a CLL phenotype, and their relationship to B-CLL.
  • Some new subtypes or variants of follicular lymphoma with distinct clinicopathologic and/or molecular genetic characteristics have been described, including primary follicular lymphomas of the duodenum and pediatric follicular lymphomas.
  • Furthermore, the impact of some probably early, or precursor lesions, such as follicular lymphoma in situ is discussed.

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  • [Cites] Cancer Cell. 2003 Feb;3(2):185-97 [12620412.001]
  • [Cites] Blood. 2002 May 15;99(10):3806-12 [11986240.001]
  • [Cites] Blood. 2002 May 1;99(9):3376-82 [11964306.001]
  • [Cites] Blood. 2002 Mar 15;99(6):1959-64 [11877266.001]
  • [Cites] N Engl J Med. 2009 Feb 12;360(7):659-67 [19213679.001]
  • [Cites] N Engl J Med. 2008 Aug 7;359(6):575-83 [18687638.001]
  • [Cites] Am J Surg Pathol. 2003 Apr;27(4):522-31 [12657939.001]
  • [Cites] Am J Surg Pathol. 2005 Dec;29(12):1661-4 [16327439.001]
  • [Cites] Blood. 2005 Dec 15;106(13):4315-21 [16123218.001]
  • [Cites] Leukemia. 2004 Oct;18(10):1722-6 [15356642.001]
  • [Cites] Am J Clin Pathol. 2004 Apr;121(4):464-72 [15080297.001]
  • [Cites] Semin Oncol. 2003 Apr;30(2):110-5 [12720118.001]
  • [Cites] Hum Pathol. 2006 May;37(5):528-33 [16647949.001]
  • (PMID = 19669189.001).
  • [ISSN] 1868-9256
  • [Journal-full-title] Journal of hematopathology
  • [ISO-abbreviation] J Hematop
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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58. Jabłońska J, Jesionek-Kupnicka D: Usefulness of immunohistochemistry in identification of prognostically important subgroups (GCB and ABC) in a heterogeneous group of diffuse large B-cell lymphomas--a review article. Pol J Pathol; 2008;59(3):121-7
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  • [Title] Usefulness of immunohistochemistry in identification of prognostically important subgroups (GCB and ABC) in a heterogeneous group of diffuse large B-cell lymphomas--a review article.
  • Although diffuse large B cell lymphomas (DLBCL) are considered in the WHO classification a specific histopathological type, their diversity in the clinical features, morphology and molecular aberrations strongly suggest that these tumors represent a heterogeneous group of neoplasms rather than a single clinicopathological entity.
  • Although it has been proven that gene expression profiling using cDNA microarrays could identify prognostically important subgroup of DLBCL: germinal center B-cell (GCB)-like DLBCL and activated B-cell (ABC)-like DLBCL, this method is impractical as a clinical tool.
  • Employing various immunohistochemical antibodies, such as CD10, CD138, anti-Bcl-2, anti-Bcl-6, MUM1 and anti-p53, several groups have aimed at subclassifying DLBCL into the GCB and ABC subgroups with comparable differences in clinical behavior.
  • [MeSH-major] Biomarkers, Tumor / analysis. Immunohistochemistry. Lymphoma, Large B-Cell, Diffuse / classification. Lymphoma, Large B-Cell, Diffuse / diagnosis

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  • (PMID = 19097355.001).
  • [ISSN] 1233-9687
  • [Journal-full-title] Polish journal of pathology : official journal of the Polish Society of Pathologists
  • [ISO-abbreviation] Pol J Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 41
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59. Robbiani DF, Bunting S, Feldhahn N, Bothmer A, Camps J, Deroubaix S, McBride KM, Klein IA, Stone G, Eisenreich TR, Ried T, Nussenzweig A, Nussenzweig MC: AID produces DNA double-strand breaks in non-Ig genes and mature B cell lymphomas with reciprocal chromosome translocations. Mol Cell; 2009 Nov 25;36(4):631-41
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  • [Title] AID produces DNA double-strand breaks in non-Ig genes and mature B cell lymphomas with reciprocal chromosome translocations.
  • Cancer-initiating translocations such as those associated with lymphomas require the formation of paired DNA double-strand breaks (DSBs).
  • Activation-induced cytidine deaminase (AID) produces widespread somatic mutation in mature B cells; however, the extent of "off-target" DSB formation and its role in translocation-associated malignancy is unknown.
  • Here, we show that deregulated expression of AID causes widespread genome instability, which alone is insufficient to induce B cell lymphoma; transformation requires concomitant loss of the tumor suppressor p53.
  • Mature B cell lymphomas arising as a result of deregulated AID expression are phenotypically diverse and harbor clonal reciprocal translocations involving a group of Immunoglobulin (Ig) and non-Ig genes that are direct targets of AID.
  • This group includes miR-142, a previously unknown micro-RNA target that is translocated in human B cell malignancy.
  • We conclude that AID produces DSBs throughout the genome, which can lead to lymphoma-associated chromosome translocations in mature B cells.

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  • [Cites] J Cell Biol. 2004 May 24;165(4):459-64 [15159415.001]
  • [Cites] J Clin Invest. 2004 Jun;113(12):1711-21 [15199406.001]
  • [Cites] Immunol Rev. 2004 Aug;200:5-11 [15242391.001]
  • [Cites] Cell. 2004 Aug 20;118(4):431-8 [15315756.001]
  • [Cites] Nat Immunol. 2004 Nov;5(11):1117-23 [15489857.001]
  • [Cites] Nature. 1983 Apr 14;302(5909):575-81 [6300689.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 May;81(10):3180-4 [6203114.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8867-71 [2682663.001]
  • [Cites] Infect Immun. 1990 Nov;58(11):3671-8 [1977706.001]
  • [Cites] Curr Biol. 1994 Jan 1;4(1):1-7 [7922305.001]
  • [Cites] Mol Cell Biol. 1998 Jun;18(6):3495-501 [9584189.001]
  • [Cites] Science. 1998 Jun 12;280(5370):1750-2 [9624052.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11816-21 [9751748.001]
  • [Cites] J Exp Med. 2004 Nov 1;200(9):1103-10 [15520243.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):307-15 [15549092.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1590-5 [15668392.001]
  • [Cites] Adv Immunol. 2005;86:43-112 [15705419.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):251-62 [15803153.001]
  • [Cites] Nat Cell Biol. 2005 Jul;7(7):675-85 [15965469.001]
  • [Cites] Leukemia. 2005 Jul;19(7):1278-80 [15843816.001]
  • [Cites] Nature. 2006 Mar 2;440(7080):105-9 [16400328.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2752-7 [16477013.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jun 6;103(23):8798-803 [16723391.001]
  • [Cites] Genes Dev. 2006 Jun 15;20(12):1539-44 [16778072.001]
  • [Cites] Cancer Res. 2006 Aug 15;66(16):7837-9 [16912154.001]
  • [Cites] DNA Repair (Amst). 2006 Sep 8;5(9-10):1234-45 [16793349.001]
  • [Cites] J Med Genet. 2007 Jan;44(1):51-8 [16971479.001]
  • [Cites] Adv Immunol. 2007;94:75-107 [17560272.001]
  • [Cites] Annu Rev Biochem. 2007;76:1-22 [17328676.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1401-14 [17604727.001]
  • [Cites] Pathol Int. 2007 Aug;57(8):474-84 [17610471.001]
  • [Cites] Cell. 2007 Jul 13;130(1):63-75 [17599403.001]
  • [Cites] Nat Immunol. 2007 Aug;8(8):801-8 [17641661.001]
  • [Cites] J Exp Med. 2007 Sep 3;204(9):2225-32 [17724134.001]
  • [Cites] J Exp Med. 2007 Nov 26;204(12):2989-3001 [17998390.001]
  • [Cites] Annu Rev Genet. 2007;41:107-20 [17576170.001]
  • [Cites] Nat Genet. 2008 Jan;40(1):108-12 [18066064.001]
  • [Cites] Nature. 2008 Feb 14;451(7180):841-5 [18273020.001]
  • [Cites] Mol Immunol. 2008 Apr;45(7):1883-92 [18067961.001]
  • [Cites] Annu Rev Immunol. 2008;26:481-511 [18304001.001]
  • [Cites] Annu Rev Immunol. 2008;26:261-92 [18370922.001]
  • [Cites] Immunity. 2008 May;28(5):621-9 [18450484.001]
  • [Cites] Immunity. 2008 May;28(5):630-8 [18455451.001]
  • [Cites] Nature. 2009 Apr 30;458(7242):1127-30 [19407794.001]
  • [Cites] Cell. 2009 May 1;137(3):391-5 [19410533.001]
  • [Cites] Nat Struct Mol Biol. 2009 May;16(5):517-27 [19412186.001]
  • [Cites] Cell. 2009 May 15;137(4):609-22 [19450511.001]
  • [Cites] Annu Rev Immunol. 2002;20:165-96 [11861601.001]
  • [Cites] Cell Cycle. 2009 Aug;8(15):2408-12 [19556863.001]
  • [Cites] Nature. 2009 Jul 9;460(7252):231-6 [19587764.001]
  • [Cites] Ann Trop Med Parasitol. 2000 Jan;94(1):23-35 [10723521.001]
  • [Cites] Cell. 2000 Sep 1;102(5):553-63 [11007474.001]
  • [Cites] Science. 2001 Feb 23;291(5508):1541-4 [11222858.001]
  • [Cites] J Exp Med. 2008 Jun 9;205(6):1357-68 [18474627.001]
  • [Cites] J Natl Cancer Inst Monogr. 2008;(39):8-11 [18647994.001]
  • [Cites] J Exp Med. 2008 Sep 1;205(9):1949-57 [18678733.001]
  • [Cites] J Exp Med. 2008 Oct 27;205(11):2585-94 [18838546.001]
  • [Cites] Oncogene. 2008 Oct 27;27(50):6462-72 [18955973.001]
  • [Cites] Cell. 2008 Dec 12;135(6):1028-38 [19070574.001]
  • [Cites] Cell. 2008 Dec 12;135(6):1130-42 [19070581.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2717-22 [19196992.001]
  • [Cites] Oncogene. 2001 Sep 10;20(40):5580-94 [11607811.001]
  • [Cites] Nature. 2001 Dec 6;414(6864):660-5 [11740565.001]
  • [Cites] Cell. 2002 Apr;109 Suppl:S45-55 [11983152.001]
  • [Cites] Nature. 2002 Jul 4;418(6893):99-103 [12097915.001]
  • [Cites] Nat Rev Immunol. 2002 Dec;2(12):920-32 [12461565.001]
  • [Cites] J Exp Med. 2003 May 5;197(9):1173-81 [12732658.001]
  • [Cites] Immunol Rev. 2003 Aug;194:177-95 [12846815.001]
  • [Cites] Cell. 2003 Aug 8;114(3):359-70 [12914700.001]
  • [Cites] Nat Rev Cancer. 2003 Sep;3(9):639-49 [12951583.001]
  • [Cites] Science. 2004 Jan 2;303(5654):83-6 [14657504.001]
  • [Cites] Nat Immunol. 2004 May;5(5):481-7 [15077110.001]
  • [Cites] J Exp Med. 2004 May 3;199(9):1235-44 [15117971.001]
  • (PMID = 19941823.001).
  • [ISSN] 1097-4164
  • [Journal-full-title] Molecular cell
  • [ISO-abbreviation] Mol. Cell
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI037526; United States / NIAID NIH HHS / AI / R01 AI037526-16; United States / NIAID NIH HHS / AI / AI037526-16; United States / NIGMS NIH HHS / GM / GM07739; United States / Intramural NIH HHS / / ; United States / NIAID NIH HHS / AI / AI037526; United States / NIAID NIH HHS / AI / R37 AI037526; United States / NIGMS NIH HHS / GM / T32 GM007739
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs; 0 / Mirn142 microRNA, mouse; 0 / Proto-Oncogene Proteins c-myc; 0 / Tumor Suppressor Protein p53; EC 3.5.4.- / AICDA (activation-induced cytidine deaminase); EC 3.5.4.5 / Cytidine Deaminase
  • [Other-IDs] NLM/ NIHMS163437; NLM/ PMC2805907
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60. Arai M, Sasaki A, Saito N, Nakazato Y: Immunohistochemical analysis of cleaved caspase-3 detects high level of apoptosis frequently in diffuse large B-cell lymphomas of the central nervous system. Pathol Int; 2005 Mar;55(3):122-9
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  • [Title] Immunohistochemical analysis of cleaved caspase-3 detects high level of apoptosis frequently in diffuse large B-cell lymphomas of the central nervous system.
  • The purpose of the present paper was to examine the level of apoptosis and the relationships among apoptosis, apoptosis-associated proteins, and proliferating potential in lymphoma tissues to clarify the characteristics of apoptosis in diffuse large B-cell lymphomas (DLBCL) of the central nervous system (CNS).
  • The formalin-fixed, paraffin-embedded tissues of CNS and non-CNS DLBCL (20 cases each) were studied by terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) and immunohistochemistry, using antibodies against single-stranded DNA (ssDNA), cleaved caspase-3, bcl-2, bax, p53, Fas and Ki-67.
  • The cleaved caspase-3 immunohistochemistry detected apoptosis of the lymphoma cells most sensitively compared to TUNEL and ssDNA immunohistochemistry.
  • High expression (grade + + or + + +) of cleaved caspase-3 was found more frequently in CNS DLBCL (11 cases, 55%) than non-CNS DLBCL (three cases, 15%; P = 0.009).
  • Bax-positivity of lymphoma cells was increased in six cases of CNS DLBCL, which also showed high positivity of cleaved caspase-3.
  • The present study indicates that the number of apoptotic cells and expression level of cleaved caspase-3 were significantly higher in CNS DLBCL than non-CNS DLBCL, and that the correlation of bax and cleaved caspase-3 expression was often present in CNS DLBCL.
  • [MeSH-major] Apoptosis. Brain Neoplasms / enzymology. Caspases / metabolism. Lymphoma, B-Cell / enzymology. Lymphoma, Large B-Cell, Diffuse / enzymology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Caspase 3. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Immunoenzyme Techniques. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Male. Middle Aged

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  • (PMID = 15743320.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
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61. Abramson JS, Chen W, Juszczynski P, Takahashi H, Neuberg D, Kutok JL, Takeyama K, Shipp MA: The heat shock protein 90 inhibitor IPI-504 induces apoptosis of AKT-dependent diffuse large B-cell lymphomas. Br J Haematol; 2009 Feb;144(3):358-66
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  • [Title] The heat shock protein 90 inhibitor IPI-504 induces apoptosis of AKT-dependent diffuse large B-cell lymphomas.
  • Gene expression profiling was utilized to characterize HSP90 isoform expression in primary human diffuse large B-cell lymphomas (DLBCLs).
  • Thereafter, we assessed the activity of the HSP90 inhibitor, IPI-504, in an extensive panel of DLBCL cell lines.
  • IPI-504, which interacts with the conserved ATP-binding site in both HSP90 isoforms, inhibited proliferation and induced apoptosis in the majority of DLBCL cell lines at low micromolar concentrations.
  • IPI-504-sensitive cell lines expressed high levels of the HSP90 client protein, pAKT, and exhibited dose-dependent decreases in pAKT levels following IPI-504 treatment and significantly reduced proliferation following AKT RNAi.
  • Furthermore, the combination of low-dose (<1 micromol/l) IPI-504 and the AKT/Pi3K pathway inhibitor, LY24009, was synergistic in IPI-504-sensitive DLBCL cell lines.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzoquinones / pharmacology. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Lactams, Macrocyclic / pharmacology. Lymphoma, Large B-Cell, Diffuse / drug therapy
  • [MeSH-minor] Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Doxorubicin / pharmacology. Enzyme Activation. Gene Deletion. Gene Expression Profiling. Humans. Oligonucleotide Array Sequence Analysis. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein Isoforms / analysis. Protein Isoforms / metabolism. Protein Kinase Inhibitors / pharmacology. Proto-Oncogene Proteins c-akt / genetics. Proto-Oncogene Proteins c-akt / metabolism. RNA, Small Interfering / pharmacology

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  • [Cites] Biochem Pharmacol. 2006 Nov 15;72(10):1246-56 [16979140.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17408-13 [17090671.001]
  • [Cites] Exp Hematol. 2006 Dec;34(12):1670-9 [17157164.001]
  • [Cites] Clin Cancer Res. 2007 Mar 1;13(5):1591-600 [17332306.001]
  • [Cites] Leukemia. 2000 Jul;14(7):1161-73 [10914538.001]
  • [Cites] Blood. 2000 Sep 15;96(6):2284-91 [10979978.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Sep 26;97(20):10832-7 [10995457.001]
  • [Cites] J Natl Cancer Inst. 2000 Oct 4;92(19):1564-72 [11018092.001]
  • [Cites] Bone Marrow Transplant. 2000 Oct;26(7):797-800 [11042664.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):1799-804 [11280726.001]
  • [Cites] Eur J Cancer. 2001 Sep;37(13):1590-8 [11527683.001]
  • [Cites] Oncogene. 2002 Feb 14;21(8):1159-66 [11850835.001]
  • [Cites] Trends Mol Med. 2002;8(4 Suppl):S55-61 [11927289.001]
  • [Cites] Clin Cancer Res. 2002 May;8(5):986-93 [12006510.001]
  • [Cites] Nat Rev Cancer. 2002 Jul;2(7):489-501 [12094235.001]
  • [Cites] Int J Cancer. 2002 Jul 1;100(1):37-42 [12115584.001]
  • [Cites] Blood. 2002 Oct 15;100(8):3041-4 [12351420.001]
  • [Cites] J Biol Chem. 2002 Oct 18;277(42):39858-66 [12176997.001]
  • [Cites] Bone Marrow Transplant. 2003 Feb;31(4):315 [12621472.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):213-7 [12676580.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2139-44 [12727831.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] Br J Cancer. 2004 Jan 26;90(2):304-5 [14974481.001]
  • [Cites] FEBS Lett. 2004 Mar 26;562(1-3):11-5 [15069952.001]
  • [Cites] Nat Cell Biol. 2004 Jun;6(6):507-14 [15146192.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] Blood. 1990 Feb 1;75(3):781-6 [2297578.001]
  • [Cites] J Biol Chem. 1994 Feb 18;269(7):5241-8 [8106507.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Aug 30;91(18):8324-8 [8078881.001]
  • [Cites] Cancer Chemother Pharmacol. 1995;36(4):305-15 [7628050.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Dec 10;93(25):14536-41 [8962087.001]
  • [Cites] Cell. 1997 Apr 18;89(2):239-50 [9108479.001]
  • [Cites] Cell. 1997 Jul 11;90(1):65-75 [9230303.001]
  • [Cites] J Biol Chem. 1997 Sep 19;272(38):23843-50 [9295332.001]
  • [Cites] Cancer Chemother Pharmacol. 1998;42(4):273-9 [9744771.001]
  • [Cites] Anticancer Res. 1998 Nov-Dec;18(6B):4705-8 [9891544.001]
  • [Cites] FEBS Lett. 1999 Sep 3;457(3):343-7 [10471805.001]
  • [Cites] Int J Cancer. 2005 Jan 10;113(2):179-88 [15455381.001]
  • [Cites] Blood. 2005 Jan 1;105(1):308-16 [15331441.001]
  • [Cites] Blood. 2005 Feb 1;105(3):1246-55 [15388581.001]
  • [Cites] Haematologica. 2005 Feb;90(2):274-5 [15710591.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1885-93 [15774780.001]
  • [Cites] Clin Cancer Res. 2005 Apr 15;11(8):3102-8 [15837766.001]
  • [Cites] Blood. 2005 Jul 1;106(1):318-27 [15784732.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1164-74 [15855278.001]
  • [Cites] Blood. 2005 Aug 15;106(4):1392-9 [15870177.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):761-72 [16175177.001]
  • [Cites] Leuk Lymphoma. 2005 Nov;46(11):1671-4 [16236621.001]
  • [Cites] Cancer Res. 2005 Nov 15;65(22):10536-44 [16288046.001]
  • [Cites] Oncogene. 2005 Nov 14;24(50):7482-92 [16288295.001]
  • [Cites] Br J Haematol. 2006 Feb;132(4):503-11 [16412023.001]
  • [Cites] Clin Cancer Res. 2006 Jan 15;12(2):584-90 [16428504.001]
  • [Cites] Blood. 2006 Feb 1;107(3):1092-100 [16234364.001]
  • [Cites] Mol Cell Biol. 2006 Jul;26(14):5348-59 [16809771.001]
  • [Cites] J Med Chem. 2006 Jul 27;49(15):4606-15 [16854066.001]
  • [Cites] Cell Death Differ. 2006 Sep;13(9):1434-41 [16311509.001]
  • [Cites] Br J Haematol. 2006 Oct;135(1):68-71 [16925576.001]
  • (PMID = 19036086.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA092625
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Lactams, Macrocyclic; 0 / Protein Isoforms; 0 / Protein Kinase Inhibitors; 0 / RNA, Small Interfering; 4GY0AVT3L4 / tanespimycin; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ NIHMS501907; NLM/ PMC4029164
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62. Dawson DW, Hong JS, Shen RR, French SW, Troke JJ, Wu YZ, Chen SS, Gui D, Regelson M, Marahrens Y, Morse HC 3rd, Said J, Plass C, Teitell MA: Global DNA methylation profiling reveals silencing of a secreted form of Epha7 in mouse and human germinal center B-cell lymphomas. Oncogene; 2007 Jun 21;26(29):4243-52
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  • [Title] Global DNA methylation profiling reveals silencing of a secreted form of Epha7 in mouse and human germinal center B-cell lymphomas.
  • Most human lymphomas originate from transformed germinal center (GC) B lymphocytes.
  • While activating mutations and translocations of MYC, BCL2 and BCL6 promote specific GC lymphoma subtypes, other genetic and epigenetic modifications that contribute to malignant progression in the GC remain poorly defined.
  • Recently, aberrant expression of the TCL1 proto-oncogene was identified in major GC lymphoma subtypes.
  • TCL1 transgenic mice offer unique models of both aggressive GC and marginal zone B-cell lymphomas, further supporting a role for TCL1 in B-cell transformation.
  • Here, restriction landmark genomic scanning was employed to discover tumor-associated epigenetic alterations in malignant GC and marginal zone B-cells in TCL1 transgenic mice.
  • EPHA7 was hypermethylated and repressed in both mouse and human GC B-cell non-Hodgkin lymphomas, with the potential to influence tumor progression and spread.
  • These data provide the first set of hypermethylated genes with the potential to complement TCL1-mediated GC B-cell transformation and spread.

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  • [Cites] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790.001]
  • [Cites] Clin Immunol. 2003 Oct;109(1):80-8 [14585279.001]
  • [Cites] Neoplasia. 2003 Sep-Oct;5(5):445-56 [14670182.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):910-9 [14871820.001]
  • [Cites] Clin Chem. 2004 Mar;50(3):490-9 [14726470.001]
  • [Cites] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):29-39 [15000147.001]
  • [Cites] Cancer Res. 2004 Apr 1;64(7):2424-33 [15059895.001]
  • [Cites] Oncogene. 1995 Jan 5;10(1):97-108 [7824284.001]
  • [Cites] Neuron. 1996 Jul;17(1):9-19 [8755474.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):837-41 [9041182.001]
  • [Cites] Blood. 1997 Nov 1;90(9):3613-22 [9345045.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9809-14 [10449776.001]
  • [Cites] Cytokine Growth Factor Rev. 2004 Dec;15(6):419-33 [15561600.001]
  • [Cites] Nat Genet. 2005 Mar;37(3):265-74 [15723065.001]
  • [Cites] Curr Opin Hematol. 2005 Jul;12(4):292-7 [15928486.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Jun;6(6):462-75 [15928710.001]
  • [Cites] IUBMB Life. 2005 Jun;57(6):421-31 [16012051.001]
  • [Cites] Nat Rev Cancer. 2005 Aug;5(8):640-8 [16056259.001]
  • [Cites] Oncogene. 2005 Aug 25;24(36):5637-47 [16007213.001]
  • [Cites] Curr Top Microbiol Immunol. 2005;294:31-49 [16329192.001]
  • [Cites] Blood Rev. 2006 Jan;20(1):1-13 [16426940.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11713-8 [16864779.001]
  • [Cites] Blood. 2006 Sep 15;108(6):1991-8 [16728701.001]
  • [Cites] Blood. 2000 Jan 1;95(1):221-30 [10607706.001]
  • [Cites] Nat Genet. 2000 Feb;24(2):132-8 [10655057.001]
  • [Cites] Cancer Res. 2000 Apr 15;60(8):2095-100 [10786666.001]
  • [Cites] Nature. 2000 Nov 9;408(6809):203-6 [11089974.001]
  • [Cites] Lab Invest. 2001 Apr;81(4):555-64 [11304575.001]
  • [Cites] Blood. 2001 May 15;97(10):3226-33 [11342453.001]
  • [Cites] J Natl Cancer Inst. 2002 Jan 2;94(1):26-32 [11773279.001]
  • [Cites] Genome Res. 2002 Apr;12(4):656-64 [11932250.001]
  • [Cites] Trends Neurosci. 2002 May;25(5):239-43 [11972959.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6955-60 [12011454.001]
  • [Cites] Methods. 2002 Jun;27(2):144-9 [12095273.001]
  • [Cites] Cancer Lett. 2002 Nov 8;185(1):1-12 [12142073.001]
  • [Cites] Oncogene. 2002 Oct 10;21(46):7011-26 [12370823.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14392-7 [12381789.001]
  • [Cites] Eur J Immunol. 2002 Dec;32(12):3745-55 [12516569.001]
  • [Cites] Genes Dev. 2003 Jun 15;17(12):1429-50 [12815065.001]
  • [Cites] Adv Exp Med Biol. 2003;532:39-49 [12908548.001]
  • [Cites] Blood. 2003 Dec 15;102(13):4431-40 [12907451.001]
  • (PMID = 17260020.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA107300; United States / NCI NIH HHS / CA / T32CA09056; United States / NCI NIH HHS / CA / R01 CA090571; United States / NEI NIH HHS / EY / PN2 EY018228; United States / PHS HHS / / T32A107126; United States / NIGMS NIH HHS / GM / R01 GM073981; United States / NICHD NIH HHS / HD / R01 HD041451; United States / Intramural NIH HHS / / ; United States / NEI NIH HHS / EY / PN2 EY018228-02; United States / NCI NIH HHS / CA / T32 CA009120; United States / NCI NIH HHS / CA / T32 CA009056; United States / NCI NIH HHS / CA / T32CA009120; United States / NICHD NIH HHS / HD / HD041451; United States / NEI NIH HHS / EY / EY018228-02; United States / NIGMS NIH HHS / GM / R01GM073981
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Validation Studies
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, EphA7
  • [Other-IDs] NLM/ NIHMS131749; NLM/ PMC2756834
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63. Kodama K, Massone C, Chott A, Metze D, Kerl H, Cerroni L: Primary cutaneous large B-cell lymphomas: clinicopathologic features, classification, and prognostic factors in a large series of patients. Blood; 2005 Oct 1;106(7):2491-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary cutaneous large B-cell lymphomas: clinicopathologic features, classification, and prognostic factors in a large series of patients.
  • In the new World Health Organization/European Organization for Research and Treatment of Cancer (WHO/EORTC) classification of cutaneous lymphomas, large B-cell lymphomas (LBCLs) are divided into 3 groups: LBCL, leg-type (LBCLLT); follicle center lymphoma, diffuse type (FCLDT); and LBCL, others (LBCLO).
  • Ninety-three cases of primary cutaneous LBCL were analyzed for clinicopathologic features, expression of several markers including Bcl-2, Bcl-6, MUM-1, and FOX-P1, in situ hybridization for Epstein-Barr virus, and molecular analyses of IGH gene rearrangement and of Borrelia burgdorferi and human herpesvirus 8 DNA.
  • Our study shows that accurate morphologic and phenotypic analyses allow us to stratify most patients into the prognostically different categories of LBCLLT and FCLDT.
  • [MeSH-major] Lymphoma, B-Cell / diagnosis. Lymphoma, B-Cell / metabolism. Skin Neoplasms / diagnosis. Skin Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Borrelia burgdorferi / metabolism. DNA Primers / chemistry. Female. Forkhead Transcription Factors / biosynthesis. Gene Rearrangement. Genes, Immunoglobulin Heavy Chain / genetics. Herpesvirus 4, Human / metabolism. Herpesvirus 8, Human / metabolism. Humans. Immunohistochemistry. In Situ Hybridization. Interferon Regulatory Factors / biosynthesis. Male. Middle Aged. Phenotype. Polymerase Chain Reaction. Prognosis. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Repressor Proteins / biosynthesis. Time Factors. Treatment Outcome

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  • (PMID = 15947086.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / FOXP1 protein, human; 0 / Forkhead Transcription Factors; 0 / Interferon Regulatory Factors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Repressor Proteins; 0 / interferon regulatory factor-4
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64. Vieira L, Martinho A, Antunes O, Silva E, Ambrósio AP, Geraldes MC, Nascimento R, Silva C, Pereira JM, Júnior EC, Jordan P: Combined molecular diagnosis of B-cell lymphomas with t(11;14)(q13;q32) or t(14;18)(q32;q21) using multiplex- and long distance inverse-polymerase chain reaction. Diagn Mol Pathol; 2008 Jun;17(2):73-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined molecular diagnosis of B-cell lymphomas with t(11;14)(q13;q32) or t(14;18)(q32;q21) using multiplex- and long distance inverse-polymerase chain reaction.
  • Translocations t(14;18)(q32;q21) and t(11;14)(q13;q32) are recurrent findings in follicular lymphoma (FL) and mantle cell lymphoma (MCL), respectively.
  • Taken together, we show that multiplex-PCR combined with long distance inverse-PCR detected a t(14;18) in 82% of FL patients and a t(11;14) in 91% of MCL patients, demonstrating that this 2-step protocol is an effective approach for molecular detection of t(11;14) and t(14;18) in B-cell lymphomas.
  • [MeSH-major] Chromosomes, Human, Pair 11 / genetics. Chromosomes, Human, Pair 14 / genetics. Chromosomes, Human, Pair 18 / genetics. Lymphoma, B-Cell / diagnosis. Polymerase Chain Reaction / methods. Translocation, Genetic
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cyclin D. Cyclins / genetics. DNA, Neoplasm / genetics. Female. Gene Fusion. Genes, bcl-2. Humans. Immunoglobulin Heavy Chains / genetics. Male. Middle Aged. Molecular Diagnostic Techniques

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  • (PMID = 18382373.001).
  • [ISSN] 1533-4066
  • [Journal-full-title] Diagnostic molecular pathology : the American journal of surgical pathology, part B
  • [ISO-abbreviation] Diagn. Mol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclin D; 0 / Cyclins; 0 / DNA, Neoplasm; 0 / Immunoglobulin Heavy Chains
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65. Boons GJ: Liposomes modified by carbohydrate ligands can target B cells for the treatment of B-cell lymphomas. Expert Rev Vaccines; 2010 Nov;9(11):1251-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Liposomes modified by carbohydrate ligands can target B cells for the treatment of B-cell lymphomas.
  • In vivo targeting of B-cell lymphoma with glycan ligands of CD22.
  • A strategy has been developed to deliver selectively chemotherapeutic drugs to B cells by employing doxorubicin-loaded liposomes modified by a ligand for the B-cell-specific cell-surface protein CD22, also known as Siglec-2.
  • The liposomes bound in a rapid and saturable manner to the human Burkitt lymphoma Daudi B-cell line and exhibited significantly higher cytotoxicity in vitro and in vivo compared with similar untargeted liposomes.
  • The CD22-targeted liposome bound to B cells isolated from lymphoma patients and although binding was proportional to CD22 expression on the cell surface, low levels of expression on chronic lymphocytic leukemia cells were sufficient to effect cell neutralization.
  • The glycan-based strategy for delivery of chemotherapeutic agents may provide a new strategy for the treatment of B-cell lymphomas.

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  • [CommentOn] Blood. 2010 Jun 10;115(23):4778-86 [20181615.001]
  • (PMID = 21087105.001).
  • [ISSN] 1744-8395
  • [Journal-full-title] Expert review of vaccines
  • [ISO-abbreviation] Expert Rev Vaccines
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA088986; United States / NCI NIH HHS / CA / R01CA088986
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS258963; NLM/ PMC3016876
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66. Hoeller S, Schneider A, Haralambieva E, Dirnhofer S, Tzankov A: FOXP1 protein overexpression is associated with inferior outcome in nodal diffuse large B-cell lymphomas with non-germinal centre phenotype, independent of gains and structural aberrations at 3p14.1. Histopathology; 2010 Jul;57(1):73-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] FOXP1 protein overexpression is associated with inferior outcome in nodal diffuse large B-cell lymphomas with non-germinal centre phenotype, independent of gains and structural aberrations at 3p14.1.
  • AIMS: To determine the molecular epidemiology and prognostic importance of structural and numeric FOXP1 gene aberrations with respect to BCL-6 gene and to FOXP1 protein expression in 389 diffuse large B-cell lymphomas (DLBCL) from the pre-rituximab era on tissue microarrays.
  • Seven percent of cases with known BCL-6 and FOXP1 gene status (n = 159) showed an isolated FOXP1 gain, 19% an isolated BCL-6 gain and 18% a trisomy 3.
  • FOXP1 gains (isolated and due to trisomy 3) were more frequent in nodal than extranodal DLBCL and in non-germinal centre B-cell-like (non-GCB) DLBCL than in GCB DLBCL.
  • By immunohistochemistry, FOXP1 protein was more often overexpressed in non-GCB than in GCB cases.
  • FOXP1 overexpression was associated with poor disease-specific survival in all DLBCL, particularly in nodal and non-GCB cases.
  • [MeSH-major] Chromosomes, Human, Pair 3 / genetics. Forkhead Transcription Factors / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / pathology. Repressor Proteins / genetics

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  • (PMID = 20579129.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FOXP1 protein, human; 0 / Forkhead Transcription Factors; 0 / Repressor Proteins
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67. Sarosiek KA, Nechushtan H, Lu X, Rosenblatt JD, Lossos IS: Interleukin-4 distinctively modifies responses of germinal centre-like and activated B-cell-like diffuse large B-cell lymphomas to immuno-chemotherapy. Br J Haematol; 2009 Nov;147(3):308-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin-4 distinctively modifies responses of germinal centre-like and activated B-cell-like diffuse large B-cell lymphomas to immuno-chemotherapy.
  • Diffuse large B-cell lymphomas (DLBCLs) can be classified into two subtypes: germinal-centre B-cell (GCB)-like and Activated B-cell (ABC)-like tumours, which are associated with longer or shorter patient overall survival, respectively.
  • We hypothesized that these differences may contribute to the different clinical behaviour and outcome of DLBCL subtypes.
  • Herein, we demonstrated that IL-4 increased the sensitivity of GCB-like DLBCL to doxorubicin-induced apoptosis and complement-dependent rituximab cell killing.
  • The distinct effects of IL-4 on doxorubicin sensitivity in GCB-like and ABC-like DLBCL cells may be partially attributed to the contrasting effects of the cytokine on Bcl-2 and Bad protein levels in the DLBCL subtypes.
  • These findings suggest that the different effects of IL-4 on chemotherapy and immunotherapy-induced cytotoxicity of GCB- and ABC-like DLBCL could contribute to the different clinical outcomes exhibited by patients with these two subtypes of DLBCL.

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  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3121-7 [16754935.001]
  • [Cites] Blood. 2008 Nov 15;112(10):4098-108 [18716132.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4178-86 [16946303.001]
  • [Cites] Mol Cell Biol. 2007 Mar;27(6):2166-79 [17210636.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Blood. 2000 Jun 15;95(12):3900-8 [10845926.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 29;97(18):10209-13 [10954754.001]
  • [Cites] Blood. 2001 Sep 1;98(5):1352-7 [11520782.001]
  • [Cites] Cell Immunol. 2001 Aug 1;211(2):131-42 [11591117.001]
  • [Cites] J Immunol Methods. 2001 Dec 1;258(1-2):183-91 [11684135.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] N Engl J Med. 2002 Jan 24;346(4):235-42 [11807147.001]
  • [Cites] Br J Haematol. 2001 Dec;115(4):807-11 [11843813.001]
  • [Cites] Blood. 2002 Apr 1;99(7):2285-90 [11895757.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Leuk Lymphoma. 2002 Jun;43(6):1313-21 [12153001.001]
  • [Cites] Leukemia. 2003 Apr;17(4):789-95 [12682639.001]
  • [Cites] J Clin Oncol. 2003 Apr 15;21(8):1466-71 [12697868.001]
  • [Cites] J Immunol. 2003 Aug 15;171(4):1722-31 [12902471.001]
  • [Cites] N Engl J Med. 2004 Apr 29;350(18):1828-37 [15115829.001]
  • [Cites] Gynecol Oncol. 2004 Sep;94(3):785-95 [15350374.001]
  • [Cites] Blood. 1990 Mar 1;75(5):1114-8 [2306518.001]
  • [Cites] Cell. 1997 Sep 19;90(6):1073-83 [9323135.001]
  • [Cites] FEBS Lett. 1997 Nov 17;417(3):360-4 [9409752.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2924-32 [15591113.001]
  • [Cites] Blood. 2005 May 15;105(10):3979-86 [15677569.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3205-11 [16373664.001]
  • [Cites] Leuk Lymphoma. 2007 Jul;48(7):1290-8 [17613756.001]
  • [Cites] Cell Res. 2007 Nov;17(11):942-55 [17968425.001]
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):447-54 [18086797.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):4027-35 [16818702.001]
  • (PMID = 19694722.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA109335-03; United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / R01 CA122105; United States / NCI NIH HHS / CA / R01 CA109335-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; 207137-56-2 / Interleukin-4; 4F4X42SYQ6 / Rituximab; 80168379AG / Doxorubicin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
  • [Other-IDs] NLM/ NIHMS139972; NLM/ PMC2763052
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68. Cattoretti G, Pasqualucci L, Ballon G, Tam W, Nandula SV, Shen Q, Mo T, Murty VV, Dalla-Favera R: Deregulated BCL6 expression recapitulates the pathogenesis of human diffuse large B cell lymphomas in mice. Cancer Cell; 2005 May;7(5):445-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Deregulated BCL6 expression recapitulates the pathogenesis of human diffuse large B cell lymphomas in mice.
  • Diffuse large B cell lymphomas (DLBCL) derive from germinal center (GC) B cells and display chromosomal alterations deregulating the expression of BCL6, a transcriptional repressor required for GC formation.
  • To investigate the role of BCL6 in DLBCL pathogenesis, we have engineered mice that express BCL6 constitutively in B cells by mimicking a chromosomal translocation found in human DLBCL.
  • These mice display increased GC formation and perturbed post-GC differentiation characterized by a decreased number of post-isotype switch plasma cells.
  • Subsequently, these mice develop a lymphoproliferative syndrome that culminates with the development of lymphomas displaying features typical of human DLBCL.
  • These results define the oncogenic role of BCL6 in the pathogenesis of DLBCL and provide a faithful mouse model of this common disease.
  • [MeSH-major] DNA-Binding Proteins / genetics. Disease Models, Animal. Gene Expression / genetics. Lymphoma, B-Cell / pathology. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Animals. Cell Differentiation / genetics. Chromosome Aberrations. Genes, Immunoglobulin / genetics. Germinal Center / chemistry. Germinal Center / metabolism. Germinal Center / pathology. Hemagglutinins / genetics. Humans. Lymphoma, Non-Hodgkin / genetics. Lymphoma, Non-Hodgkin / pathology. Lymphoproliferative Disorders / genetics. Lymphoproliferative Disorders / pathology. Mice. Mice, Inbred C57BL. Mice, Inbred Strains. Mice, Knockout. Mice, Transgenic. Plasma Cells / chemistry. Plasma Cells / metabolism. Plasma Cells / pathology. Promoter Regions, Genetic / genetics. Spleen / chemistry. Spleen / metabolism. Spleen / pathology. Splenomegaly / pathology. Survival Analysis. Time Factors


69. Yang F, Xian RR, Li Y, Polony TS, Beemon KL: Telomerase reverse transcriptase expression elevated by avian leukosis virus integration in B cell lymphomas. Proc Natl Acad Sci U S A; 2007 Nov 27;104(48):18952-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomerase reverse transcriptase expression elevated by avian leukosis virus integration in B cell lymphomas.
  • In this study, we identified avian leukosis virus (ALV) proviral integration sites in rapid-onset B cell lymphomas arising <12 weeks after infection of chicken embryos.

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  • [Cites] Nature. 2000 Aug 10;406(6796):641-5 [10949306.001]
  • [Cites] Int J Cancer. 2006 Sep 15;119(6):1276-84 [16615118.001]
  • [Cites] Oncogene. 2003 Feb 20;22(7):1073-86 [12592394.001]
  • [Cites] Oncogene. 2003 Jun 12;22(24):3813-20 [12802289.001]
  • [Cites] Oncogene. 2003 Jun 19;22(25):3911-6 [12813464.001]
  • [Cites] Mol Cell Biol. 1988 Nov;8(11):4858-67 [2850470.001]
  • [Cites] J Virol. 1989 Apr;63(4):1630-40 [2538646.001]
  • [Cites] Mol Cell Biol. 1989 Jun;9(6):2657-64 [2548084.001]
  • [Cites] J Virol. 1992 Jan;66(1):512-23 [1309260.001]
  • [Cites] Curr Top Microbiol Immunol. 1991;171:1-25 [1814689.001]
  • [Cites] Poult Sci. 2003 Jun;82(6):917-26 [12817446.001]
  • [Cites] Nat Rev Cancer. 2003 Aug;3(8):623-7 [12894250.001]
  • [Cites] J Virol. 2003 Sep;77(17):9378-87 [12915553.001]
  • [Cites] Nucleic Acids Res. 2004 Jan 1;32(Database issue):D523-7 [14681473.001]
  • [Cites] Cytogenet Genome Res. 2003;102(1-4):309-17 [14970722.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):4983-90 [15297398.001]
  • [Cites] Nature. 1981 Apr 9;290(5806):475-80 [6261142.001]
  • [Cites] Cell. 1981 Aug;25(2):421-31 [6269747.001]
  • [Cites] Nature. 1982 Jan 21;295(5846):209-14 [6276760.001]
  • [Cites] Cell. 1987 Dec 24;51(6):887-98 [3319189.001]
  • [Cites] J Virol. 1988 Apr;62(4):1423-32 [2831403.001]
  • [Cites] J Virol Methods. 1994 Oct;49(3):269-84 [7868645.001]
  • [Cites] Science. 1995 Sep 1;269(5228):1236-41 [7544491.001]
  • [Cites] Nucleic Acids Res. 1997 Jul 1;25(13):2595-7 [9185569.001]
  • [Cites] J Virol. 1997 Sep;71(9):6526-33 [9261372.001]
  • [Cites] Eur J Cancer. 1997 Apr;33(5):787-91 [9282118.001]
  • [Cites] Cell. 1997 Oct 3;91(1):25-34 [9335332.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10827-32 [9380719.001]
  • [Cites] Exp Cell Res. 1998 Oct 10;244(1):33-42 [9770346.001]
  • [Cites] Nature. 1999 Jul 29;400(6743):464-8 [10440377.001]
  • [Cites] Trends Mol Med. 2004 Nov;10(11):542-8 [15519280.001]
  • [Cites] Stem Cells. 2005 Apr;23(4):516-29 [15790773.001]
  • [Cites] Science. 2005 Aug 19;309(5738):1253-6 [16037417.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Sep 30;335(3):925-36 [16105662.001]
  • [Cites] J Virol. 2005 Sep;79(18):12035-44 [16140779.001]
  • [Cites] J Virol. 2006 Jan;80(1):281-95 [16352553.001]
  • [Cites] J Exp Med. 2006 May 15;203(5):1307-17 [16651385.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11306-11 [16847266.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2005;70:205-8 [16869755.001]
  • [Cites] Nat Rev Cancer. 2002 Nov;2(11):879-84 [12415258.001]
  • (PMID = 18024587.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA048746; United States / NCI NIH HHS / CA / R01 CA124596; United States / NIGMS NIH HHS / GM / T32 GM007231; United States / NCI NIH HHS / CA / R01 CA48746
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.7.49 / Telomerase
  • [Other-IDs] NLM/ PMC2141889
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70. Larouche J, Berger F, Chassagne-Clement C, Sebban C, Ghesquieres H, Salles G, Coiffier B: Lymphoma recurrence 5 years or more following diffuse large B-cell lymphoma: Clinical characteristics and outcome. J Clin Oncol; 2009 May 20;27(15_suppl):8562

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lymphoma recurrence 5 years or more following diffuse large B-cell lymphoma: Clinical characteristics and outcome.
  • : 8562 Background: Diffuse large B-cell lymphoma (DLBCL) usually relapses early following treatment but some relapses happen 5 years or later.
  • Few data exist regarding clinical characteristics and outcome of these patients (pts).
  • METHODS: We performed a retrospective analysis of all pts from two centers in Lyon/France between 1980-2003 who presented a biopsy proven relapse 5 years or later following diagnosis of DLBCL.
  • Clinical characteristics at diagnosis were: median age 57 y; stage I-II 63% (34/54); IPI low/low intermediate 84% (41/49) and extranodal involvement (EN) 66% (35/53).
  • IHC at diagnosis: CD20 100% (46/46), CD10 28% (10/36), bcl-6 53% (9/17), MUM1 48% (11/23), bcl-2 68% (19/28), germinal-center phenotype (GC) 57% (12/21) and non-GC 43% (9/21).
  • Median time from diagnosis to relapse was 7.4 years (5-20.5 years).
  • MUM1 expression at diagnosis was associated with DLBCL histology at relapse (p=0.037).
  • Clinical characteristics at relapse were: median age 66 y; stage I-II 48% (26/54); 73% (31/43) with DLBCL at relapse had EN.
  • 54% (15/28) with DLBCL at relapse had a GC phenotype and 46% (13/28) a non-GC phenotype.
  • CONCLUSIONS: Patients with DLBCL who present a late relapse usually had localized stage, favorable IPI and extranodal involvement at diagnosis.

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  • (PMID = 27960984.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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71. Mozos A, Ye H, Chuang WY, Chu JS, Huang WT, Chen HK, Hsu YH, Bacon CM, Du MQ, Campo E, Chuang SS: Most primary adrenal lymphomas are diffuse large B-cell lymphomas with non-germinal center B-cell phenotype, BCL6 gene rearrangement and poor prognosis. Mod Pathol; 2009 Sep;22(9):1210-7
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  • [Title] Most primary adrenal lymphomas are diffuse large B-cell lymphomas with non-germinal center B-cell phenotype, BCL6 gene rearrangement and poor prognosis.
  • Primary adrenal lymphoma is extremely rare, accounting for <1% of non-Hodgkin lymphomas, and lymphoma-associated chromosomal translocations have yet to be reported in this entity.
  • The mean tumor size at diagnosis was 8.5 cm.
  • All cases presented with stage IE disease without regional nodal involvement.
  • Histologically, eight cases were diffuse large B-cell lymphoma, all of which carried a non-germinal center B-cell phenotype.
  • Fluorescence in situ hybridization revealed BCL6 gene rearrangement in 5 (83%) of 6 diffuse large B-cell lymphomas investigated.
  • The remaining cases were one case each of plasmablastic lymphoma and extranodal NK/T-cell lymphoma, nasal type, the first and third case of primary adrenal lymphoma of these particular lymphoma subtypes in the English literature, respectively.
  • At a median follow-up of 4.5 months, 7 patients died of lymphoma, 1 died of an unrelated disease, 1 was alive with disease, and 1 was alive without disease.
  • The prognosis of these patients was poor as compared with those with nodal diffuse large B-cell lymphoma.
  • We speculate that the poor outcome of primary adrenal lymphoma might be related to the bulky tumor size at presentation, non-germinal center B-cell phenotype, and frequent BCL-6 gene rearrangement.
  • [MeSH-major] Adrenal Gland Neoplasms / pathology. B-Lymphocytes / pathology. DNA-Binding Proteins / genetics. Gene Rearrangement. Lymphoma, Large B-Cell, Diffuse / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Female. Germinal Center / immunology. Germinal Center / pathology. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Middle Aged. Neoplasm Staging. Phenotype. Prognosis. Retrospective Studies

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  • (PMID = 19525926.001).
  • [ISSN] 1530-0285
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / DNA-Binding Proteins
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72. He H, Cheng L, Weiss LM, Chu PG: Clinical outcome of incidental pelvic node malignant B-cell lymphomas discovered at the time of radical prostatectomy. Leuk Lymphoma; 2007 Oct;48(10):1976-80
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  • [Title] Clinical outcome of incidental pelvic node malignant B-cell lymphomas discovered at the time of radical prostatectomy.
  • Incidental pelvic node malignant B-cell lymphomas diagnosed at the time of radical prostatectomy are rare.
  • Their clinical outcome has not been studied.
  • We studied thirteen such cases with long-term clinical follow-up.
  • Of 13 cases, 9 were chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), 3 marginal zone B-cell lymphoma (MZL) and 1 mantle cell lymphoma (MCL).
  • All 13 patients did not receive radiation or chemotherapy; and five of 13 cases showed hematologic evidence of lymphoma progression between 1 and 5 months after radical prostatectomy.
  • After progression, the mantle cell lymphoma patient received aggressive chemotherapy and had systemic dissemination.
  • None of 13 patients had died from lymphoma or prostate carcinoma at the last follow-up.
  • In conclusion, most incidental pelvic node lymphomas (8/13) showed no evidence of systemic dissemination to peripheral blood or bone marrow after a mean 42.8 weeks of follow-up despite the fact that no additional treatment was given.
  • Strong consideration should be given to withholding further treatment in patients diagnosed with pelvic low-grade B-cell lymphoma at the time of radical prostatectomy until disease progression occurs.
  • [MeSH-major] Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / therapy. Neoplasms, Second Primary / therapy. Prostatic Neoplasms / surgery. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Disease-Free Survival. Follow-Up Studies. Humans. Male. Middle Aged. Models, Biological. Neoplasm Metastasis. Prognosis. Prostatectomy. Time Factors. Treatment Outcome

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  • (PMID = 17917966.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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73. Mayall F, Johnson S: Immunoflow cytometry compared with PCR for the identification of clonality in FNAs of T-cell-rich B-cell lymphomas. Cytopathology; 2007 Apr;18(2):117-9
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  • [Title] Immunoflow cytometry compared with PCR for the identification of clonality in FNAs of T-cell-rich B-cell lymphomas.
  • OBJECTIVE: The study aimed to compare the utility of immunoflow cytometry (IFC) with two IgH polymerase chain reaction (PCR) methods for the identification of clonality in fine needle aspirations (FNAs) from T-cell-rich B-cell lymphomas (TCRBCLs).
  • Seven of these were cases in which the original diagnosis had been made by FNA cytology with IFC and cell block immunohistochemistry (IHC).
  • Formalin-fixed paraffin-embedded FNA cell block or histology tissue from these specimens had also been submitted for IgH PCR clonality studies using primers FR2a/VLJH and primers FR3a/VLJH.
  • RESULTS: All 10 case demonstrated B-cell clonality for at least one of the primer sets on PCR, but none showed light chain restriction on IFC.
  • All TCRBCLs were positive for CD20 and CD79a but negative for CD10 and BCl-2.
  • CONCLUSIONS: If IgH PCR clonality assays had a turnaround time of 1 or 2 days, there might be a strong case for these studies supporting or even replacing IFC, in the FNA diagnosis of lymphoid lesions.
  • [MeSH-major] Biopsy, Fine-Needle. Flow Cytometry / methods. Lymphoma, B-Cell / pathology. Polymerase Chain Reaction / methods. T-Lymphocytes / pathology
  • [MeSH-minor] Antigens, CD / metabolism. Biomarkers, Tumor / metabolism. Clone Cells. Genes, Immunoglobulin Light Chain. Humans. Immunophenotyping

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  • (PMID = 17397497.001).
  • [ISSN] 0956-5507
  • [Journal-full-title] Cytopathology : official journal of the British Society for Clinical Cytology
  • [ISO-abbreviation] Cytopathology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor
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74. Lin KB, Freeman SA, Gold MR: Rap GTPase-mediated adhesion and migration: A target for limiting the dissemination of B-cell lymphomas? Cell Adh Migr; 2010 Jul-Sep;4(3):327-32
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  • [Title] Rap GTPase-mediated adhesion and migration: A target for limiting the dissemination of B-cell lymphomas?
  • B-cell lymphomas, which arise in lymphoid organs, can spread rapidly via the circulatory system and form solid tumors within multiple organs.
  • Rate-limiting steps in this metastatic process may be the adhesion of lymphoma cells to vascular endothelial cells, their exit from the vasculature and their migration to tissue sites that will support tumor growth.
  • Thus proteins that control B cell adhesion and migration are likely to be key factors in lymphoma dissemination, and hence potential targets for therapeutic intervention.
  • The Rap GTPases are master regulators of integrin activation, cell motility and the underlying cytoskeletal, adhesion and membrane dynamics.
  • We have recently shown that Rap activation is critical for B-lymphoma cells to undergo transendothelial migration in vitro and in vivo.
  • As a consequence, suppressing Rap activation impairs the ability of intravenously injected B-lymphoma cells to form solid tumors in the liver and other organs.
  • We discuss this work in the context of targeting Rap, its downstream effectors, or other regulators of B cell adhesion and migration as an approach for limiting the dissemination of B-lymphoma cells and the development of secondary tumors.

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  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):9064-9 [10922060.001]
  • [Cites] Endocr Relat Cancer. 1999 Mar;6(1):21-3 [10732782.001]
  • [Cites] Nat Immunol. 2000 Jul;1(1):31-6 [10881171.001]
  • [Cites] Leuk Lymphoma. 2001 Feb;40(5-6):631-45 [11426535.001]
  • [Cites] Nature. 2001 Jul 19;412(6844):341-6 [11460166.001]
  • [Cites] J Immunol. 2002 Aug 1;169(3):1365-71 [12133960.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349.001]
  • [Cites] J Cell Biol. 2003 Apr 28;161(2):417-27 [12707305.001]
  • [Cites] Nat Immunol. 2003 Aug;4(8):741-8 [12845325.001]
  • [Cites] Nat Rev Immunol. 2003 Nov;3(11):867-78 [14668803.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12009-19 [14701796.001]
  • [Cites] Nat Rev Immunol. 2004 May;4(5):360-70 [15122201.001]
  • [Cites] Nat Neurosci. 2004 Sep;7(9):923-9 [15286792.001]
  • [Cites] Nat Med. 2004 Sep;10(9):982-6 [15334074.001]
  • [Cites] Dev Cell. 2004 Oct;7(4):585-95 [15469846.001]
  • [Cites] J Cell Biol. 2004 Oct 11;167(1):111-22 [15479739.001]
  • [Cites] J Biol Chem. 1998 Oct 30;273(44):29218-23 [9786933.001]
  • [Cites] J Biol Chem. 2005 Feb 11;280(6):5022-31 [15569673.001]
  • [Cites] J Clin Invest. 2005 Mar;115(3):680-7 [15696195.001]
  • [Cites] Curr Opin Cell Biol. 2005 Apr;17(2):123-8 [15780587.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):251-62 [15803153.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):898-906 [16424023.001]
  • [Cites] Nat Immunol. 2006 Sep;7(9):919-28 [16892067.001]
  • [Cites] Eur J Immunol. 2006 Aug;36(8):2235-49 [16821235.001]
  • [Cites] Curr Biol. 2006 Sep 19;16(18):1796-806 [16979556.001]
  • [Cites] Blood. 2006 Dec 15;108(13):4178-86 [16946303.001]
  • [Cites] J Cell Sci. 2007 Jan 1;120(Pt 1):17-22 [17182900.001]
  • [Cites] J Cell Biol. 2007 Mar 12;176(6):863-75 [17353362.001]
  • [Cites] Immunity. 2007 Jun;26(6):784-97 [17570692.001]
  • [Cites] J Biol Chem. 2007 Oct 19;282(42):30629-42 [17716979.001]
  • [Cites] Immunity. 2008 Jan;28(1):88-99 [18191593.001]
  • [Cites] Immunity. 2008 Jan;28(1):75-87 [18191594.001]
  • [Cites] Blood. 2008 May 1;111(9):4627-36 [18319399.001]
  • [Cites] Nat Immunol. 2008 Sep;9(9):953-9 [18711432.001]
  • [Cites] J Immunol. 2008 Sep 1;181(5):3373-83 [18714009.001]
  • [Cites] Nat Med. 2009 Mar;15(3):313-8 [19234460.001]
  • [Cites] Nat Med. 2009 Mar;15(3):300-5 [19234461.001]
  • [Cites] Nat Med. 2009 Mar;15(3):306-12 [19234463.001]
  • [Cites] Science. 2009 May 15;324(5929):895-9 [19443776.001]
  • [Cites] Cancer Res. 2009 Jun 15;69(12):4962-8 [19470770.001]
  • [Cites] Hematol Oncol Clin North Am. 2009 Aug;23(4):791-827 [19577170.001]
  • [Cites] J Biol Chem. 2009 Aug 21;284(34):22865-77 [19561089.001]
  • [Cites] Nat Genet. 2009 Oct;41(10):1133-7 [19783987.001]
  • [Cites] Oncogene. 2010 Jan 28;29(4):608-15 [19838206.001]
  • [Cites] Science. 1999 Dec 10;286(5447):2098-102 [10617422.001]
  • [Cites] Nat Immunol. 2001 Feb;2(2):123-8 [11175804.001]
  • (PMID = 20212359.001).
  • [ISSN] 1933-6926
  • [Journal-full-title] Cell adhesion & migration
  • [ISO-abbreviation] Cell Adh Migr
  • [Language] ENG
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; EC 3.6.5.2 / rap GTP-Binding Proteins
  • [Other-IDs] NLM/ PMC2958603
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75. Lu X, Chen J, Sasmono RT, Hsi ED, Sarosiek KA, Tiganis T, Lossos IS: T-cell protein tyrosine phosphatase, distinctively expressed in activated-B-cell-like diffuse large B-cell lymphomas, is the nuclear phosphatase of STAT6. Mol Cell Biol; 2007 Mar;27(6):2166-79
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  • [Title] T-cell protein tyrosine phosphatase, distinctively expressed in activated-B-cell-like diffuse large B-cell lymphomas, is the nuclear phosphatase of STAT6.
  • Diffuse large B-cell lymphomas (DLBCLs) consist of clinically distinct subtypes: germinal center B-cell (GCB)-like and activated-B-cell (ABC)-like tumors, characterized by long and short survival, respectively.
  • Among the differentially expressed PTPs, only T-cell PTP (TCPTP) localizes to the nucleus.

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  • [Cites] EMBO J. 1999 Nov 15;18(22):6307-18 [10562543.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • [Cites] Semin Immunol. 2000 Aug;12(4):379-86 [10995584.001]
  • [Cites] J Biol Chem. 2000 Dec 15;275(50):39718-26 [10993888.001]
  • [Cites] J Biol Chem. 2001 Oct 5;276(40):37700-7 [11479308.001]
  • [Cites] J Biol Chem. 2001 Dec 7;276(49):46313-8 [11514572.001]
  • [Cites] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286.001]
  • [Cites] Mol Endocrinol. 2002 Jan;16(1):58-69 [11773439.001]
  • [Cites] Curr Biol. 2002 Mar 19;12(6):446-53 [11909529.001]
  • [Cites] Bioorg Med Chem Lett. 2002 Apr 22;12(8):1219-23 [11934592.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Mol Cell Biol. 1996 Oct;16(10):5811-20 [8816495.001]
  • [Cites] J Biol Chem. 1997 May 16;272(20):12968-77 [9148903.001]
  • [Cites] J Immunol. 1997 Aug 1;159(3):1255-64 [9233621.001]
  • [Cites] J Biol Chem. 1997 Aug 22;272(34):21548-57 [9261175.001]
  • [Cites] J Exp Med. 1997 Aug 29;186(5):683-93 [9271584.001]
  • [Cites] J Immunol. 1997 Oct 15;159(8):3757-66 [9378962.001]
  • [Cites] J Biol Chem. 1997 Nov 14;272(46):29322-9 [9361013.001]
  • [Cites] Mol Cell Biol. 1998 Mar;18(3):1622-34 [9488479.001]
  • [Cites] J Immunol. 1998 Jul 1;161(1):302-10 [9647237.001]
  • [Cites] Adv Exp Med Biol. 1998;452:37-43 [9889957.001]
  • [Cites] Gene. 1999 Sep 17;237(2):351-60 [10521659.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525.001]
  • [Cites] Nat Immunol. 2005 Mar;6(3):253-60 [15696169.001]
  • [Cites] Blood. 2005 Apr 1;105(7):2924-32 [15591113.001]
  • [Cites] Curr Opin Cell Biol. 2005 Apr;17(2):203-9 [15780598.001]
  • [Cites] Mol Cell Biol. 2002 Aug;22(16):5662-8 [12138178.001]
  • [Cites] J Biol Chem. 2002 Sep 27;277(39):36563-9 [12121972.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Oct 4;297(4):811-7 [12359225.001]
  • [Cites] J Biol Chem. 2003 Feb 7;278(6):3903-11 [12459556.001]
  • [Cites] Mol Cell Biol. 2003 Mar;23(6):2096-108 [12612081.001]
  • [Cites] Leukemia. 2003 Apr;17(4):789-95 [12682639.001]
  • [Cites] J Biol Chem. 2003 May 9;278(19):16520-7 [12615921.001]
  • [Cites] Nat Rev Immunol. 2003 Nov;3(11):900-11 [14668806.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3075-86 [14701875.001]
  • [Cites] FASEB J. 2004 Jan;18(1):8-30 [14718383.001]
  • [Cites] Cell. 2004 Jun 11;117(6):699-711 [15186772.001]
  • [Cites] Blood. 1991 May 1;77(9):1859-70 [2018830.001]
  • [Cites] Science. 1991 Nov 1;254(5032):713-6 [1948050.001]
  • [Cites] J Clin Invest. 1993 Jan;91(1):88-93 [8423237.001]
  • [Cites] Biochemistry. 1993 Mar 9;32(9):2194-201 [8443161.001]
  • [Cites] Cancer Res. 1995 May 15;55(10):2173-6 [7743520.001]
  • [Cites] Cancer Res. 1995 Sep 1;55(17):3692-6 [7641177.001]
  • (PMID = 17210636.001).
  • [ISSN] 0270-7306
  • [Journal-full-title] Molecular and cellular biology
  • [ISO-abbreviation] Mol. Cell. Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / CA109335
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / STAT6 Transcription Factor; 207137-56-2 / Interleukin-4; EC 3.1.3.48 / PTPN2 protein, human; EC 3.1.3.48 / Protein Tyrosine Phosphatase, Non-Receptor Type 2; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  • [Other-IDs] NLM/ PMC1820499
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76. Polo JM, Juszczynski P, Monti S, Cerchietti L, Ye K, Greally JM, Shipp M, Melnick A: Transcriptional signature with differential expression of BCL6 target genes accurately identifies BCL6-dependent diffuse large B cell lymphomas. Proc Natl Acad Sci U S A; 2007 Feb 27;104(9):3207-12
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  • [Title] Transcriptional signature with differential expression of BCL6 target genes accurately identifies BCL6-dependent diffuse large B cell lymphomas.
  • Diffuse large B cell lymphomas (DLBCLs) often express BCL6, a transcriptional repressor required for the formation of normal germinal centers.
  • This set of genes was enriched in modulators of transcription, chromatin structure, protein ubiquitylation, cell cycle, and DNA damage responses.
  • In a panel of DLBCL cell lines analyzed by expression arrays and classified according to their gene expression profiles, only BCR tumors were highly sensitive to the BCL6 peptide inhibitor, BPI.

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  • [Cites] Nat Genet. 2000 May;25(1):25-9 [10802651.001]
  • [Cites] Nature. 2004 Dec 2;432(7017):635-9 [15577913.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):31-6 [11134512.001]
  • [Cites] Behav Brain Res. 2001 Nov 1;125(1-2):279-84 [11682119.001]
  • [Cites] J Biol Chem. 2002 Apr 12;277(15):13286-93 [11825903.001]
  • [Cites] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054.001]
  • [Cites] Adv Exp Med Biol. 2002;512:21-8 [12405183.001]
  • [Cites] Bioinformatics. 2003 Feb 12;19(3):368-75 [12584122.001]
  • [Cites] Cell. 2003 Apr 18;113(2):207-19 [12705869.001]
  • [Cites] Bioinformatics. 2003 May 1;19(7):891-2 [12724301.001]
  • [Cites] Nat Med. 2004 Dec;10(12):1329-35 [15531890.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1851-61 [15550490.001]
  • [Cites] Cancer Cell. 2005 May;7(5):445-55 [15894265.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Mol Cell Biol. 2006 Jul;26(14):5348-59 [16809771.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 19;100(17):9991-6 [12900505.001]
  • [Cites] Genome Res. 2004 Jan;14(1):62-6 [14707170.001]
  • [Cites] Methods Enzymol. 2004;376:315-34 [14975315.001]
  • [Cites] J Immunol. 2004 Jul 15;173(2):1158-65 [15240705.001]
  • [Cites] Cell. 2004 Oct 1;119(1):75-86 [15454082.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 28;101(39):14198-203 [15375218.001]
  • [Cites] Science. 1993 Oct 29;262(5134):747-50 [8235596.001]
  • [Cites] Blood. 1995 Jul 1;86(1):45-53 [7795255.001]
  • [Cites] Science. 1997 Apr 25;276(5312):589-92 [9110977.001]
  • [Cites] Nat Genet. 1997 Jun;16(2):161-70 [9171827.001]
  • [Cites] Genes Dev. 1998 Jul 1;12(13):1953-61 [9649500.001]
  • [Cites] Blood. 1999 Oct 1;94(7):2403-13 [10498613.001]
  • [Cites] Immunity. 2000 Aug;13(2):199-212 [10981963.001]
  • (PMID = 17360630.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA092625; United States / NCI NIH HHS / CA / R01 CA104348; United States / NCI NIH HHS / CA / P01CA092625
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCL6 protein, human; 0 / DNA-Binding Proteins; 0 / Peptides
  • [Other-IDs] NLM/ PMC1805543
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77. Natkunam Y, Zhao S, Mason DY, Chen J, Taidi B, Jones M, Hammer AS, Hamilton Dutoit S, Lossos IS, Levy R: The oncoprotein LMO2 is expressed in normal germinal-center B cells and in human B-cell lymphomas. Blood; 2007 Feb 15;109(4):1636-42
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The oncoprotein LMO2 is expressed in normal germinal-center B cells and in human B-cell lymphomas.
  • We previously developed a multivariate model based on the RNA expression of 6 genes (LMO2, BCL6, FN1, CCND2, SCYA3, and BCL2) that predicts survival in diffuse large B-cell lymphoma (DLBCL) patients.
  • Immunohistologic analysis of over 1200 normal and neoplastic tissue and cell lines showed that LMO2 protein is expressed as a nuclear marker in normal germinal-center (GC) B cells and GC-derived B-cell lines and in a subset of GC-derived B-cell lymphomas.
  • It was rarely expressed in mature T, natural killer (NK), and plasma cell neoplasms and was absent from nonhematolymphoid tissues except for endothelial cells.
  • Hierarchical cluster analysis of immunohistologic data in DLBCL demonstrated that the expression profile of the LMO2 protein was similar to that of other GC-associated proteins (HGAL, BCL6, and CD10) but different from that of non-GC proteins (MUM1/IRF4 and BCL2).

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  • [Cites] Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):320-4 [10618416.001]
  • [Cites] Mech Dev. 2000 Mar 1;91(1-2):5-17 [10704826.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Blood. 2004 Mar 1;103(5):1909-11 [14604958.001]
  • [Cites] N Engl J Med. 2004 Feb 26;350(9):913-22 [14985489.001]
  • [Cites] N Engl J Med. 2004 Apr 29;350(18):1828-37 [15115829.001]
  • [Cites] J Immunol Methods. 1986 May 1;89(1):61-72 [3084658.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4367-71 [2034676.001]
  • [Cites] J Pathol. 2000 Aug;191(4):452-61 [10918222.001]
  • [Cites] Mod Pathol. 2001 Jul;14(7):686-94 [11455001.001]
  • [Cites] Blood. 2002 Feb 15;99(4):1136-43 [11830458.001]
  • [Cites] Am J Pathol. 2002 Nov;161(5):1557-65 [12414504.001]
  • [Cites] Int J Hematol. 2002 Nov;76(4):295-8 [12463590.001]
  • [Cites] Blood. 2003 Jan 1;101(1):78-84 [12393466.001]
  • [Cites] Histopathology. 2003 Sep;43(3):209-19 [12940773.001]
  • [Cites] Science. 2003 Oct 17;302(5644):415-9 [14564000.001]
  • [Cites] Oncogene. 1991 Oct;6(10):1887-93 [1923511.001]
  • [Cites] J Mol Biol. 1992 Aug 5;226(3):747-61 [1507224.001]
  • [Cites] N Engl J Med. 1993 Sep 30;329(14):987-94 [8141877.001]
  • [Cites] Cell. 1994 Jul 15;78(1):45-57 [8033210.001]
  • [Cites] Br J Haematol. 1996 May;93(2):280-6 [8639417.001]
  • [Cites] Science. 1997 Nov 7;278(5340):1059-64 [9353180.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3890-5 [9520463.001]
  • [Cites] Semin Oncol. 1998 Aug;25(4):483-91 [9728598.001]
  • [Cites] Blood. 2004 Dec 15;104(13):4173-80 [15054041.001]
  • [Cites] Blood. 2005 May 15;105(10):3979-86 [15677569.001]
  • [Cites] Blood. 2005 Nov 1;106(9):3183-90 [16046532.001]
  • [Cites] Mol Ther. 2006 Jan;13(1):15-25 [16260184.001]
  • [Cites] J Clin Oncol. 2006 Feb 20;24(6):995-1007 [16418498.001]
  • [Cites] J Pathol. 2006 Aug;209(4):454-63 [16739114.001]
  • [Cites] Nature. 2000 Feb 3;403(6769):503-11 [10676951.001]
  • (PMID = 17038524.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA034233; United States / NCI NIH HHS / CA / CA34233; United States / NCI NIH HHS / CA / CA33399; United States / NCI NIH HHS / CA / R37 CA033399; United States / NCI NIH HHS / CA / R01 CA109335; United States / NCI NIH HHS / CA / CA109335
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / LIM Domain Proteins; 0 / LMO2 protein, human; 0 / Metalloproteins; 0 / Proto-Oncogene Proteins
  • [Other-IDs] NLM/ PMC1794056
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78. Forde P, Grant C, Smith E, Farrell M, Brett F, Bolger C, Grogan L, Breathnach O: Primary central nervous system lymphoma: An Irish clinical experience. J Clin Oncol; 2009 May 20;27(15_suppl):e13032

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary central nervous system lymphoma: An Irish clinical experience.
  • : e13032 Background: North American studies have demonstrated an increase in incidence of primary CNS lymphoma in recent decades.
  • To our knowledge there have been no studies analyzing primary CNS lymphoma in the Irish setting.
  • METHODS: The records of 78 patients diagnosed with primary CNS lymphoma at our institution between January 1999 and October 2008 were reviewed.
  • Patient's age, sex, and time to diagnosis were noted.
  • Histology and radiology was reviewed for cell of origin, CD20 status, and sites of involvement.
  • Median time from hospital presentation to histological diagnosis was 17 days (4-790).
  • 92% (74) of primary CNS lymphomas were B cell and CD20 positive with 8% (4) being T cell.
  • One-third of patients had multifocal brain involvement by lymphoma.
  • CONCLUSIONS: In comparison with international published series primary CNS lymphoma in Ireland is diagnosed at an older median age, has a more even sex distribution and a relatively higher incidence of T cell origin.
  • Multifocal tumor involvement was also more frequent than in other series possibly indicating later clinical presentations.
  • The wide range in time to diagnosis indicates the difficulties associated with diagnosing this uncommon condition.

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  • (PMID = 27962876.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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79. Ruiz A, Reischl U, Swerdlow SH, Hartke M, Streubel B, Procop G, Tubbs RR, Cook JR: Extranodal marginal zone B-cell lymphomas of the ocular adnexa: multiparameter analysis of 34 cases including interphase molecular cytogenetics and PCR for Chlamydia psittaci. Am J Surg Pathol; 2007 May;31(5):792-802
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extranodal marginal zone B-cell lymphomas of the ocular adnexa: multiparameter analysis of 34 cases including interphase molecular cytogenetics and PCR for Chlamydia psittaci.
  • Extranodal marginal zone B-cell lymphomas of MALT type (MALT lymphomas) show site-dependent variations in their morphologic, phenotypic, and/or cytogenetic findings.
  • This report describes a comprehensive analysis of 34 ocular adnexa MALT lymphomas, including interphase fluorescence in situ hybridization for MALT lymphoma-associated cytogenetic abnormalities and polymerase chain reaction for Chlamydia psittaci, which has recently been suggested to be associated with ocular adnexa lymphomas.
  • A typical morphologic pattern was identified in 79% of cases, while overtly monocytoid cytology (12%), predominantly plasmacytic features (9%), and lymphoepithelial lesions (3%) were uncommon.
  • Plasmacytic differentiation (41%) was associated with stage IV disease (P=0.036) and gains of chromosomes 3 and/or 18q (P=0.021) (79%).
  • This study identifies the characteristic morphologic, phenotypic, and cytogenetic findings in ocular adnexa MALT lymphoma, including a subset differing from those arising at other anatomic sites.
  • The lack of C. psittaci in this series, in contrast to some prior reports, indicates that there may also be geographic heterogeneity in the pathogenesis of ocular adnexa MALT lymphoma.
  • [MeSH-major] Chlamydia Infections / pathology. Chlamydophila psittaci / isolation & purification. Lymphoma, B-Cell, Marginal Zone / pathology. Orbital Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. DNA, Bacterial / analysis. DNA, Neoplasm / analysis. Female. Humans. Interphase / genetics. Male. Middle Aged. Polymerase Chain Reaction. Retrospective Studies

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  • (PMID = 17460465.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Bacterial; 0 / DNA, Neoplasm
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80. Goteri G, Olivieri A, Ranaldi R, Lucesole M, Filosa A, Capretti R, Pieramici T, Leoni P, Rubini C, Fabris G, Lo Muzio L: Bone marrow histopathological and molecular changes of small B-cell lymphomas after rituximab therapy: comparison with clinical response and patients outcome. Int J Immunopathol Pharmacol; 2006 Apr-Jun;19(2):421-31
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bone marrow histopathological and molecular changes of small B-cell lymphomas after rituximab therapy: comparison with clinical response and patients outcome.
  • This study correlates bone marrow changes after Rituximab (RTX) treatment with the clinical characteristics and outcome of 26 patients with small B-cell lymphomas.
  • Clinical, histological and molecular responses to RTX were correlated to the clinical outcome of the patients.
  • Sixteen out of twenty-six patients obtained a complete clinical remission (CR).
  • A favourable histology--follicular lymphoma (FL), hairy cell leukaemia (HCL) and marginal zone lymphoma (MZL)--was associated with a higher frequency of clinical CR and histological remission (HR), in comparison with mantle cell lymphoma (MCL), chronic lymphocytic leukaemia (CLL) and lymphoplasmacytic lymphoma (LPL).
  • 1) complete lymphoid cell disappearance (9 patients); or 2) nodular/interstitial T-cell infiltration (10 patients).
  • 1) persistence of CD20+ small lymphoid cells in 1 patient with MCL;.
  • 2) loss of CD20 antigen expression in 4 patients with CLL; or 3) persistence only of clusters of monotypic plasma cells in 2 patients with LPL.
  • The percentage of lymphomatous infiltrate after RTX was higher in patients who subsequently died of the disease.
  • Molecular response showed no correlations with the further clinical course in 12 patients achieving a complete clinical remission.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Bone Marrow / metabolism. Bone Marrow / pathology. Lymphoma, B-Cell / drug therapy. Lymphoma, B-Cell / pathology

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  • (PMID = 16831308.001).
  • [ISSN] 0394-6320
  • [Journal-full-title] International journal of immunopathology and pharmacology
  • [ISO-abbreviation] Int J Immunopathol Pharmacol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
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81. Levine B, Sinha SC, Kroemer G: Bcl-2 family members: Dual regulators of apoptosis and autophagy. Autophagy; 2008 Jul 01;4(5):600-606
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  • [Title] Bcl-2 family members: Dual regulators of apoptosis and autophagy.
  • In normal conditions, Beclin 1 is bound to and inhibited by Bcl-2 or the Bcl-2 homolog Bcl-X<sub>L</sub>.
  • This interaction involves a Bcl-2 homology 3 (BH3) domain in Beclin 1 and the BH3 binding groove of Bcl-2/Bcl-X<sub>L</sub>.
  • Other proteins containing BH3 domains, called BH3-only proteins, can competitively disrupt the interaction between Beclin 1 and Bcl-2/Bcl-X<sub>L</sub> to induce autophagy.
  • Nutrient starvation, which is a potent physiologic inducer of autophagy, can stimulate the dissociation of Beclin 1 from its inhibitors, either by activating BH3-only proteins (such as Bad) or by posttranslational modifications of Bcl-2 (such as phosphorylation) that may reduce its affinity for Beclin 1 and BH3-only proteins.
  • Thus, anti-apoptotic Bcl-2 family members and pro-apoptotic BH3-only proteins may participate in the inhibition and induction of autophagy, respectively.
  • This hitherto neglected crosstalk between the core machineries regulating autophagy and apoptosis may redefine the role of Bcl-2 family proteins in oncogenesis and tumor progression.

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  • (PMID = 28186856.001).
  • [ISSN] 1554-8635
  • [Journal-full-title] Autophagy
  • [ISO-abbreviation] Autophagy
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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82. Castro JE, Sandoval-Sus JD, Melo-Cardenas J, Darrah D, Urquiza M, Pakbaz RS, Prussak CE, Kipps TJ: Phase I study of intranodal direct injection of adenovirus encoding recombinant CD40-ligand (Ad-ISF35) in patients with chronic lymphocytic leukemia. J Clin Oncol; 2009 May 20;27(15_suppl):3003

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of intranodal direct injection of adenovirus encoding recombinant CD40-ligand (Ad-ISF35) in patients with chronic lymphocytic leukemia.
  • : 3003 Background: Transduction of chronic lymphocytic leukemia (CLL) cells with replication-defective adenovirus (Ad) encoding a genetically engineered, membrane-stablized CD154 (ISF35) converts transduced, and "bystander" non-transduced, CLL cells into proficient antigen presenting cells that can induce immunity against autologous leukemia cells.
  • Preclinical studies demonstrated that direct injection of Ad-ISF35 into lymphoma nodules can induce potent anti-lymphoma immune responses in test animals, capable of eradicating lethal tumors at distal sites and protect against recurrent disease upon subsequent re-challenge with syngeneic tumor.
  • Pts, ages 45-71 yrs, with rapidly progressive disease (median CLL doubling time of 3.7 months) each received a single ultrasound guided IDI of 1 to 30 x 10<sup>10</sup> Ad-ISF35 viral particles in 4 different dose cohorts.
  • Although there was no evidence for dissemination of Ad-ISF35 beyond the injected lymph node, IDI of Ad-ISF35 induced blood CLL cells to express death receptors, pro-apoptotic proteins, and immune co-stimulatory molecules similar to those induced on "bystander" CLL cells co-cultured with Ad-ISF35 transduced cells in vitro.
  • Importantly, IDI of Ad-ISF35 resulted in significant reductions in blood leukemia cell counts and a median reduction of 53.2% (range 25-75.4%) in the size of lymph nodes and/or spleen, which was durable (≥ 4 months) in 9 pts.
  • Despite aggressive disease prior to treatment, the median treatment-free survival was 5.3 months and 3 pts have yet to require additional treatment after 1-year follow-up.
  • CONCLUSIONS: Single IDI of Ad-ISF35 was safe and effective in inducing systemic biologic and clinical responses in pts with CLL.
  • IDI of Ad-ISF35 might be effective in the treatment of CLL and related lymphomas.

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  • (PMID = 27962049.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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83. Townsend AR, Millward M, Price T, Mainwaring P, Spencer A, Longenecker A, Palladino MA, Lloyd GK, Spear MA, Padrik P: Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm). J Clin Oncol; 2009 May 20;27(15_suppl):3582

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical trial of NPI-0052 in advanced malignancies including lymphoma and leukemia (advanced malignancies arm).
  • : 3582 Background: The novel structure (non-peptide based) of NPI-0052 (NPI) appears to lead to unique proteasome inhibition (PI), toxicology and signal transduction profiles.
  • Preclinical research suggests improvements in therapeutic ratio and activity in hematologic and solid tumor models, leading to clinical trials in patients with myeloma, lymphomas, leukemias, and solid tumors.
  • METHODS: Patients with solid tumor, lymphoma or leukemia diagnoses without standard treatment options were treated with IV NPI on Days 1, 8 and 15 of 28-day cycles in a 3+3 design dose escalation to a Recommended Phase 2 Dose (RP2D).
  • Enrollment then began in 10 patient lymphoma and CLL RP2D cohorts.
  • Stable disease was induced in 31% of patients, including one each with mantle cell, Hodgkin's lymphoma, follicular lymphoma, sarcoma, prostate carcinoma, and two with melanoma.

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  • (PMID = 27961753.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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84. Snuderl M, Kolman OK, Chen YB, Hsu JJ, Ackerman AM, Dal Cin P, Ferry JA, Harris NL, Hasserjian RP, Zukerberg LR, Abramson JS, Hochberg EP, Lee H, Lee AI, Toomey CE, Sohani AR: B-cell lymphomas with concurrent IGH-BCL2 and MYC rearrangements are aggressive neoplasms with clinical and pathologic features distinct from Burkitt lymphoma and diffuse large B-cell lymphoma. Am J Surg Pathol; 2010 Mar;34(3):327-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] B-cell lymphomas with concurrent IGH-BCL2 and MYC rearrangements are aggressive neoplasms with clinical and pathologic features distinct from Burkitt lymphoma and diffuse large B-cell lymphoma.
  • B-cell lymphomas with concurrent IGH-BCL2 and MYC rearrangements, also known as "double-hit" lymphomas (DHL), are rare neoplasms characterized by highly aggressive clinical behavior, complex karyotypes, and a spectrum of pathologic features overlapping with Burkitt lymphoma (BL), diffuse large B-cell lymphoma (DLBCL) and B-lymphoblastic lymphoma/leukemia (B-LBL).
  • The clinical and pathologic spectrum of this rare entity, including comparison to other high-grade B-cell neoplasms, has not been well defined.
  • We conducted a retrospective analysis of clinical and pathologic features of 20 cases of DHL seen at our institution during a 5-year period.
  • Six patients had a history of grade 1 to 2 follicular lymphoma; review of the prior biopsy specimens in 2 of 5 cases revealed blastoid morphology.
  • Eighteen patients had Ann Arbor stage 3 or 4 disease and all had elevated serum lactate dehydrogenase (LDH) levels at presentation.
  • Extranodal disease was present in 17/20 (85%), bone marrow involvement in 10/17 (59%) and central nervous system (CNS) disease in 5/11 (45%).
  • Fourteen patients (70%) died within 8 months of diagnosis.
  • Twelve DHL cases (60%) were classified as B-cell lymphoma, unclassifiable, with features intermediate between DLBCL and BL, 7 cases (35%) as DLBCL, not otherwise specified, and 1 case as B-LBL.
  • DHL is a high-grade B-cell neoplasm with a poor prognosis, resistance to multiagent chemotherapy, and clinical and pathologic features distinct from other high-grade B-cell neoplasms.
  • Familiarity with the morphologic and immunophenotypic spectrum of DHL is important in directing testing to detect concurrent IGH-BCL2 and MYC rearrangements when a karyotype is unavailable.
  • The aggressive clinical behavior and combination of genetic abnormalities seen in these cases may warrant categorization as a separate entity in future classifications and call for novel therapeutic approaches.
  • [MeSH-major] Burkitt Lymphoma / genetics. Gene Expression Regulation, Neoplastic. Gene Rearrangement, B-Lymphocyte, Heavy Chain. Genes, Immunoglobulin Heavy Chain. Lymphoma, B-Cell / genetics. Lymphoma, Large B-Cell, Diffuse / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-myc / genetics
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols. Child. Drug Resistance, Neoplasm. Female. Humans. Immunophenotyping. In Situ Hybridization, Fluorescence. Kaplan-Meier Estimate. Karyotyping. Male. Middle Aged. Neoplasm Staging. Polymerase Chain Reaction. Predictive Value of Tests. Proportional Hazards Models. Retrospective Studies. Risk Assessment. Terminology as Topic. Time Factors. Treatment Outcome. World Health Organization. Young Adult

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  • [Cites] Am J Surg Pathol. 2000 Apr;24(4):525-34 [10757399.001]
  • [Cites] Leukemia. 2000 Nov;14(11):1960-6 [11069032.001]
  • [Cites] Cancer Genet Cytogenet. 2000 Nov;123(1):52-4 [11120335.001]
  • [Cites] Cancer Genet Cytogenet. 2001 Apr 1;126(1):45-51 [11343778.001]
  • [Cites] Arch Pathol Lab Med. 2003 May;127(5):610-3 [12708908.001]
  • [Cites] Blood. 2004 Jan 1;103(1):275-82 [14504078.001]
  • [Cites] Arch Pathol Lab Med. 2004 Feb;128(2):210-3 [14736281.001]
  • [Cites] Int J Hematol. 2004 Jun;79(5):474-9 [15239399.001]
  • [Cites] Blood. 1983 Nov;62(5):1142-6 [6605167.001]
  • [Cites] Proc Natl Acad Sci U S A. 1984 Nov;81(22):7166-70 [6334305.001]
  • [Cites] Am J Clin Pathol. 1986 May;85(5):636-40 [3486584.001]
  • [Cites] N Engl J Med. 1987 Nov 5;317(19):1185-9 [3657890.001]
  • [Cites] N Engl J Med. 1988 May 26;318(21):1373-8 [3285208.001]
  • [Cites] Oncogene. 1988 May;2(5):431-5 [3131717.001]
  • [Cites] J Clin Invest. 1989 Nov;84(5):1454-9 [2509518.001]
  • [Cites] Genes Chromosomes Cancer. 1990 Jul;2(2):147-58 [2278969.001]
  • [Cites] Oncogene. 1991 Jan;6(1):145-8 [1992441.001]
  • [Cites] Leukemia. 1991 Jan;5(1):83-7 [1999960.001]
  • [Cites] Leukemia. 1991 Jun;5(6):473-8 [1711639.001]
  • [Cites] Hematol Oncol. 1991 Mar-Apr;9(2):63-78 [1869243.001]
  • [Cites] Ann Hematol. 1991 Nov;63(5):282-7 [1958753.001]
  • [Cites] Ann Hematol. 1992 Feb;64(2):101-4 [1554791.001]
  • [Cites] N Engl J Med. 1993 Sep 30;329(14):987-94 [8141877.001]
  • [Cites] Leukemia. 1994 Apr;8(4):560-3 [8152251.001]
  • [Cites] Cancer Genet Cytogenet. 1994 Jun;74(2):87-94 [8019967.001]
  • [Cites] Am J Clin Pathol. 1995 Apr;103(4):472-8 [7726146.001]
  • [Cites] Ann Oncol. 1998 Jan;9(1):55-61 [9541684.001]
  • [Cites] Blood. 1998 Nov 1;92(9):3152-62 [9787151.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1558-67 [10334544.001]
  • [Cites] Am J Surg Pathol. 2005 Jan;29(1):121-4 [15613866.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Aug;43(4):414-23 [15852472.001]
  • [Cites] Hum Pathol. 2005 May;36(5):571-5 [15948125.001]
  • [Cites] Am J Surg Pathol. 2005 Aug;29(8):1086-94 [16006805.001]
  • [Cites] Am J Surg Pathol. 2005 Nov;29(11):1490-6 [16224216.001]
  • [Cites] Leukemia. 2005 Dec;19(12):2313-23 [16193090.001]
  • [Cites] Am J Surg Pathol. 2005 Dec;29(12):1652-60 [16327438.001]
  • [Cites] Mod Pathol. 2006 Jan;19(1):25-33 [16258503.001]
  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2419-30 [16760442.001]
  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2431-42 [16760443.001]
  • [Cites] Br J Haematol. 2006 Aug;134(3):294-301 [16848772.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Nov;171(1):52-6 [17074591.001]
  • [Cites] J Clin Pathol. 2007 Sep;60(9):1061-4 [17182663.001]
  • [Cites] Haematologica. 2007 Oct;92(10):1335-42 [18024371.001]
  • [Cites] Am J Clin Pathol. 2008 Jan;129(1):157-66 [18089500.001]
  • [Cites] Curr Protoc Hum Genet. 2007 Jan;Chapter 8:Unit 8.8 [18428417.001]
  • [Cites] Haematologica. 2008 Sep;93(9):1327-34 [18698080.001]
  • [Cites] Blood. 2008 Sep 15;112(6):2248-60 [18612102.001]
  • [Cites] Am J Surg Pathol. 2008 Nov;32(11):1593-607 [18753947.001]
  • [Cites] Br J Haematol. 2009 Mar;144(5):716-25 [19120369.001]
  • [Cites] Leukemia. 2009 Feb;23(2):225-34 [18923440.001]
  • [Cites] Leukemia. 2009 Apr;23(4):777-83 [19151788.001]
  • [Cites] Haematologica. 2009 Jul;94(7):935-43 [19535347.001]
  • [Cites] Blood. 2009 Sep 10;114(11):2273-9 [19597184.001]
  • [Cites] Haematologica. 2007 Oct;92(10):1297-301 [18024366.001]
  • (PMID = 20118770.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R37 CA076404; United States / NIGMS NIH HHS / GM / T32 GM074897; United States / NIGMS NIH HHS / GM / T32 GM074897-07
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MYC protein, human; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Proto-Oncogene Proteins c-myc
  • [Other-IDs] NLM/ NIHMS305320; NLM/ PMC3152212
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85. Baum PR, Cerveny C, Gordon B, Nilsson C, Wiens J, Rafiq S, Lapalombella R, Muthusamy N, Byrd JC, Wahl A: Evaluation of the effect of TRU-016, an anti-CD37 directed SMIP in combination with other therapeutic drugs in models of non-Hodgkin's lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):8571

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of the effect of TRU-016, an anti-CD37 directed SMIP in combination with other therapeutic drugs in models of non-Hodgkin's lymphoma.
  • : 8571 Background: TRU-016, a single chain anti-CD37 Fc fusion molecule has been shown to display pro-apoptotic and Fc-dependent cellular cytotoxicity activities against primary CLL cells and NHL cell lines.
  • The pro-apoptotic signal generated by TRU-016 binding to CD37 on CLL cells has been shown to be caspase-independent and distinct from the signal generated by many other therapeutics including rituximab.
  • We have tested drug combinations using the mantle cell lymphoma line Rec-1 and diffuse large B-cell lymphoma line SU-DHL-6 in vitro and extended these results to in vivo settings using the follicular lymphoma cell line DOHH2 treated with the combination of TRU-016 and bendamustine.
  • METHODS: To determine TRU-016 interactions with the established therapeutics rituximab, doxorubicin, rapamycin, and bendamustine, drugs were tested alone or in combination with TRU-016 and the anti-proliferative effects on cell lines measured after 96 hours.
  • To determine if in vitro synergy could be recapitulated in vivo, SCID mice were implanted with DOHH2 cells and therapeutic treatment was initiated when tumor volumes reached 200 mm<sup>3</sup>.
  • This demonstrates that the in vitro synergy results were extendable to a more complex in vivo disease model.
  • CONCLUSIONS: TRU-016 in combination with rituximab, rapamycin, or bendamustine increases cell killing of NHL cells.
  • Furthermore, the combination of TRU-016 and bendamustine displayed greater in vivo anti-tumor activity than either agent alone against a follicular lymphoma tumor model.

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  • (PMID = 27961015.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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86. Gil Deza E, Dragosky M, Annetta I, Marquez M, Corzo A, Gercovich N, Morgenfeld E, Tognelli F, Rivarola E, Gercovich FG: Primary breast lymphomas: An Argentinian cooperative study. J Clin Oncol; 2009 May 20;27(15_suppl):e19555

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary breast lymphomas: An Argentinian cooperative study.
  • : e19555 Background: Primary Breast Lymphomas are rare tumors (less than 1% of all primary breast tumors).
  • Because of that, the records of two institutions dedicated exclusively to the treatment of cancer (Hospital Municipal de Oncologia "Maria Curie" and Instituto Oncologico Henry Moore) have been working together in a single series.
  • OBJECTIVE: To make a retrospective study of the clinical onset, treatment and evolution of the patients with Primary Breast Lymphoma (PBL).
  • A database containing characteristics of the population, clinical onset, treatments, evolution and survival Results: Gender F/M=2/15 pt.
  • Pathology: Hodgkin's Lymphoma = 1 pt, NHL follicular = 8 pt, Large-Cell Diffuse NHL = 6 pt, lymphoplasmocytic NHL = 1 pt, Marginal Zone NHL = 1 pt.
  • 2) Sixteen out of 17 were non-Hodgkin lymphomas.

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  • (PMID = 27961091.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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87. Gratzinger D, Advani R, Zhao S, Talreja N, Tibshirani RJ, Horning SJ, Levy R, Lossos IS, Gascoyne RD, Natkunam Y: Prognostic significance of vascular endothelial growth factor (VEGF), VEGF receptors (VEGFR), and vascularity in diffuse large B-cell lymphoma treated with immunochemotherapy (R-CHOP). J Clin Oncol; 2009 May 20;27(15_suppl):8581

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of vascular endothelial growth factor (VEGF), VEGF receptors (VEGFR), and vascularity in diffuse large B-cell lymphoma treated with immunochemotherapy (R-CHOP).
  • : 8581 Background: Diffuse large B cell lymphoma (DLBCL) cells coexpress VEGF, VEGFR1 and VEGFR2.
  • METHODS: 162 pts with de novo DLBCL treated with R-CHOP and median followup of 44 months were evaluated retrospectively with immunohistochemistry on tissue microarrays.
  • Scoring: VEGF, VEGFR1, VEGFR2, and phosphoVEGFR2 (pVEGFR2) in lymphoma cells (categorical variable) <5%, none; 5-30%, weak; >30%, strong.

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  • (PMID = 27962266.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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88. Yoo C, Sohn B, Kim J, Yoon D, Huh J, Kim S, Lee D, Kim S, Lee J, Suh C: The prognostic significance of the number of extranodal sites in the patients with disseminated diffuse large B-cell lymphoma treated with R-CHOP. J Clin Oncol; 2009 May 20;27(15_suppl):8570

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The prognostic significance of the number of extranodal sites in the patients with disseminated diffuse large B-cell lymphoma treated with R-CHOP.
  • : 8570 Background: The combination of rituximab and CHOP chemotherapy (R-CHOP) has improved survival of patients with diffuse large B-cell lymphoma (DLBCL).

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  • (PMID = 27961016.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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89. Gisselbrecht C, Glass B, Mounier N, Gill D, Linch D, Trneny M, Bosly A, Shpilberg O, Ketterer N, Moskowitz C, Schmitz N: R-ICE versus R-DHAP in relapsed patients with CD20 diffuse large B-cell lymphoma (DLBCL) followed by autologous stem cell transplantation: CORAL study. J Clin Oncol; 2009 May 20;27(15_suppl):8509

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] R-ICE versus R-DHAP in relapsed patients with CD20 diffuse large B-cell lymphoma (DLBCL) followed by autologous stem cell transplantation: CORAL study.
  • : 8509 Background: Salvage chemotherapy followed by high dose therapy and autologous stem cell transplantation (ASCT) is the standard of treatment for chemosensitive relapses in diffuse large B cell lymphoma.
  • Patients with prior exposure to rituximab had more refractory disease and adverse prognostic factors.

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  • (PMID = 27960863.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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90. Nabil IN Jr, Allam W, Alaoui K, Errihani H: Primary nasopharyngeal non Hodgkin lymphoma: A retrospective investigation of 26 patients. J Clin Oncol; 2009 May 20;27(15_suppl):e19552

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary nasopharyngeal non Hodgkin lymphoma: A retrospective investigation of 26 patients.
  • : e19552 Background: Primary nasopharyngeal non-Hodgkin lymphoma (NNHL) was uncommon.
  • In this retrospective study we report our experience dealing with this disease at the National Institute of Oncology.
  • METHODS: We retrospectively analyzed various characteristics of Primary NNHL: patient demographics, clinical and histological diagnosis, disease stage, treatment effects and outcome, in 26 patients treated at our institution between January 2001 and December 2007.
  • The major symptoms at first diagnosis were: nasal obstruction (88.6%), hypoacousia (88.4%), epistaxis (33.3%) and rhinorrhea (15.3%).
  • Clinical examination founded bilateral cervical lymph nodes in 17 cases (65%).
  • Histological analysis showed follicular lymphoma in 7 cases (26.9%), large B-cell lymphoma in 11 cases (42,3%) and T lymphoma in 4 cases ( 15,3%).
  • At the end of total treatment, 18 patients (69.2%) achieved complete response and remained disease free while 4 (15.4%) achieved partial response (>70%) and 4 (15.4%) were progressive (these patients received second line chemotherapy).
  • After 110 months median flow-up, median disease free and overall survival were not reached.
  • CONCLUSIONS: From our study and from the literature, we conclude that histological characteristics, principle of treatment and outcome of primary NNHL patients are similar to that of patients with nodal lymphoma.

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  • (PMID = 27961093.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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91. Sohn B, Yoon D, Kim S, Lee D, Kim S, Huh J, Lee J, Suh C: Outcomes in patients with primary gastric diffuse large B-cell lymphoma after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy. J Clin Oncol; 2009 May 20;27(15_suppl):e19543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcomes in patients with primary gastric diffuse large B-cell lymphoma after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy.
  • : e19543 Background: The optimal therapy for primary gastric diffuse large B- cell lymphoma (DLBCL) still needs to be defined.
  • METHODS: We searched AMC Registry for Non-Hodgkin's Lymphoma and found 26 patients with primary gastric DLBCL, who received R-CHOP as first-line chemotherapy.
  • Ten of 26 patients had localized disease.
  • Remaining patients had disseminated disease.
  • After analyses of 10 patients with localized disease, we found that these patients had received a total 38 cycles, with a median of 3 cycles per patient.
  • In patients with localized disease, CR was observed in 10 of 10 patients (100%), and both 3-year EFS and OS was 100% (10 of 10 patients).
  • In analyses with 16 patients with disseminated disease, all patients had received a total 91 cycles, with a median of 6 cycles per patient.
  • CR after R-CHOP treatment was observed in 10 of 16 patients (62.5%), partial response in 3 patients, stable disease in 1 patient, and progressive disease in 1 patient.
  • Three-year EFS and OS was 61.1% and 57.8% in patients with disseminated disease.
  • Combination with rituximab in CHOP regimen showed excellent prognosis especially in patients with localized disease.
  • In localized disease, CR was 100%, 3-year EFS and OS was 100%.
  • In disseminated disease, CR was 62.5%, 3-year EFS and OS was 61.1% and 57.8%.

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  • (PMID = 27960994.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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92. Vose J, Loberiza F, Armitage J, Bierman P, Bociek R, Dornan D: Effects of FCGR3A and FCGR2A polymorphisms on outcomes of patients with diffuse large B-cell lymphoma treated with CHOP-like chemotherapy versus CHOP-rituximab. J Clin Oncol; 2009 May 20;27(15_suppl):8567

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of FCGR3A and FCGR2A polymorphisms on outcomes of patients with diffuse large B-cell lymphoma treated with CHOP-like chemotherapy versus CHOP-rituximab.
  • : 8567 Background: The addition of rituximab to cyclophosphamide/ doxorubicin/ vincristine/ prednisone (R-CHOP) therapy for diffuse large B-cell lymphoma (DLBCL) has significantly improved the outcome for many patients (pts).
  • In a multivariate analysis for risk of progression or death: FCGR2A : H/H vs. H/R or R/R by treatment type: CHOP-like [RR 0.63 (95% CI 0.37-1.08), p=0.10] and R-CHOP [RR 0.59 (0.36-0.96), p=0.04] and for FCGR3A V/V vs. F/V or F/F by treatment arm: CHOP-like [RR 0.75 (0.36-1.54), p=0.43] and R-CHOP [RR 2.28(0.70-7.44), p=0.17].
  • However, our study also suggests that a trend toward association of certain polymorphisms with clinical outcomes.

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  • (PMID = 27961024.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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93. Gaffar HA, Elfayomy A, Elmaghraby A, Elnemr MM, Elsawy WH: bcl-2 expression and possibility of bladder preservation using combined modality treatment in muscle-invasive transtional cell carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e16133

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] bcl-2 expression and possibility of bladder preservation using combined modality treatment in muscle-invasive transtional cell carcinoma.
  • To evaluate the combined modality treatment and selective bladder preservation and to evaluate BCL-2 expression that may predict treatment response and survival.
  • METHODS: 66 eligible patients with T2-4a NxM0 transitional cell carcinoma received two courses of gemcitabine and cisplatin followed by 45 Gy of pelvic radiotherapy in 1.8 Gy fractions with concomitant cisplatin.
  • Immunohistochemistry was used to assess the tumor cell expression of BCL-2.
  • Bcl-2 was expressed in 35 (53%) of the patients.
  • Bcl-2 immunoreactivity was inversely correlated with of histological grade (p = 0.0232) and was not correlated with gender distribution (p = 0.4666), the clinical stage (T) (p = 0.4325) or response to treatment (p = 0.6234).
  • No significant difference was noted between the cause-specific survival rate of patients with positive Bcl-2 expression and those with negative BCL-2 expression.
  • CONCLUSIONS: this combined approach of chemotherapy and radiation therapy with bladder preservation should be considered as an option for muscle-invasive transitional cell carcinoma of bladder.
  • Assessment of Bcl-2 protein expression may be used to predict a clinical response to this combined modality approach.

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  • (PMID = 27963367.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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94. Lopez R, Gallardo E, Ruibal A, Leon L, Sanchez-Salmon A, Abdulkader I, Gude F, Curiel T, Barandela J, Gayoso L: HIF expression and Max-SUV-18F-FDG-PET in non-small cell lung cancer (NSCLC) patients. J Clin Oncol; 2009 May 20;27(15_suppl):e22010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HIF expression and Max-SUV-18F-FDG-PET in non-small cell lung cancer (NSCLC) patients.
  • WI) to construct a TMA block, according to conventional protocols for the study of immunohistochemical expression of HIF-1α, HIF-2 α, EGFR, bcl-2, MIB1, p16, p63 and cyclins A, B1, D1 and D3.
  • Sections were scored as positive if >10% of cells stained positively.
  • Staining patterns were correlated to clinical variables.
  • RESULTS: HIF- 1α expression was observed in 84/96 patients (34/39 adenocarcinomas and 50/57 squamous cell carcinomas), however it did not correlate with clinical stage (I-II: 41/45 vs III-IV: 44/51).
  • HIF-2 α expression was observed in 60/103 cases (27/42 adenocarcinomas and 33/61 squamous cell carcinomas) and it did not correlate with clinical stage ((I-II: 28/45 vs III-IV: 32/57).
  • After multivariate analysis, only the clinical stage (RR: 2,2) was a prognostic factor. CONCLUSIONS:.
  • 1) HIF-1α and HIF-2 α expressions are frequent in patients with NSCLCs and it did not correlate with clinical stage;.

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  • (PMID = 27963184.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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95. Psyrri D, Pectasides E, Weinberger P, Sasaki C, Burtness B, Fountzilas G: Outcome and molecular features of head and neck squamous cell carcinomas (HNSCC) bearing a p16 high phenotype. J Clin Oncol; 2009 May 20;27(15_suppl):6031

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome and molecular features of head and neck squamous cell carcinomas (HNSCC) bearing a p16 high phenotype.
  • : 6031 Background: We have previously demonstrated that p16 expression defines a biologically distinct subgroup of oropharyngeal squamous cell cancers (OSCC).
  • Protein expression levels for a panel of 13 markers (EGFR, MET, STAT 3, ERK 1/2, pAkt, PI3Kp85, PI3Kp110, PTEN, p53, Bcl-2, E-cadherin, β-catenin, NFκB) were analyzed using AQUA.
  • p16 positive tumors also expressed higher levels of PTEN (p = 0.0009), PI3Kp110 (p = 0.03), NFκB (p = 0.007), and Bcl-2 (p = 0.005).

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  • (PMID = 27962428.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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96. Yi J, Kim S, Lee S, Park S, Ko Y, Choi J, Kim W: Clinical usefulness of PET/CT in initial staging and response evaluation of primary gastric lymphoma. J Clin Oncol; 2009 May 20;27(15_suppl):e19541

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical usefulness of PET/CT in initial staging and response evaluation of primary gastric lymphoma.
  • : e19541 Background: Positron emission tomography (PET)/computed tomography (CT) scan has a well-established role in the management of non-Hodgkin's lymphoma (NHL).
  • However, in case of the primary gastric lymphoma, which is the most frequent extranodal NHL, the role of PET/CT scan is still controversial.
  • METHODS: We retrospectively analyzed 42 patients with primary gastric lymphoma who underwent PET/CT scans; 32 patients with diffuse large B-cell lymphoma (DLBCL) and 10 patients with extranodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma) were analyzed.
  • After corresponding treatment, response was evaluated by conventional CT scans or PET/CT scans and endoscopy with biopsy Results: Nine patients were up-staged based on the results of their PET/CT scan compared to CT (7 DLBCL, 2 MALT lymphomas) while six patients were down-staged by the PET/CT scan.
  • Three patients with DLBCL, who showed an initially high SUVmax, died of disease progression.
  • All of these gastric lesions were grossly and pathologically benign lesions without evidence of lymphoma cells.
  • CONCLUSIONS: PET/CT scan can help staging patients with primary gastric lymphoma, and the maximum SUV has possibility to have prognostic value.

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  • (PMID = 27960998.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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97. Flinn IW, Byrd JC, Furman RR, Brown JR, Lin TS, Bello C, Giese NA, Yu AS: Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies. J Clin Oncol; 2009 May 20;27(15_suppl):3543

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preliminary evidence of clinical activity in a phase I study of CAL-101, a selective inhibitor of the p1108 isoform of phosphatidylinositol 3-kinase (P13K), in patients with select hematologic malignancies.
  • The PI3K p110δ isoform is highly expressed in cells of hematopoietic origin and plays a key role in B cell maturation and function.
  • In vitro studies of 0.1 to 10 μM CAL-101 showed inhibition of pAKT expression and/or apoptotic effects against primary chronic lymphocytic leukemia (CLL) and acute myeloid leukemia (AML) cells and against a range of leukemia and lymphoma cell lines.
  • METHODS: In an ongoing phase 1 dose escalation study in sequential cohorts of 3 patients with relapsed/refractory CLL or select B-cell non-Hodgkin's lymphoma, CAL-101 is administered orally twice daily for 28 days per cycle.
  • Clinical response is evaluated according to NCI criteria at the end of Cycles 1 and 2 and every 2 cycles thereafter.
  • Two of 6 patients attained partial response and 4 have stable disease.
  • Partial responses were observed after 2 cycles of 50 mg in a patient with mantle cell lymphoma with 6 prior therapies, and after 1 cycle of 100 mg in a patient with follicular lymphoma with 6 prior therapies, including autologous stem cell transplant.
  • Disease specific cohort expansion will occur at the maximally tolerated dose, and patients with AML will be added.
  • CONCLUSIONS: Early results from a phase 1 study of the oral PI3K p110δ inhibitor CAL-101 show that it is well tolerated and has preliminary clinical activity in patients with B-cell malignancies.

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  • (PMID = 27961357.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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98. Passalacqua R, Brighenti M, Naldi N, Potenzoni D, Monica B, Fumagalli M, Lazzarelli S, Caminiti C: Long-term effects of a program of bladder preservation using chemotherapy plus radiotherapy in muscle invasive bladder cancer (BC). Analysis of biologic predictive factors and health-related quality of life (QOL). J Clin Oncol; 2009 May 20;27(15_suppl):e16014

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Moreover we investigated whether p53, Ki67, bcl-2, c-erbB-2 protein expression predict the achievement of a complete response (CR).
  • At the response evaluation, pts with biopsy proven residual disease were considered incomplete responders (IR) and underwent immediate cystectomy.
  • Paraffin embedded blocks of the primary tumors were collected and Ki67, p53, bcl-2 and c-erbB-2 protein expression were evaluated in a blind fashion.

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  • (PMID = 27962925.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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99. Rajnics P, Demeter J, Csomor J, Krenács L, Pajor L, Kollár B, Kertész Z, Egyed M: Rare primary extranodal lymphomas: diffuse large B-cell lymphomas of the genital tract. Ann Hematol; 2009 Dec;88(12):1223-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare primary extranodal lymphomas: diffuse large B-cell lymphomas of the genital tract.
  • Primary non-Hodgkin's lymphoma (NHL) of the genital tract is a rare entity.
  • Etiology and pathogenesis of these NHLs are unknown, although there might be a possible association between chronic inflammation and lymphomas.
  • The most common histological subtype is the diffuse large B-cell lymphoma.
  • We report two cases of uterine lymphoma and one case of prostate lymphoma in this paper.
  • The symptoms and the differential diagnosis are also discussed.
  • The two young patients are disease-free nowadays; the older patient with poor prognostic histological-type lymphoma relapsed in a short time and died after second relapse.
  • A multicenter analysis is necessary to evaluate the long-term results of chemoimmunotherapy in these rare extranodal lymphoma entities.
  • [MeSH-major] Lymphoma, Large B-Cell, Diffuse / pathology. Prostatic Neoplasms / pathology. Uterine Neoplasms / pathology

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  • MedlinePlus Health Information. consumer health - Uterine Cancer.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
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  • (PMID = 19352660.001).
  • [ISSN] 1432-0584
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
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100. Amara K, Trimeche M, Ziadi S, Laatiri A, Hachana M, Korbi S: Prognostic significance of aberrant promoter hypermethylation of CpG islands in patients with diffuse large B-cell lymphomas. Ann Oncol; 2008 Oct;19(10):1774-86
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prognostic significance of aberrant promoter hypermethylation of CpG islands in patients with diffuse large B-cell lymphomas.
  • BACKGROUND: Diffuse large B-cell lymphoma (DLBCL) exhibits heterogeneous clinical features and a marked variable response to treatment.
  • Overall survival (OS) and disease-free survival (DFS) rates were calculated by the Kaplan-Meier method and differences were compared with the log-rank test.
  • In addition, hypermethylation of P16 was significantly associated with advanced clinical stages and B symptoms (P = 0.041 and 0.012).






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