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BACKGROUND: Hematopoiesis outside the bone marrow is known to occur in patients with severe anemia, leukemia, polycythemia, or myelofibrosis, and in patients affected by chronic poisoning by marrow-toxic substances.

A hematoxylin-eosin-stained biopsy specimen showed whorls of tumor cells, diagnostic of a meningioma.

Flow cytometric evaluation confirmed the clinical suspicion of an underlying chronic lymphocytic leukemia.

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(PMID = 17714768.001).

[ISSN] 0090-3019

[Journal-full-title] Surgical neurology

[ISO-abbreviation] Surg Neurol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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B cell CLL/lymphoma-2 (BCL-2) and its relatives comprise the BCL-2 family of proteins, which were originally characterized with respect to their roles in controlling outer mitochondrial membrane integrity and apoptosis.

Here we will discuss the mechanisms and functions of the BCL-2 family in the context of these pathways, highlighting the complex integration and regulation of the BCL-2 family in cell fate decisions.

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[Cites] Mol Cell. 2009 Nov 13;36(3):355-63 [19917245.001]

[Cites] Mol Cell. 2009 Nov 13;36(3):487-99 [19917256.001]

[Cites] Mol Cell. 2009 Nov 25;36(4):696-703 [19941828.001]

[Cites] Nature. 2010 Jan 7;463(7277):103-7 [20023629.001]

[Cites] J Biol Chem. 2008 Apr 18;283(16):10892-903 [18281291.001]

[Cites] J Biol Chem. 2007 Apr 27;282(17):13123-32 [17337444.001]

[Cites] Nat Rev Mol Cell Biol. 2007 May;8(5):405-13 [17377525.001]

[Cites] Apoptosis. 2007 May;12(5):897-911 [17453159.001]

[Cites] J Cell Biol. 2007 Apr 23;177(2):277-87 [17452531.001]

[Cites] EMBO J. 2007 May 16;26(10):2527-39 [17446862.001]

[Cites] Cell Death Differ. 2007 Jun;14(6):1086-94 [17332775.001]

[Cites] Autophagy. 2007 Jul-Aug;3(4):374-6 [17438366.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Jul 10;104(28):11649-54 [17606912.001]

[Cites] Genes Dev. 2007 Aug 1;21(15):1937-48 [17671092.001]

[Cites] Nat Cell Biol. 2007 Sep;9(9):1057-65 [17721514.001]

[Cites] Autophagy. 2007 Nov-Dec;3(6):561-8 [17643073.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19500-5 [18048346.001]

[Cites] Cell. 2008 Jan 11;132(1):27-42 [18191218.001]

[Cites] J Biol Chem. 2000 May 26;275(21):16202-12 [10821866.001]

[Cites] Genes Dev. 2000 Aug 15;14(16):2060-71 [10950869.001]

[Cites] J Biol Chem. 2001 Mar 2;276(9):6453-62 [11102440.001]

[Cites] Dev Cell. 2001 Oct;1(4):515-25 [11703942.001]

[Cites] Dev Cell. 2002 Jan;2(1):55-67 [11782314.001]

[Cites] Cancer Cell. 2002 Feb;1(1):19-30 [12086884.001]

[Cites] Cancer Cell. 2002 Sep;2(3):183-92 [12242151.001]

[Cites] Cell. 2002 Nov 1;111(3):331-42 [12419244.001]

[Cites] J Cell Biol. 2002 Dec 23;159(6):931-8 [12499352.001]

[Cites] Mol Cell. 2003 Mar;11(3):577-90 [12667443.001]

[Cites] Science. 2003 Apr 4;300(5616):135-9 [12624178.001]

[Cites] J Biol Chem. 2003 Sep 19;278(38):36373-9 [12783892.001]

[Cites] Science. 2004 Feb 13;303(5660):1010-4 [14963330.001]

[Cites] Biochim Biophys Acta. 2004 Mar 1;1644(2-3):83-94 [14996493.001]

[Cites] Nat Cell Biol. 2004 May;6(5):443-50 [15077116.001]

[Cites] Mol Biol Cell. 2004 Nov;15(11):5001-11 [15356267.001]

[Cites] Nature. 1988 Sep 29;335(6189):440-2 [3262202.001]

[Cites] Cell. 1989 Apr 7;57(1):79-88 [2649247.001]

[Cites] Nature. 1990 Nov 22;348(6299):331-3 [2250704.001]

[Cites] J Biol Chem. 1997 May 23;272(21):13829-34 [9153240.001]

[Cites] J Virol. 1998 Nov;72(11):8586-96 [9765397.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):105-10 [15613488.001]

[Cites] Mol Cell. 2005 Feb 4;17(3):393-403 [15694340.001]

[Cites] Science. 2005 Feb 18;307(5712):1101-4 [15718471.001]

[Cites] Mol Cell. 2005 Feb 18;17(4):525-35 [15721256.001]

[Cites] Nature. 2005 Jun 2;435(7042):677-81 [15902208.001]

[Cites] Science. 2005 Sep 9;309(5741):1732-5 [16151013.001]

[Cites] J Biol Chem. 2005 Oct 21;280(42):35742-50 [16115883.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Dec 13;102(50):17975-80 [16330765.001]

[Cites] Nat Rev Mol Cell Biol. 2006 Feb;7(2):97-108 [16493416.001]

[Cites] Mol Cell. 2006 Mar 17;21(6):761-73 [16543146.001]

[Cites] Science. 2006 Apr 28;312(5773):572-6 [16645094.001]

[Cites] Cancer Cell. 2006 May;9(5):351-65 [16697956.001]

[Cites] Cell. 2006 Jul 14;126(1):163-75 [16839884.001]

[Cites] Cell. 2006 Jul 14;126(1):177-89 [16839885.001]

[Cites] J Cell Biol. 2006 Sep 25;174(7):915-21 [16982799.001]

[Cites] Mol Cell Biol. 2006 Oct;26(20):7397-408 [17015472.001]

[Cites] J Clin Oncol. 2006 Oct 10;24(29):4738-45 [16966688.001]

[Cites] Nature. 2006 Oct 12;443(7112):658-62 [17035996.001]

[Cites] Cancer Cell. 2006 Nov;10(5):389-99 [17097561.001]

[Cites] Nat Cell Biol. 2006 Dec;8(12):1348-58 [17115033.001]

[Cites] J Clin Invest. 2007 Jan;117(1):112-21 [17200714.001]

[Cites] Science. 2007 Feb 9;315(5813):856-9 [17289999.001]

[Cites] Nat Rev Cancer. 2008 Feb;8(2):121-32 [18202696.001]

[Cites] Dev Cell. 2008 Feb;14(2):193-204 [18267088.001]

[Cites] Nat Immunol. 2008 Apr;9(4):405-14 [18327259.001]

[Cites] Trends Cell Biol. 2008 Apr;18(4):157-64 [18314333.001]

[Cites] Mol Cell. 2008 May 9;30(3):369-80 [18471982.001]

[Cites] J Exp Med. 2008 May 12;205(5):1029-36 [18443228.001]

[Cites] Mol Biol Cell. 2008 Jun;19(6):2402-12 [18353969.001]

[Cites] Mol Cell. 2008 Jun 20;30(6):678-88 [18570871.001]

[Cites] Nature. 2008 Jul 10;454(7201):232-5 [18454133.001]

[Cites] J Biol Chem. 2008 Jul 25;283(30):21294-304 [18524770.001]

[Cites] Mol Cell. 2008 Aug 22;31(4):557-69 [18691924.001]

[Cites] Mol Cell. 2008 Aug 22;31(4):570-85 [18722181.001]

[Cites] Cell Death Differ. 2008 Oct;15(10):1564-71 [18551131.001]

[Cites] Nature. 2008 Oct 23;455(7216):1076-81 [18948948.001]

[Cites] Nature. 2008 Dec 4;456(7222):605-10 [19052620.001]

[Cites] Cell. 2008 Dec 12;135(6):1074-84 [19062087.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20327-32 [19074266.001]

[Cites] Mol Cell. 2009 Jan 16;33(1):15-29 [19150424.001]

[Cites] J Biol Chem. 2009 Jan 30;284(5):2719-28 [19029119.001]

[Cites] Clin Cancer Res. 2009 Feb 15;15(4):1126-32 [19228717.001]

[Cites] Nature. 2009 May 21;459(7245):428-32 [19363473.001]

[Cites] Autophagy. 2009 Jul;5(5):720-2 [19395874.001]

[Cites] Cell Death Differ. 2009 Aug;16(8):1135-45 [19300452.001]

[Cites] Science. 2009 Jul 24;325(5939):477-81 [19556461.001]

[Cites] Apoptosis. 2009 Aug;14(8):929-34 [19629695.001]

[Cites] Nat Cell Biol. 2009 Aug;11(8):958-66 [19578372.001]

[Cites] J Cell Biol. 2009 Aug 10;186(3):355-62 [19651893.001]

[Cites] Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14397-402 [19706527.001]

(PMID = 20159550.001).

[ISSN] 1097-4164

[Journal-full-title] Molecular cell

[ISO-abbreviation] Mol. Cell

[Language] eng

[Grant] United States / NCI NIH HHS / CA / F32 CA101444; United States / NIAID NIH HHS / AI / R01 AI040646; United States / NIAID NIH HHS / AI / R01 AI040646-16

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Proto-Oncogene Proteins c-bcl-2

[Number-of-references] 89

[Other-IDs] NLM/ NIHMS337530; NLM/ PMC3222298

   

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When these titanocenes were tested against LLC-PK cells, the IC(50) values obtained were of 24, 36, and 41 microM respectively.

The most cytotoxic titanocene in this paper (5a) with an IC(50) value of 24 microM is found to be almost ten times less cytotoxic than cis-platin, which showed an IC(50) value of 3.3 microM when tested on the epithelial pig kidney LLC-PK cell line, and approximately 2 times less cytotoxic than its dimethylamino-functionalised analogue.

[MeSH-minor] Animals. Cyclopentanes. Inhibitory Concentration 50. LLC-PK1 Cells. Structure-Activity Relationship. Swine

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(PMID = 18336326.001).

[ISSN] 1573-4064

[Journal-full-title] Medicinal chemistry (Shāriqah (United Arab Emirates))

[ISO-abbreviation] Med Chem

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclopentanes; 0 / Morpholines; 0 / Organometallic Compounds; 1271-29-0 / titanocene; 19W699IKIE / fulvene

   

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The cytotoxicity of the compounds was assessed by the MTT method using LLC-MK2 cells.

Trans-methylpluviatolide displayed low toxicity for LLC-MK2 cells, with an IC50 of 6.53 mM.

[MeSH-minor] Animals. Cell Line. Macrophages / drug effects. Macrophages / metabolism. Mice. Molecular Structure. Nitric Oxide / biosynthesis. Structure-Activity Relationship

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(PMID = 18479721.001).

[ISSN] 0031-9422

[Journal-full-title] Phytochemistry

[ISO-abbreviation] Phytochemistry

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Lactones; 0 / Lignans; 0 / Trypanocidal Agents; 0 / methylpluviatolide; 31C4KY9ESH / Nitric Oxide

   

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[Title] A prospective study of 728 cases of non-Hodgkin lymphoma from a single laboratory in Shanghai, China.

The frequency of subtypes of lymphoid neoplasms was determined in a prospective series of 831 patients presenting at 29 Shanghai hospitals over a 4-year period.

Diagnosis and classification was established in a single laboratory according to the 2001 WHO classification system.

The frequency of non-Hodgkin lymphoma was 87.6% (n = 728) and Hodgkin lymphoma was 12.4% (n = 103).

The most prevalent NHL subtypes diagnosed using WHO criteria were diffuse large B cell lymphoma (DLBCL), precursor B lymphoblastic leukemia/lymphoma and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL).

Although a low incidence has been reported in some Asian populations, CLL/SLL was commonly encountered, indicating that chronic lymphoid neoplasms are not rare in Shanghai.

Consistent with previous reports, our findings indicate a decrease in the frequency of follicular lymphoma and an increase in T cell neoplasms compared to the West.

Precursor T lymphoblastic leukemia/lymphoma, anaplastic large T cell lymphoma, aggressive NK cell leukemia, angioimmunoblastic T cell lymphoma and peripheral T cell lymphoma were prominent subtypes of T cell NHL.

[MeSH-major] Asian Continental Ancestry Group / statistics & numerical data. Lymphoma, Non-Hodgkin / classification. Lymphoma, Non-Hodgkin / ethnology

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[Cites] Int J Cancer. 1984 Aug 15;34(2):143-8 [6381328.001]

[Cites] Ann Oncol. 2004 Jul;15(7):1091-6 [15205204.001]

[Cites] Cancer. 1996 Oct 15;78(8):1813-9 [8859197.001]

[Cites] Blood. 1995 Mar 1;85(5):1151-68 [7858247.001]

[Cites] Blood. 1994 Sep 1;84(5):1361-92 [8068936.001]

[Cites] Cancer Lett. 1999 Jan 8;135(1):73-81 [10077224.001]

[Cites] Cancer. 1994 Jul 1;74(1):174-81 [8004573.001]

[Cites] Hematol Oncol Clin North Am. 1991 Oct;5(5):983-1001 [1938764.001]

[Cites] Int J Hematol. 2007 Jan;85(1):18-25 [17261497.001]

[Cites] Cancer. 2007 Apr 1;109(7):1360-4 [17326056.001]

[Cites] Hum Pathol. 1987 Sep;18(9):924-8 [3497862.001]

[Cites] Appl Immunohistochem Mol Morphol. 2005 Dec;13(4):323-32 [16280661.001]

[Cites] Cancer. 2000 Oct 1;89(7):1586-92 [11013375.001]

[Cites] Br J Haematol. 1999 Nov;107(2):353-6 [10583224.001]

[Cites] Zhonghua Bing Li Xue Za Zhi. 2005 Jan;34(1):22-7 [15796877.001]

[Cites] Pathol Int. 2002 Jan;52(1):1-12 [11940200.001]

[Cites] Rev Clin Exp Hematol. 2002 Jun;6(2):114-41; discussion 200-2 [12196212.001]

[Cites] Cancer. 1998 Aug 15;83(4):806-12 [9708949.001]

[Cites] Int J Cancer. 2007;120 Suppl 12:1-39 [17405121.001]

[Cites] J Clin Oncol. 1998 Aug;16(8):2780-95 [9704731.001]

(PMID = 18648906.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / DNA, Neoplasm

   

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[Title] B lymphocytes in humans express ZAP-70 when activated in vivo.

Recently, this important signaling element was detected in leukemic B cells from a subgroup of patients with B cell chronic lymphocytic leukemia (B-CLL).

The cDNA sequence of B cell ZAP-70 was the same as that in T cells.

Germinal center B cells and plasma cells had a substantial proportion of ZAP-70+ cells, while memory and follicular mantle B cells, which contain low numbers of activated B cells, expressed relatively little ZAP-70.

A cell fraction of IgD+, CD38+ B cells, which are comprised of many in vivo activated B cells, exhibited the highest levels of ZAP-70.

In these B cells, the expression of ZAP-70 correlated with that of CD38 and not with that of CD5, a hallmark of B-CLL cells.

B-CLL cells are activated cells and their ZAP-70 expression reflects a normal property of activated B cells populations rather than a neoplastic aberration.

[MeSH-major] B-Lymphocytes / immunology. Gene Expression Regulation, Enzymologic / immunology. Lymphocyte Activation / immunology. ZAP-70 Protein-Tyrosine Kinase / immunology

[MeSH-minor] Antigens, CD38 / immunology. Antigens, CD5 / immunology. Cells, Cultured. Germinal Center / cytology. Germinal Center / immunology. Humans. Immunoglobulin D / immunology. Killer Cells, Natural / cytology. Killer Cells, Natural / enzymology. Killer Cells, Natural / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Membrane Glycoproteins / immunology. Palatine Tonsil / cytology. Palatine Tonsil / immunology. T-Lymphocytes / cytology. T-Lymphocytes / enzymology. T-Lymphocytes / immunology

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(PMID = 16482508.001).

[ISSN] 0014-2980

[Journal-full-title] European journal of immunology

[ISO-abbreviation] Eur. J. Immunol.

[Language] eng

[Grant] United States / NCRR NIH HHS / RR / M01 RR018535; United States / NCI NIH HHS / CA / R01 CA 81554; United States / NCI NIH HHS / CA / R01 CA 87956

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, CD5; 0 / Immunoglobulin D; 0 / Membrane Glycoproteins; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human

   

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[Title] Dendritic cell-based immunogens for B-cell chronic lymphocytic leukemia.

Hybrids generated from tumor cells and dendritic cells (DC) have been proposed as tools for treating malignant disease.

Here, we study the underlying principles and the feasibility for the adjuvant therapy of human B cell chronic-lymphocytic leukemia (B-CLL).

CLL cells and allogeneic DC were only mixed or additionally fused.

Using a combination of FACS and fluorescence microscopic analyses, we show that DC-CLL hybrids can be successfully generated.

We made a systematic comparison of the immunostimulatory capacities of different stimulator cell populations, including DC-CLL fusion samples, unfused mixtures of DC and CLL cells as well as DC or tumor cells alone.

This could be explained by the capture of antigens from surrounding leukemia cells by DC during co-cultivation.

Although fusion frequencies were low, PBMC stimulation was significantly more effective when the mixtures were subjected to cell fusion.

The most potent stimulus was provided by DC-CLL fusion samples derived from mature DC, probably due to their enhanced costimulatory capacity.

In summary, DC-tumor cell hybrids might be feasible in the treatment of B-CLL.

It should be considered that FACS analysis is not sufficient to assess fusion frequencies and that interactions between unfused DC and CLL cells also result in PBMC activation.

[MeSH-major] Dendritic Cells / immunology. Leukemia, Lymphocytic, Chronic, B-Cell / immunology

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(PMID = 16516377.001).

[ISSN] 0304-3835

[Journal-full-title] Cancer letters

[ISO-abbreviation] Cancer Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD11c; 0 / Antigens, CD19; 0 / Antigens, CD3; 0 / Antigens, CD5; 0 / Antigens, CD80; 0 / Antigens, CD86; 0 / CD83 antigen; 0 / HLA-DR Antigens; 0 / Immunoglobulins; 0 / Membrane Glycoproteins; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma

   

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[Title] Does reduced-intensity allogeneic transplantation confer a survival advantage to patients with poor prognosis chronic lymphocytic leukaemia? A case-control retrospective analysis.

BACKGROUND: Reduced-intensity conditioning (RIC) allogeneic haemopoietic cell transplantation (allo-HCT) is increasingly considered as a therapeutic option for younger patients with poor-risk chronic lymphocytic leukaemia (CLL).

In this retrospective analysis, we assessed the outcomes of CLL patients undergoing RIC allo-HCT compared with a group of matched controls that were candidates for transplantation but did not have a suitable donor or refused the procedure.

Haemopoietic cell grafts were harvested from HLA-matched siblings (27) and unrelated donors (7).

Matching variables were age at diagnosis and time to first CLL-specific therapy.

RESULTS: Both patient groups were well balanced in terms of cytogenetics by FISH, CD38 and ZAP-70 expression, and immunoglobulin heavy-chain variable region mutational status.

Median overall survival was 113 months for HCT patients and 85 months for controls when calculated from time of diagnosis (P = 0.072) and 103 and 67 months, respectively, when calculated from time of first therapy (P = 0.041).

CONCLUSION: RIC allo-HCT is a reasonable option for patients with high-risk CLL.

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(PMID = 19596701.001).

[ISSN] 1569-8041

[Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology

[ISO-abbreviation] Ann. Oncol.

[Language] ENG

[Publication-type] Journal Article

[Publication-country] England

   

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[Title] Chronic lymphoid leukaemia: clinico-haematological correlation and outcome in a single institution in Niger Delta region of Nigeria.

Sixty patients were prospectively studied with the aim of analyzing the clinical and laboratory features and outcome of patients diagnosed with chronic lymphocytic leukaemia (CLL) in a major referral center in Niger Delta region of Nigeria for 10 years (1995-2005).

The peripheral blood, bone marrow cytology, clinical features and stage at diagnosis were studied.

The CLL incidence was 36.4% of total leukaemias.

There was a strong association between the blood counts at diagnosis and outcome of therapy.

The 2-year survival for young (<55 years) and older (>55 years) CLL patients was 27.2% and 28.9%, respectively, which is still very poor because of a number of strong limiting factors.

CLL is not rare in Southern Nigeria and its presentations are similar to cases seen worldwide.

[MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / mortality

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(PMID = 17988297.001).

[ISSN] 1751-5521

[Journal-full-title] International journal of laboratory hematology

[ISO-abbreviation] Int J Lab Hematol

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

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[Title] Chronic lymphocytic leukemia and treatment resistance in cancer: the role of the p53 pathway.

The importance of studying p53 pathway defects in CLL has been fostered by the demonstration of the fundamentally different clinical course of patients with 17p deletion, where the clinical course is, contrary to most patients with CLL, very poor.

The demonstration of the resistance to chemotherapy and mutation of the remaining TP53 allele explains the clinical presentation of CLL with 17p deletion.

Here we review recent evidence that TP53 mutation in the absence of the deletion of 17p shows a similar clinical and biological course in CLL.

[MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Tumor Suppressor Protein p53 / genetics

[MeSH-minor] Ataxia Telangiectasia Mutated Proteins. Cell Cycle Proteins / genetics. Chromosomes, Human, Pair 17. DNA Damage. DNA-Binding Proteins / genetics. Drug Resistance, Neoplasm. Gene Deletion. Humans. MicroRNAs / genetics. Protein-Serine-Threonine Kinases / genetics. Survival Analysis. Tumor Suppressor Proteins / genetics

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(PMID = 19098429.001).

[ISSN] 1551-4005

[Journal-full-title] Cell cycle (Georgetown, Tex.)

[ISO-abbreviation] Cell Cycle

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / MicroRNAs; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / Protein-Serine-Threonine Kinases

[Number-of-references] 37

   

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We demonstrate the effect of proteasome inhibitors in mitochondrial release of apoptosis-inducing factor (AIF) in cisplatin-exposed renal tubular epithelial cells (LLC-PK(1) cells) and in a model of cisplatin nephrotoxicity.

Downregulation of Mcl-1 by small interfering RNA promoted Bax activation and cytochrome c and AIF release, suggesting that cisplatin-induced Mcl-1 depletion and associated Bax activation are involved in the release of AIF.

[MeSH-minor] Animals. Blotting, Western. Immunoprecipitation. LLC-PK1 Cells. Male. Mice. Mice, Inbred C57BL. Swine

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(PMID = 19699182.001).

[ISSN] 1873-2968

[Journal-full-title] Biochemical pharmacology

[ISO-abbreviation] Biochem. Pharmacol.

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; Q20Q21Q62J / Cisplatin

   

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[Title] ABO genotyping in leukemia patients reveals new ABO variant alleles.

The aim of the present study was to perform ABO genotyping in patients with leukemia.

Blood samples were collected from 108 Brazilian patients with chronic myeloid leukemia (N = 69), chronic lymphoid leukemia (N = 13), acute myeloid leukemia (N = 15), and acute lymphoid leukemia (N = 11).

We identified 22 new ABO*variants in the coding region of the ABO gene in 25 individuals with leukemia (23.2%).

The majority of ABO variants was detected in O alleles (15/60.0%).

Elucidation of the diversity of this gene in leukemia and in other diseases is important for the determination of the effect of changes in an amino acid residue on the specificity and activity of ABO glycosyltransferases and their function.

In conclusion, this is the first report of a large number of patients with leukemia genotyped for ABO.

The findings of this study indicate that there is a high level of recombinant activity in the ABO gene in leukemia patients, revealing new ABO variants.

[MeSH-major] ABO Blood-Group System / genetics. Alleles. Genetic Variation. Leukemia / blood

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(PMID = 18273824.001).

[ISSN] 1676-5680

[Journal-full-title] Genetics and molecular research : GMR

[ISO-abbreviation] Genet. Mol. Res.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Brazil

[Chemical-registry-number] 0 / ABO Blood-Group System; 9007-49-2 / DNA

   

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BACKGROUND: The current manual sample processing method recommended for use with the TRUGENE HBV Genotyping Kit (TRUGENE HBV; Bayer HealthCare LLC, Tarrytown, NY) is labor-intensive and may be prone to specimen cross-contamination.

Performance of TRUGENE HBV used in conjunction with MP sample processing was evaluated further using 22 clinical serum specimens containing low titers of HBV DNA.

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(PMID = 16023890.001).

[ISSN] 1386-6532

[Journal-full-title] Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology

[ISO-abbreviation] J. Clin. Virol.

[Language] eng

[Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / DNA, Viral

   

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[Title] Active compounds isolated from traditional Chinese prescription Wen-Pi-Tang protecting against peroxynitrite-induced LLC-PK(1) cell damage.

Wen-Pi-Tang, a traditional Chinese prescription, has been widely used for the treatment of patients with moderate chronic renal failure in China.

Although the protective effect of Wen-Pi-Tang on peroxynitrite (ONOO(-))-induced renal tubular epithelial LLC-PK(1) cell damage was elucidated in our previous research, the active components of Wen-Pi-Tang have not yet been fully clarified.

Therefore, the major bioactivity of Wen-Pi-Tang against ONOO(-)-induced cytotoxicity in LLC-PK(1) cells was thought to be mediated by (+)-catechin.

Although we cannot disregard the synergetic effect of various components in Wen-Pi-Tang, (+)-catechin is a major active compound protecting against ONOO(-)-induced LLC-PK(1) cell damage and may be used as an index to qualify the ONOO(-)-inhibitory activity of Wen-Pi-Tang extract.

[MeSH-minor] Animals. Cell Line. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Epithelial Cells / pathology. Free Radicals / metabolism. Molsidomine / analogs & derivatives. Molsidomine / pharmacology. Nitric Oxide Donors / pharmacology. Swine

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(PMID = 18711772.001).

[ISSN] 0192-415X

[Journal-full-title] The American journal of Chinese medicine

[ISO-abbreviation] Am. J. Chin. Med.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Singapore

[Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Free Radicals; 0 / Nitric Oxide Donors; 0 / wen-pi-tang; 14691-52-2 / Peroxynitrous Acid; 5O5U71P6VQ / linsidomine; 8R1V1STN48 / Catechin; D46583G77X / Molsidomine

   

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[Title] Aspirin induces apoptosis in human leukemia cells independently of NF-kappaB and MAPKs through alteration of the Mcl-1/Noxa balance.

Aspirin and other non-steroidal anti-inflammatory drugs induce apoptosis in most cell types.

In this study we examined the mechanism of aspirin-induced apoptosis in human leukemia cells.

Our results show that aspirin induced apoptosis in leukemia Jurkat T cells independently of NF-kappaB.

This alteration of the Mcl-1/Noxa balance was also found in other leukemia cell lines and primary chronic lymphocytic leukemia cells (CLL).

Furthermore, in CLL cells aspirin induced an increase in the protein levels of Noxa.

[MeSH-major] Apoptosis / drug effects. Aspirin / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / enzymology. Mitogen-Activated Protein Kinases / metabolism. NF-kappa B / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism

[MeSH-minor] Apoptosis Regulatory Proteins / metabolism. Cell Line, Tumor. Cell Survival / drug effects. Cycloheximide / pharmacology. Cytochromes c / secretion. Drug Screening Assays, Antitumor. Enzyme Activation / drug effects. Humans. JNK Mitogen-Activated Protein Kinases / metabolism. MAP Kinase Kinase Kinases / metabolism. Mitochondria / drug effects. Mitochondria / secretion. Myeloid Cell Leukemia Sequence 1 Protein. Proto-Oncogene Proteins / metabolism

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(PMID = 19936928.001).

[ISSN] 1573-675X

[Journal-full-title] Apoptosis : an international journal on programmed cell death

[ISO-abbreviation] Apoptosis

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / BBC3 protein, human; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / NF-kappa B; 0 / PMAIP1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 9007-43-6 / Cytochromes c; 98600C0908 / Cycloheximide; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; EC 2.7.11.25 / MAP3K8 protein, human; R16CO5Y76E / Aspirin

   

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Previous studies demonstrated that NK-dependant increases in CCL22 secretion selectively recruit Tregs toward murine lungs bearing Lewis Lung Carcinoma (LLC).

To extend the in vitro studies, the present studies utilized in vivo depletion of NK cells to ascertain the contribution of NK-derived CCL22 toward total CCL22 and subsequent Treg levels in both normal and LLC-bearing lungs.

However, NK depletion had the unexpected effect of increasing both CCL22 secretion and Treg levels in the lungs of NK-depleted LLC-bearing mice.

Flow cytometry and a series of both immunomagnetic and FACS isolations were used to identify the CCL22-producing cellular fractions in LLC-bearing lungs.

A novel CD11b(+)CD11c(+) cell population was identified that accumulates in large numbers in NK-depleted LLC-bearing lung tissue.

These CD11b(+)CD11c(+) cells secreted large amounts of CCL22 that may overcompensate for the loss of NK-derived CCL22 in the lungs of NK-depleted LLC-bearing mice.

Taken together, these data suggest that NK cells play both a positive and negative role in the regulation of CCL22 secretion and, in turn, the recruitment of Tregs toward LLC-bearing lungs.

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[Cites] J Exp Med. 2000 Feb 21;191(4):661-8 [10684858.001]

[Cites] J Immunol. 2009 Mar 1;182(5):2753-65 [19234170.001]

[Cites] Int Immunol. 2001 Apr;13(4):459-63 [11282985.001]

[Cites] J Leukoc Biol. 2001 Apr;69(4):531-7 [11310838.001]

[Cites] J Exp Med. 2001 Sep 17;194(6):847-53 [11560999.001]

[Cites] Science. 2001 Oct 19;294(5542):605-9 [11567106.001]

[Cites] J Clin Oncol. 2003 Jun 15;21(12):2342-8 [12805336.001]

[Cites] Annu Rev Immunol. 2004;22:329-60 [15032581.001]

[Cites] Semin Immunol. 2004 Apr;16(2):89-98 [15036232.001]

[Cites] Nat Med. 2004 Sep;10(9):942-9 [15322536.001]

[Cites] J Reticuloendothel Soc. 1979 Jun;25(6):623-33 [385867.001]

[Cites] Boll Ist Sieroter Milan. 1985;64(1):25-34 [3859302.001]

[Cites] J Natl Cancer Inst. 1986 Apr;76(4):745-50 [3457207.001]

[Cites] J Natl Cancer Inst. 1986 Dec;77(6):1255-60 [3491925.001]

[Cites] J Immunol. 1995 Aug 1;155(3):1151-64 [7636184.001]

[Cites] Clin Exp Metastasis. 1998 Apr;16(3):275-82 [9568645.001]

[Cites] J Immunol. 1998 Nov 1;161(9):5027-38 [9794440.001]

[Cites] Diabetes. 2005 Feb;54(2):434-42 [15677501.001]

[Cites] J Immunol. 2009 Dec 15;183(12):8044-53 [19933856.001]

[Cites] Cancer Res. 2005 Jun 15;65(12):5211-20 [15958566.001]

[Cites] J Immunol. 2005 Nov 1;175(9):6169-76 [16237114.001]

[Cites] Cancer Res. 2006 Jun 1;66(11):5716-22 [16740709.001]

[Cites] Cancer Immunol Immunother. 2008 Jan;57(1):123-31 [17522861.001]

[Cites] Blood. 2008 Jan 15;111(2):761-6 [17967942.001]

[Cites] Int J Cancer. 2008 May 15;122(10):2286-93 [18224687.001]

[Cites] Nat Rev Cancer. 2008 Aug;8(8):618-31 [18633355.001]

[Cites] Blood. 2001 Mar 15;97(6):1733-41 [11238115.001]

(PMID = 20198623.001).

[ISSN] 1097-0215

[Journal-full-title] International journal of cancer

[ISO-abbreviation] Int. J. Cancer

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01CA8566; United States / NIDCR NIH HHS / DE / R01 DE018168-02; United States / NCI NIH HHS / CA / 1R01CA128837; United States / NCI NIH HHS / CA / R01 CA085266-06; United States / NCI NIH HHS / CA / R01 CA085266; United States / NIDCR NIH HHS / DE / R01DE018168; United States / NIDCR NIH HHS / DE / R01 DE018168; United States / NCI NIH HHS / CA / CA128837-01A2; United States / NCI NIH HHS / CA / R01 CA128837; United States / NCI NIH HHS / CA / R01 CA128837-01A2; United States / NIDCR NIH HHS / DE / DE018168-02

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD11c; 0 / CCL22 protein, human; 0 / Chemokine CCL22; 37758-47-7 / G(M1) Ganglioside; 71012-19-6 / asialo GM1 ganglioside

[Other-IDs] NLM/ NIHMS189166; NLM/ PMC2947555

   

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[Title] Redundant role for Zap70 in B cell development and activation.

Expression of the Syk family tyrosine kinase Zap70 is strongly correlated with poor clinical outcome in chronic lymphocytic leukemia, the most common human leukemia characterized by B cell accumulation.

The expression of Zap70 may reflect the specific cell of origin of the tumor or may contribute to pathology.

Thus, the normal role of Zap70 in B cell physiology is of great interest.

While initial studies reported that Zap70 expression in the mouse was limited to T and NK cells, more recent work has shown expression in early B cell progenitors and in splenic B cells, suggesting that the kinase may play a role in the development or activation of B cells.

In this study, we show that Zap70 is expressed in all developing subsets of B cells as well as in recirculating B cells, marginal zone B cells and peritoneal B1 cells.

[MeSH-major] B-Lymphocytes / metabolism. Cell Differentiation. ZAP-70 Protein-Tyrosine Kinase / metabolism

[MeSH-minor] Animals. B-Lymphocyte Subsets / cytology. B-Lymphocyte Subsets / metabolism. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Calcium Signaling / physiology. Cell Proliferation. Flow Cytometry. Hemocyanin / immunology. Immunoblotting. Intracellular Signaling Peptides and Proteins / deficiency. Intracellular Signaling Peptides and Proteins / genetics. Intracellular Signaling Peptides and Proteins / metabolism. Lymphocyte Activation. Mice. Mice, Inbred C57BL. Mice, Inbred Strains. Mice, Knockout. Mice, Mutant Strains. Mice, Transgenic. Peritoneal Cavity / cytology. Precursor Cells, B-Lymphoid / cytology. Precursor Cells, B-Lymphoid / metabolism. Protein-Tyrosine Kinases / deficiency. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. Receptors, Antigen, B-Cell / physiology. Spleen / cytology. Spleen / immunology. Syk Kinase. Vaccination

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(PMID = 18465772.001).

[ISSN] 0014-2980

[Journal-full-title] European journal of immunology

[ISO-abbreviation] Eur. J. Immunol.

[Language] eng

[Grant] United Kingdom / Medical Research Council / / MC/ U117527252; United Kingdom / Medical Research Council / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Intracellular Signaling Peptides and Proteins; 0 / Receptors, Antigen, B-Cell; 0 / trinitrophenyl keyhole limpet hemocyanin; 9013-72-3 / Hemocyanin; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / SYK protein, human; EC 2.7.10.2 / Syk Kinase; EC 2.7.10.2 / Syk protein, mouse; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / Zap70 protein, mouse

   

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The comparison between the dose distributions measured on films and computed by TPS, after a precise image registration procedure performed by a commercial piece of software (FILMQA, 3cognition LLC (Division of ISP), Wayne, NJ), allowed the authors to measure the repositioning errors, obtaining about 0.5 mm in case of central spherical PTV and about 1.5 mm in case of peripheral irregular PTV.

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(PMID = 19673186.001).

[ISSN] 0094-2405

[Journal-full-title] Medical physics

[ISO-abbreviation] Med Phys

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] Plasmablastic lymphoma: Cytologic findings in 5 cases with unusual presentation.

BACKGROUND: Plasmablastic lymphoma (PBL) is a rare form of non-Hodgkin lymphoma that was once believed to occur primarily in the oral cavity of human immunodeficiency virus-positive individuals.

The presence of the following was evaluated: cellularity, plasmablastic cells, background necrosis (BN), single-cell necrosis (SCN), lymphoglandular bodies (LGB), tingible-body macrophages (TBM), 3-dimensional clusters/sheets, and cytoplasmic vacuoles.

Two patients had the acquired immunodeficiency syndrome and 3 had second non-PBL related malignancies including endometrial carcinoma, lung adenocarcinoma, and small lymphocytic lymphoma.

However, although these findings may suggest PBL, a definitive diagnosis requires adjunctive studies including immunohistochemistry and flow cytometry.

[MeSH-major] Lymphoma, Non-Hodgkin / metabolism. Lymphoma, Non-Hodgkin / pathology

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[Copyright] (c) 2008 American Cancer Society.

(PMID = 18683216.001).

[ISSN] 0008-543X

[Journal-full-title] Cancer

[ISO-abbreviation] Cancer

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] A randomized, double-blind, placebo-controlled, clinical study of the general effects of a standardized Lycium barbarum (Goji) Juice, GoChi.

BACKGROUND: This randomized, double-blind, placebo-controlled clinical trial is the first study reported from outside China that has examined the general effects of the orally consumed goji berry, Lycium barbarum, as a standardized juice (GoChi; FreeLife International LLC, Phoenix, AZ) to healthy adults for 14 days.

METHODS: Based upon the medicinal properties of Lycium barbarum in traditional Asian medicine, we examined by questionnaire subjective ratings (0-5) of general feelings of well-being, neurologic/psychologic traits, gastrointestinal, musculoskeletal, and cardiovascular complaints as well as any adverse effects.

CONCLUSIONS: These results clearly indicate that daily consumption of GoChi for 14 days increases subjective feelings of general well-being, and improves neurologic/psychologic performance and gastrointestinal functions.

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(PMID = 18447631.001).

[ISSN] 1075-5535

[Journal-full-title] Journal of alternative and complementary medicine (New York, N.Y.)

[ISO-abbreviation] J Altern Complement Med

[Language] eng

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Neuroprotective Agents; 0 / Plant Extracts

   

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We review our experience with the use of the CentriMag (Levitronix LLC, Waltham, Mass) circulatory support system in such patients whose neurologic status was uncertain.

Thus, for our 12 study patients, long-term survival was 75% at 1 month and 62.5% at 1 year.

By using this strategy, we avoided the urgent placement of expensive long-term ventricular assist devices in hemodynamically unstable patients with multisystem organ failure whose neurologic status was uncertain until end-organ recovery and excellent hemodynamic stability were achieved with the relatively inexpensive short-term CentriMag circulatory support system.

[MeSH-minor] Acute Disease. Analysis of Variance. Decision Making. Heart Transplantation / statistics & numerical data. Humans. Male. Middle Aged. Survival Analysis. Treatment Outcome

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[CommentIn] J Thorac Cardiovasc Surg. 2008 Mar;135(3):717; author reply 717-8 [18329513.001]

(PMID = 17662772.001).

[ISSN] 1097-685X

[Journal-full-title] The Journal of thoracic and cardiovascular surgery

[ISO-abbreviation] J. Thorac. Cardiovasc. Surg.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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Population pharmacokinetic and pharmacodynamic modeling was performed using NONMEM V (GloboMax LLC, Hanover, MD).

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(PMID = 17122576.001).

[ISSN] 0003-3022

[Journal-full-title] Anesthesiology

[ISO-abbreviation] Anesthesiology

[Language] eng

[Publication-type] Journal Article; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / Hypnotics and Sedatives; R60L0SM5BC / Midazolam

   

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[Title] Thalidomide-induced partial stable remission in a case of refractory progressive B Cell Chronic Lymphoid Leukemia.

[MeSH-major] Leukemia, B-Cell / drug therapy. Thalidomide / therapeutic use

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(PMID = 17544506.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Case Reports; Letter

[Publication-country] England

[Chemical-registry-number] 4Z8R6ORS6L / Thalidomide

   

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Topics include bendamustine (Treanda) for chronic lymphocytic leukemia, hepatitis B immune globulin (HepaGam B) to prevent hepatitis B infection following liver transplantation, and a fibrin sealant (Artiss) used in skin graft surgery for burn patients.

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(PMID = 19561795.001).

[ISSN] 1052-1372

[Journal-full-title] P & T : a peer-reviewed journal for formulary management

[ISO-abbreviation] P T

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Other-IDs] NLM/ PMC2683604

   

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[Title] Management of infectious complications in patients with chronic lymphocytic leukemia.

Infections remain a major cause of morbidity and mortality in patients with chronic lymphocytic leukemia (CLL).

The pathogenesis of these complications is related to immune defects inherent to the primary disease as well as to therapy-related immunosuppression.

The spectrum of infections seen has evolved with the therapeutic use of purine analogs, which induce specific cellular immune defects, as well as the monoclonal antibodies alemtuzumab and rituximab.

This overview will summarize the pathogenesis of infection in patients with CLL as well as the spectrum of infection and approaches to the prophylactic and therapeutic management of these complications.

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(PMID = 18024648.001).

[ISSN] 1520-4391

[Journal-full-title] Hematology. American Society of Hematology. Education Program

[ISO-abbreviation] Hematology Am Soc Hematol Educ Program

[Language] ENG

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 63

   

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[Title] Sequential therapy with fludarabine, high-dose cyclophosphamide, and rituximab in previously untreated patients with chronic lymphocytic leukemia produces high-quality responses: molecular remissions predict for durable complete responses.

PURPOSE: Modern combination strategies are active in chronic lymphocytic leukemia (CLL) but can have significant myelosuppression and immunosuppression that may require dose attenuation for safety.

In that study, cyclophosphamide consolidation improved the frequency of complete response (CR) four-fold.

PATIENTS AND METHODS: Thirty-six previously untreated CLL patients received therapy with fludarabine 25 mg/m(2) on days 1 through 5 every 4 weeks for six cycles, followed by consolidation with cyclophosphamide 3,000 mg/m(2) administered every 3 weeks for three cycles, followed by consolidation with weekly rituximab 375 mg/m(2) for four cycles.

Evaluation for minimal residual disease included flow cytometry and a highly sensitive clonotypic polymerase chain reaction (PCR).

The median age was 59 years (range, 37 to 71 years), 61% of patients had high-risk disease, and 58% had unmutated IgV(H) genes.

Twenty patients (56%) achieved flow cytometric CRs, and 12 patients (33%) achieved a molecular CR (PCR negative).

Patients achieving molecular CRs had an excellent prognosis with a plateau in the response duration curve, and 90% remain in clinical CR at 5 years.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy

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[Cites] Leukemia. 2000 Sep;14(9):1577-82 [10995003.001]

[Cites] N Engl J Med. 2000 Dec 14;343(24):1750-7 [11114313.001]

[Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]

[Cites] J Clin Oncol. 2001 Mar 1;19(5):1414-20 [11230486.001]

[Cites] Blood. 2001 Apr 1;97(7):1929-36 [11264154.001]

[Cites] Blood. 2001 Oct 15;98(8):2319-25 [11588025.001]

[Cites] Blood. 2003 Jan 1;101(1):6-14 [12393429.001]

[Cites] Diagn Immunol. 1985;3(3):133-8 [3931957.001]

[Cites] Leukemia. 1993 Mar;7(3):361-5 [7680398.001]

[Cites] Blood. 1993 Sep 15;82(6):1695-700 [8400226.001]

[Cites] Leukemia. 1994 Aug;8(8):1290-3 [8057664.001]

[Cites] Lancet. 1996 May 25;347(9013):1432-8 [8676625.001]

[Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]

[Cites] Blood. 2005 Jan 1;105(1):49-53 [15138165.001]

[Cites] J Clin Oncol. 2005 Jun 20;23(18):4079-88 [15767648.001]

[Cites] Blood. 2006 Jan 15;107(2):742-51 [16179374.001]

[Cites] Blood. 2006 Feb 1;107(3):885-91 [16219797.001]

[Cites] J Clin Oncol. 2006 Apr 1;24(10):1575-81 [16520464.001]

[Cites] J Clin Oncol. 2007 Mar 1;25(7):793-8 [17283364.001]

[Cites] Lancet. 2007 Jul 21;370(9583):230-9 [17658394.001]

[CommentIn] J Clin Oncol. 2009 Feb 1;27(4):479-80 [19075263.001]

(PMID = 19075280.001).

[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

[Grant] United States / NCI NIH HHS / CA / P30 CA008748; United States / NIAID NIH HHS / AI / R01 AI067823; United States / NCI NIH HHS / CA / R01 CA67823

[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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine

[Other-IDs] NLM/ PMC2645858

   

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[Title] Genomic complexity identifies patients with aggressive chronic lymphocytic leukemia.

Chronic lymphocytic leukemia (CLL) has a variable clinical course.

Presence of specific genomic aberrations has been shown to impact survival outcomes and can help categorize CLL into clinically distinct subtypes.

We studied 178 CLL patients enrolled in a prospective study at the University of Michigan, of whom 139 and 39 were previously untreated and previously treated, respectively.

Genomic complexity scores were derived and correlated with the surrogate clinical end points time to first therapy (TTFT) and time to subsequent therapy (TTST): measures of disease aggressiveness and/or therapy efficaciousness.

In univariate analysis, progressively increasing complexity scores in previously untreated CLL patients identified patients with short TTFT at high significance levels.

Similarly, TTST was significantly shorter in pretreated patients with high as opposed to low genomic complexity.

Finally, algorithmic subchromosomal complexity determination was developed, facilitating automation and future routine clinical application of CLL whole-genome analysis.

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[Cites] Blood. 1975 Aug;46(2):219-34 [1139039.001]

[Cites] Cancer. 1981 Jul 1;48(1):198-206 [7237385.001]

[Cites] Science. 1989 Apr 14;244(4901):207-11 [2565047.001]

[Cites] N Engl J Med. 1990 Sep 13;323(11):720-4 [2201915.001]

[Cites] Blood. 1994 Nov 1;84(9):3148-57 [7949187.001]

[Cites] Blood. 1995 Mar 15;85(6):1580-9 [7888675.001]

[Cites] Blood. 1996 Jun 15;87(12):4990-7 [8652811.001]

[Cites] Blood. 1998 Jun 1;91(11):4342-9 [9596683.001]

[Cites] Blood. 1998 Oct 1;92(7):2322-33 [9746770.001]

[Cites] Blood. 1999 Sep 15;94(6):1840-7 [10477712.001]

[Cites] Blood. 1999 Sep 15;94(6):1848-54 [10477713.001]

[Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]

[Cites] Bioinformatics. 2005 May 1;21(9):1958-63 [15657097.001]

[Cites] J Clin Oncol. 2005 May 20;23(15):3433-8 [15809449.001]

[Cites] Cancer Res. 2005 Jul 15;65(14):6071-9 [16024607.001]

[Cites] Blood. 2005 Nov 1;106(9):3175-82 [16014569.001]

[Cites] Blood. 2005 Dec 15;106(13):4389-96 [16131571.001]

[Cites] Annu Rev Genet. 2006;40:363-83 [16895466.001]

[Cites] Blood. 2007 Jan 15;109(2):399-404 [17003373.001]

[Cites] Blood. 2007 Feb 1;109(3):1202-10 [17053054.001]

[Cites] J Clin Oncol. 2007 Mar 1;25(7):799-804 [17283363.001]

[Cites] Leukemia. 2007 Aug;21(8):1715-22 [17541398.001]

[Cites] Clin Cancer Res. 2007 Aug 15;13(16):4777-85 [17699855.001]

[Cites] Leukemia. 2007 Dec;21(12):2442-51 [17805327.001]

[Cites] J Clin Oncol. 2007 Dec 1;25(34):5448-57 [17968022.001]

[Cites] Blood. 2008 Feb 1;111(3):1584-93 [17971485.001]

[Cites] Blood. 2006 Jan 15;107(2):742-51 [16179374.001]

[Cites] Blood. 2006 Jul 15;108(2):638-44 [16574953.001]

[Cites] Blood. 2006 Aug 1;108(3):853-61 [16601244.001]

[Cites] Nat Genet. 2006 Sep;38(9):1043-8 [16921376.001]

[Cites] J Clin Oncol. 2006 Oct 1;24(28):4634-41 [17008705.001]

[Cites] Blood. 2006 Nov 1;108(9):3152-60 [16840733.001]

[Cites] Blood. 2003 Jun 15;101(12):4944-51 [12595313.001]

[Cites] Lancet. 2004 Jan 10;363(9403):105-11 [14726163.001]

[Cites] Curr Opin Genet Dev. 2004 Feb;14(1):11-6 [15108799.001]

[Cites] Cancer Res. 2004 May 1;64(9):3060-71 [15126342.001]

[Cites] Bioinformatics. 2004 May 22;20(8):1233-40 [14871870.001]

[Cites] Blood. 2004 Sep 1;104(5):1428-34 [15138159.001]

[Cites] N Engl J Med. 2004 Aug 26;351(9):893-901 [15329427.001]

[Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]

[Cites] Blood. 2001 Jul 1;98(1):181-6 [11418478.001]

[Cites] Oncogene. 2001 Sep 10;20(40):5580-94 [11607811.001]

[Cites] Blood. 2001 Nov 1;98(9):2633-9 [11675331.001]

[Cites] Blood. 2002 Feb 1;99(3):1023-9 [11807008.001]

[Cites] Leukemia. 2002 Jan;16(1):30-5 [11840260.001]

[Cites] Blood. 2002 Aug 15;100(4):1177-84 [12149195.001]

[Cites] Blood. 2002 Aug 15;100(4):1410-6 [12149225.001]

[Cites] Blood. 2002 Dec 15;100(13):4325-36 [12393746.001]

[Cites] Blood. 2003 Feb 15;101(4):1262-9 [12406914.001]

[Cites] N Engl J Med. 2003 May 1;348(18):1764-75 [12724482.001]

[CommentIn] Blood. 2008 Sep 1;112(5):1550 [18725569.001]

(PMID = 18436738.001).

[ISSN] 1528-0020

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / R21 CA124420; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / R21 CA124420-01A1

[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 / Immunoglobulin Heavy Chains; 0 / Membrane Glycoproteins; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human

[Other-IDs] NLM/ PMC2518900

   

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[Title] Pseudohyperkalemia in chronic lymphocytic leukemia.

[MeSH-major] Hyperkalemia / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / blood

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(PMID = 18509189.001).

[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] Case Reports; Journal Article

[Publication-country] United States

   

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[Title] MicroRNA patterns associated with clinical prognostic parameters and CNS relapse prediction in pediatric acute leukemia.

BACKGROUND: Recent reports have indicated that microRNAs (miRNAs) play a critical role in malignancies, and regulations in the progress of adult leukemia.

The role of miRNAs in pediatric leukemia still needs to be established.

The purpose of this study was to investigate the aberrantly expressed miRNAs in pediatric acute leukemia and demonstrate miRNA patterns that are pediatric-specific and prognostic parameter-associated.

The most highly expressed miRNAs in pediatric ALL were miR-34a, miR-128a, miR-128b, and miR-146a, while the highly expressed miRNAs in pediatric AML were miR-100, miR-125b, miR-335, miR-146a, and miR-99a, which are significantly different from those reported for adult CLL and AML. miR-125b and miR-126 may serve as favorable prognosticators for M3 and M2 patients, respectively.

CONCLUSIONS/SIGNIFICANCE: There are existing pediatric-associated and prognostic parameter-associated miRNAs that are independent of cell lineage and could provide therapeutic direction for individual risk-adapted therapy for pediatric leukemia patients.

[MeSH-major] Central Nervous System Neoplasms / diagnosis. Leukemia / diagnosis. Leukemia / pathology. MicroRNAs

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[Cites] Cell. 2003 Apr 4;113(1):25-36 [12679032.001]

[Cites] Genes Dev. 2003 Feb 15;17(4):438-42 [12600936.001]

[Cites] J Pediatr (Rio J). 2003 Mar-Apr;79(2):149-58 [14502336.001]

[Cites] Genes Chromosomes Cancer. 2004 Feb;39(2):167-9 [14695998.001]

[Cites] Cell. 2004 Jan 23;116(2):281-97 [14744438.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2999-3004 [14973191.001]

[Cites] Genes Dev. 2004 Mar 1;18(5):504-11 [15014042.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11755-60 [15284443.001]

[Cites] N Engl J Med. 2004 Aug 26;351(9):893-901 [15329427.001]

[Cites] Nature. 2005 Feb 17;433(7027):769-73 [15685193.001]

[Cites] N Engl J Med. 2005 Feb 24;352(8):804-15 [15728813.001]

[Cites] Nature. 2005 Mar 17;434(7031):338-45 [15735639.001]

[Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13944-9 [16166262.001]

[Cites] N Engl J Med. 2005 Oct 27;353(17):1768-71 [16251533.001]

[Cites] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535.001]

[Cites] Nucleic Acids Res. 2005;33(20):e179 [16314309.001]

[Cites] Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279.001]

[Cites] Semin Oncol. 2006 Apr;33(2):167-73 [16616063.001]

[Cites] Cancer Res. 2006 Aug 1;66(15):7390-4 [16885332.001]

[Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19971-6 [18056805.001]

[Cites] Blood. 2008 Mar 1;111(5):2825-32 [18089852.001]

[Cites] Blood. 2008 Mar 15;111(6):3183-9 [18187662.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3945-50 [18308931.001]

[Cites] Blood. 2008 May 15;111(10):5078-85 [18337557.001]

[Cites] Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15535-40 [18832181.001]

[Cites] J Exp Med. 2008 Oct 27;205(11):2499-506 [18936236.001]

[Cites] J Clin Oncol. 2008 Nov 1;26(31):5078-87 [18809607.001]

[Cites] Leukemia. 2009 Feb;23(2):313-22 [18923441.001]

[Cites] Dev Biol. 1999 Dec 15;216(2):671-80 [10642801.001]

[Cites] N Engl J Med. 2000 Dec 28;343(26):1910-6 [11136261.001]

[Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Nov 26;99(24):15524-9 [12434020.001]

[Cites] J Clin Oncol. 2003 Jan 15;21(2):179-81 [12525506.001]

[Cites] N Engl J Med. 2003 May 1;348(18):1764-75 [12724482.001]

(PMID = 19915715.001).

[ISSN] 1932-6203

[Journal-full-title] PloS one

[ISO-abbreviation] PLoS ONE

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / MicroRNAs

[Other-IDs] NLM/ PMC2773830

   

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8-Chloroadenosine (8-Cl-Ado) is a ribosyl nucleoside analog currently in phase I testing for the treatment of chronic lymphocytic leukemia (CLL).

In the current study with four mantle cell lymphoma cell lines, we report a new major metabolic pathway for 8-Cl-Ado intracellular metabolism, the formation of succinyl-8-chloro-adenosine (S-8-Cl-Ado) and its monophosphate (S-8-Cl-AMP).

Consistent with fumarate as a required substrate for formation of succinyl-8-Cl-adenylate metabolites, the S-8-Cl-adenylate concentrations in multiple cell lines were associated with fumarate loss.

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[Cites] J Biol Chem. 2000 Jan 7;275(1):223-8 [10617608.001]

[Cites] Breast Cancer Res Treat. 2010 Jun;121(2):355-64 [19641990.001]

[Cites] J Chromatogr B Biomed Sci Appl. 2000 Aug 18;745(2):421-30 [11043760.001]

[Cites] Cancer Res. 2001 Jul 15;61(14):5474-9 [11454694.001]

[Cites] Nat Genet. 2002 Apr;30(4):406-10 [11865300.001]

[Cites] Cancer Chemother Pharmacol. 2002 Aug;50(2):85-94 [12172971.001]

[Cites] Cancer Res. 2003 Nov 15;63(22):7968-74 [14633728.001]

[Cites] J Biol Chem. 2004 Sep 24;279(39):40405-11 [15265873.001]

[Cites] Clin Chim Acta. 1985 Jun 14;148(3):185-96 [4042353.001]

[Cites] Anal Biochem. 1991 Mar 2;193(2):287-91 [1872474.001]

[Cites] J Inherit Metab Dis. 1997 Jun;20(2):193-202 [9211192.001]

[Cites] J Biol Chem. 1956 Sep;222(1):17-30 [13366975.001]

[Cites] Mol Cancer Ther. 2004 Nov;3(11):1411-20 [15542780.001]

[Cites] Mol Cancer Ther. 2005 Apr;4(4):569-77 [15827330.001]

[Cites] Blood. 2005 Jun 1;105(11):4455-62 [15718423.001]

[Cites] Cancer Cell. 2005 Aug;8(2):143-53 [16098467.001]

[Cites] Oncogene. 2006 Aug 7;25(34):4675-82 [16892081.001]

[Cites] J Clin Endocrinol Metab. 2006 Aug;91(8):3071-5 [16757530.001]

[Cites] J Biol Chem. 2007 Feb 16;282(7):4524-32 [17182618.001]

[Cites] Cancer Res. 2007 Oct 15;67(20):9913-20 [17942923.001]

[Cites] Mol Cell Proteomics. 2009 Jan;8(1):70-85 [18723843.001]

[Cites] Mol Cancer Ther. 2009 Mar;8(3):626-35 [19276158.001]

[Cites] Diabetes Obes Metab. 2009 May;11 Suppl 2:3-8 [19385978.001]

[Cites] Science. 2009 May 22;324(5930):1029-33 [19460998.001]

[Cites] J Clin Oncol. 2009 Jul 10;27(20):3297-302 [19487376.001]

[Cites] Mol Cell Biol. 2009 Aug;29(15):4080-90 [19470762.001]

[Cites] Biochem Pharmacol. 2009 Sep 15;78(6):583-91 [19477165.001]

[Cites] Br J Haematol. 2009 Nov;147(3):297-307 [19709085.001]

[Cites] J Inherit Metab Dis. 2000 Jun;23(4):371-4 [10896297.001]

(PMID = 20064937.001).

[ISSN] 1083-351X

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / R01 CA085915; United States / NCI NIH HHS / CA / CA 85915; United States / NCI NIH HHS / CA / CA136411; United States / NCI NIH HHS / CA / P50 CA136411

[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 / Antineoplastic Agents; 0 / Fumarates; 0 / Hypoglycemic Agents; 0 / Oligomycins; 0 / Purines; 0 / Uncoupling Agents; 146-77-0 / 2-Chloroadenosine; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 34408-14-5 / 8-chloroadenosine; 41941-56-4 / 8-chloro-cyclic adenosine monophosphate; 9100L32L2N / Metformin; AB6MNQ6J6L / Succinic Acid

[Other-IDs] NLM/ PMC2832953

   

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When titanocenes 3a-c were tested against pig kidney (LLC-PK) cells inhibitory concentrations (IC(50)) of 1.6x10(-4)M, 1.5x10(-4)M and 9.1x10(-4)M, respectively, were observed.

These values represent improved cytotoxicity against LLC-PK, when compared to their corresponding ansa substituted analogues and also in comparison to unsubstituted titanocene dichloride.

[MeSH-minor] Animals. Cell Line. Cell Survival. Drug Evaluation, Preclinical. Molecular Conformation. Molecular Structure. Swine

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(PMID = 16764931.001).

[ISSN] 0162-0134

[Journal-full-title] Journal of inorganic biochemistry

[ISO-abbreviation] J. Inorg. Biochem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organometallic Compounds; 1271-29-0 / titanocene

   

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[Title] Protein expression profiling of cytokines and cytokine receptors on purified chronic lymphocytic leukemia cells from patients with favourable prognostic indicators.

Chronic lymphocytic leukemia (CLL) cells rapidly undergo apoptosis when cultured in vitro, which contrasts with their prolonged survival in vivo.

Multiple cytokines and cytokine receptors are believed to work together to regulate the survival of CLL cells.

The aim of the current study was to measure the endogenous expression and secretion of cytokines and cytokine receptors in CLL cells when exogenous cytokines are minimized.

We demonstrated that the intracellular and secreted levels of 174 cytokines and cytokine receptors of purified CLL B-cells were not significantly different from those of normal B-cells except for the secreted levels of IL-6 and eotaxin.

IL-6 was 3.0 times lower (p = 0.038) whereas eotaxin was 2.2 times higher (p = 0.027) in CLL conditioned medium than in normal B-cell conditioned medium.

Our results suggest that, except for IL-6 and eotaxin, CLL B-cells and their normal counterparts produce and secrete similar amounts of cytokines and cytokine receptors in vitro.

[MeSH-major] Cytokines / analysis. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Receptors, Cytokine / analysis

[MeSH-minor] Adult. Aged. B-Lymphocytes / secretion. Case-Control Studies. Cells, Cultured. Chemokine CCL11 / analysis. Chemokine CCL11 / secretion. Female. Humans. Interleukin-6 / analysis. Interleukin-6 / secretion. Male. Middle Aged. Prognosis. Proteomics / methods

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(PMID = 18398743.001).

[ISSN] 1029-2403

[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 / CCL11 protein, human; 0 / Chemokine CCL11; 0 / Cytokines; 0 / Interleukin-6; 0 / Receptors, Cytokine

   

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[Title] Alemtuzumab therapy for severe autoimmune hemolysis in a patient with B-cell chronic lymphocytic leukemia.

B-cell chronic lymphocytic leukemia (B-CLL) is the most common cause of autoimmune hemolytic anemia (AIHA), and a subgroup of these patients who develop both these conditions fail to respond to corticosteroids, cytotoxic drugs, splenectomy, and iv immunoglobulins.

Alemtuzumab is a humanized anti-CD52 monoclonal antibody that is an effective therapy for B-CLL, mycosis fungoides, and T-cell prolymphocytic leukemia.

Here we present a case report of a 78-yr-old woman with B-CLL and progressive life-threatening AIHA with hemoglobin count 5.5 g/dL following fludarabine treatment, who was treated successfully with alemtuzumab.

We conclude that alemtuzumab may be indicated for the treatment of AIHA in B-CLL patients who have failed other treatments.

[MeSH-major] Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / complications

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[Cites] J Clin Oncol. 1998 May;16(5):1885-9 [9586905.001]

[Cites] Br J Haematol. 1986 Nov;64(3):479-86 [3539172.001]

[Cites] Blood. 1993 Aug 1;82(3):807-12 [7687895.001]

[Cites] Br J Haematol. 1996 Apr;93(1):151-3 [8611450.001]

[Cites] Blood. 1996 May 1;87(9):3869-76 [8611714.001]

[Cites] Eur J Haematol. 2003 May;70(5):319-21 [12694169.001]

[Cites] Hematol Cell Ther. 1997 Nov;39 Suppl 1:S41-4 [9471060.001]

[Cites] Semin Hematol. 1992 Jan;29(1):64-74 [1570545.001]

[Cites] Mol Hum Reprod. 1996 Mar;2(3):177-84 [9238677.001]

[Cites] J Clin Oncol. 2002 Sep 15;20(18):3891-7 [12228210.001]

[Cites] Blood. 2002 Aug 1;100(3):768-73 [12130484.001]

[Cites] Leuk Lymphoma. 2002 May;43(5):1007-11 [12148879.001]

[Cites] Br J Haematol. 2001 Sep;114(4):891-8 [11564082.001]

[Cites] Blood. 1989 May 1;73(6):1431-9 [2713487.001]

[Cites] Br J Haematol. 2003 Oct;123(2):278-81 [14531909.001]

[Cites] Blood. 2000 May 1;95(9):2786-92 [10779422.001]

[Cites] J Biol Chem. 1995 Mar 17;270(11):6088-99 [7890742.001]

[Cites] Immunology. 1998 Nov;95(3):427-36 [9824507.001]

[Cites] Semin Oncol. 1998 Feb;25(1):80-97 [9482530.001]

[Cites] Semin Oncol. 1998 Feb;25(1):34-41 [9482525.001]

[Cites] Leuk Lymphoma. 2002 Sep;43(9):1755-62 [12685828.001]

[Cites] Nature. 1988 Mar 24;332(6162):323-7 [3127726.001]

[Cites] Semin Hematol. 1992 Jan;29(1):3-12 [1570541.001]

[Cites] J Clin Oncol. 1997 Apr;15(4):1567-74 [9193354.001]

[Cites] Ann Oncol. 1992 Feb;3(2):171-2 [1606091.001]

(PMID = 16645240.001).

[ISSN] 1357-0560

[Journal-full-title] Medical oncology (Northwood, London, England)

[ISO-abbreviation] Med. Oncol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab

   

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[Title] Allogeneic dendritic cells pulsed with tumor lysates or apoptotic bodies as immunotherapy for patients with early-stage B-cell chronic lymphocytic leukemia.

Recently, immunotherapies with allogeneic dendritic cells (DCs) pulsed with tumor antigens to generate specific T-cell responses have been tested in clinical trials for patients with solid tumors.

This is the first report on a clinical vaccination study with DCs for patients with B-cell chronic lymphocytic leukemia (B-CLL).

The potential of allogeneic DCs pulsed ex vivo with tumor cell lysates or apoptotic bodies to stimulate antitumor immunity in patients with B-CLL in early stages was evaluated.

In one patient, a significant increase of specific cytotoxic T lymphocytes against RHAMM/CD168, a recently characterized leukemia-associated antigen, could be detected after DC vaccination.

Taken together, the study demonstrated that DC vaccination in CLL patients is feasible and safe.

[MeSH-major] Apoptosis / immunology. Cancer Vaccines / therapeutic use. Dendritic Cells / immunology. Immunotherapy / methods. Leukemia, Lymphocytic, Chronic, B-Cell / therapy. Neoplasm Proteins / immunology

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(PMID = 15990861.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD44; 0 / Cancer Vaccines; 0 / Extracellular Matrix Proteins; 0 / Neoplasm Proteins; 0 / hyaluronan-mediated motility receptor

   

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[Title] The anti-apoptotic, glucocorticoid receptor cochaperone protein BAG-1 is a long-term target for the actions of mood stabilizers.

Increasing data suggest that impairments of cellular plasticity/resilience underlie the pathophysiology of bipolar disorder.

A series of microarray studies with validating criteria have recently revealed a common, novel target for the long-term actions of the structurally highly dissimilar mood stabilizers lithium and valproate: BAG-1 [BCL-2 (B-cell CLL/lymphoma 2)-associated athanogene].

Chronic administration of both agents at therapeutic doses increased the expression of BAG-1 in rat hippocampus.

Furthermore, these findings were validated at the protein level, and the effects were seen in a time frame consistent with therapeutic effects and were specific for mood stabilizers.

Furthermore, small interfering RNA studies showed that these inhibitory effects on GR activity were mediated, at least in part, through BAG-1.

The observation that BAG-1 inhibits glucocorticoid activation suggests that mood stabilizers may counteract the deleterious effects of hypercortisolemia seen in bipolar disorder by upregulating BAG-1.

Additionally, these studies suggest that regulation of GR-mediated plasticity may play a role in the treatment of bipolar disorder and raise the possibility that agents affecting BAG-1 more directly may represent novel therapies for this devastating illness.

[MeSH-minor] Alkaline Phosphatase / genetics. Alkaline Phosphatase / metabolism. Animals. Behavior, Animal. Blotting, Western / methods. Cell Line, Tumor. Dexamethasone / pharmacology. Dose-Response Relationship, Drug. Drug Interactions. Gene Expression / drug effects. Humans. Immunohistochemistry / methods. Indoles / metabolism. Male. Molecular Weight. Neuroblastoma. RNA, Small Interfering / pharmacology. Rats. Rats, Wistar. Receptors, Glucocorticoid / metabolism. Time Factors. Transfection / methods

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(PMID = 15872096.001).

[ISSN] 1529-2401

[Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience

[ISO-abbreviation] J. Neurosci.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Antimanic Agents; 0 / BCL2-associated athanogene 1 protein; 0 / DNA-Binding Proteins; 0 / Indoles; 0 / RNA, Small Interfering; 0 / Receptors, Glucocorticoid; 0 / Transcription Factors; 47165-04-8 / DAPI; 614OI1Z5WI / Valproic Acid; 7S5I7G3JQL / Dexamethasone; 9FN79X2M3F / Lithium; EC 3.1.3.1 / Alkaline Phosphatase

   

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[Title] A fluorimetry-based ssYFP secretion assay to monitor vasopressin-induced exocytosis in LLC-PK1 cells expressing aquaporin-2.

Vasopressin (VP)-induced exocytosis was dissected in native and aquaporin-2 (AQP2)-expressing renal LLC-PK(1) cells by a fluorimetric exocytosis assay based on soluble secreted yellow fluorescent protein (ssYFP).

Fluorimetry and Western blot analysis demonstrated similar constitutive ssYFP secretion in native LLC-PK(1) and AQP2-expressing cells.

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[Cites] Am J Physiol Renal Physiol. 2005 Jun;288(6):F1103-12 [15644488.001]

[Cites] J Biol Chem. 2008 Sep 26;283(39):26643-61 [18664568.001]

[Cites] Mol Cell Proteomics. 2005 Aug;4(8):1095-106 [15905145.001]

[Cites] Histochem Cell Biol. 2005 Jul;124(1):1-12 [16049696.001]

[Cites] J Am Soc Nephrol. 2005 Oct;16(10):2881-9 [16093449.001]

[Cites] J Cell Biol. 2005 Sep 26;170(7):1113-25 [16186257.001]

[Cites] Traffic. 2005 Dec;6(12):1142-56 [16262725.001]

[Cites] Nephrol Dial Transplant. 2000;15 Suppl 6:21-2 [11143977.001]

[Cites] Am J Physiol Renal Physiol. 2001 Dec;281(6):F1092-101 [11704560.001]

[Cites] Physiol Rev. 2002 Jan;82(1):205-44 [11773613.001]

[Cites] J Biol Chem. 2002 Mar 22;277(12):10379-86 [11782489.001]

[Cites] Am J Physiol Renal Physiol. 2002 Jun;282(6):F998-1011 [11997316.001]

[Cites] J Biol Chem. 2003 Jan 10;278(2):1101-7 [12374804.001]

[Cites] EMBO Rep. 2003 Jan;4(1):88-93 [12524527.001]

[Cites] Am J Physiol Renal Physiol. 2003 May;284(5):F893-901 [12676734.001]

[Cites] Am J Physiol Cell Physiol. 2003 Oct;285(4):C750-62 [12801889.001]

[Cites] Am J Physiol Renal Physiol. 2004 Feb;286(2):F233-43 [14519593.001]

[Cites] Nat Rev Mol Cell Biol. 2004 Feb;5(2):121-32 [15040445.001]

[Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13368-73 [15326289.001]

[Cites] Mol Cell Biol. 1985 Dec;5(12):3610-6 [3915782.001]

[Cites] Am J Physiol. 1993 Aug;265(2 Pt 2):F214-24 [8396343.001]

[Cites] Experientia. 1994 Nov 30;50(11-12):1012-20 [7988659.001]

[Cites] Proc Natl Acad Sci U S A. 1995 Aug 1;92(16):7212-6 [7543677.001]

[Cites] EMBO J. 1996 Feb 1;15(3):510-9 [8599934.001]

[Cites] J Biol Chem. 1997 Jun 6;272(23):14800-4 [9169447.001]

[Cites] Am J Physiol. 1997 Jun;272(6 Pt 2):F817-22 [9227644.001]

[Cites] Am J Physiol Renal Physiol. 2000 Feb;278(2):F317-26 [10662736.001]

[Cites] Am J Physiol Renal Physiol. 2000 Mar;278(3):F388-94 [10710543.001]

[Cites] Am J Physiol Renal Physiol. 2000 Jan;278(1):F29-42 [10644653.001]

[Cites] J Cell Sci. 2000 Jun;113 ( Pt 11):1985-92 [10806109.001]

[Cites] J Clin Invest. 2000 Nov;106(9):1115-26 [11067864.001]

[Cites] J Biol Chem. 2000 Nov 24;275(47):36839-46 [10973964.001]

[Cites] Plant Cell Physiol. 2000 Sep;41(9):993-1001 [11100771.001]

[Cites] Nature. 1997 Sep 4;389(6646):81-5 [9288971.001]

[Cites] Eur J Cell Biol. 1997 Oct;74(2):133-42 [9352218.001]

[Cites] Curr Opin Neurobiol. 1997 Oct;7(5):631-9 [9384543.001]

[Cites] J Membr Biol. 1998 Jan 15;161(2):141-9 [9435270.001]

[Cites] Biochem J. 1998 Apr 15;331 ( Pt 2):669-75 [9531511.001]

[Cites] J Cell Biol. 1998 Dec 14;143(6):1485-503 [9852146.001]

[Cites] J Am Soc Nephrol. 1999 Jul;10(7):1416-29 [10405197.001]

[Cites] J Biol Chem. 2004 Nov 5;279(45):46969-80 [15319442.001]

[Cites] Am J Physiol Renal Physiol. 2005 May;288(5):F930-8 [15625084.001]

[Cites] Endocrinology. 2005 Dec;146(12):5063-70 [16150901.001]

[Cites] Am J Physiol Renal Physiol. 2006 Jan;290(1):F177-87 [15985652.001]

[Cites] Biol Cell. 2006 Apr;98(4):215-32 [16563128.001]

[Cites] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7159-64 [16641100.001]

[Cites] Am J Physiol Endocrinol Metab. 2006 Jun;290(6):E1276-86 [16418206.001]

[Cites] Am J Physiol Renal Physiol. 2006 Jul;291(1):F246-53 [16449354.001]

[Cites] Am J Physiol Renal Physiol. 2006 Oct;291(4):F882-90 [16684923.001]

[Cites] Annu Rev Cell Dev Biol. 2006;22:439-55 [16824007.001]

[Cites] Traffic. 2007 Feb;8(2):110-23 [17156409.001]

[Cites] PLoS Comput Biol. 2007 Mar 23;3(3):e57 [17381238.001]

[Cites] Nat Rev Genet. 2007 Jul;8(7):533-43 [17572691.001]

[Cites] Am J Physiol Cell Physiol. 2007 Sep;293(3):C1129-38 [17626240.001]

[Cites] J Biol Chem. 2007 Sep 28;282(39):28721-32 [17636261.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16696-701 [17940053.001]

[Cites] Neuron. 2007 Nov 21;56(4):657-69 [18031683.001]

[Cites] Semin Nephrol. 2008 May;28(3):266-78 [18519087.001]

[Cites] Curr Opin Nephrol Hypertens. 2008 Sep;17(5):491-8 [18695390.001]

[Cites] J Cell Biol. 2008 Aug 11;182(3):587-601 [18678705.001]

[Cites] J Am Soc Nephrol. 2005 Jun;16(6):1571-82 [15843469.001]

(PMID = 18799651.001).

[ISSN] 0363-6143

[Journal-full-title] American journal of physiology. Cell physiology

[ISO-abbreviation] Am. J. Physiol., Cell Physiol.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / DK-38452; United States / NIDDK NIH HHS / DK / DK-43341; United States / NIDDK NIH HHS / DK / DK-57521; United States / NIDDK NIH HHS / DK / K08 DK-075940-01

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Aquaporin 2; 0 / Luminescent Proteins; 11000-17-2 / Vasopressins

[Other-IDs] NLM/ PMC2603565

   

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[Title] Alemtuzumab as consolidation after a response to fludarabine is effective in purging residual disease in patients with chronic lymphocytic leukemia.

PURPOSE: Treatment with alemtuzumab has resulted in negative responses for minimal residual disease (MRD) in patients with chronic lymphocytic leukemia (CLL).

In a prior analysis we demonstrated that it is possible to achieved MRD negativity, as assessed by polyclonality of immunoglobulin heavy chain after consolidation with alemtuzumab.

This phase II study evaluated 34 patients with CLL who received alemtuzumab consolidation in an effort to improve the quality of their response to fludarabine-based induction.

Subsequent peripheral blood stem-cell (PBSC) collection and transplantation, tolerability, and pharmacokinetics also were assessed.

CONCLUSION: Subcutaneously administered alemtuzumab was effective, safe, and well tolerated as consolidation therapy in patients with CLL who responded to fludarabine induction therapy.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Peripheral Blood Stem Cell Transplantation

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(PMID = 16618945.001).

[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] Clinical Trial, Phase II; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Antiviral Agents; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine; P9G3CKZ4P5 / Ganciclovir

   

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[Title] Immune anaemias in patients with chronic lymphocytic leukaemia treated with fludarabine, cyclophosphamide and rituximab--incidence and predictors.

Immune anaemias (IA) [auto-immune haemolytic anaemia (AIHA) and pure red cell aplasia (PRCA)] are complications of chronic lymphocytic leukaemia (CLL).

Additional markers of haemolysis (indirect hyperbilirubinaemia, reticulocytosis, low haptoglobin and elevated lactate dehydrogenase levels) confirmed the presence of AIHA in these patients.

Thus, the incidence of IA among CLL patients treated with FCR was comparable with historical rates.

The diagnosis of AIHA can be considered even if the DAT is negative.

[MeSH-major] Anemia, Hemolytic, Autoimmune / etiology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Red-Cell Aplasia, Pure / etiology

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[CommentIn] Br J Haematol. 2007 Nov;139(4):622-3 [17979948.001]

(PMID = 17341265.001).

[ISSN] 0007-1048

[Journal-full-title] British journal of haematology

[ISO-abbreviation] Br. J. Haematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Glucocorticoids; 4F4X42SYQ6 / Rituximab; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine

   

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STI571 is used mostly in the treatment of chronic myeloid leukemia and inhibits activity of the BCR/ABL oncogenic tyrosine kinase, which is a hallmark of this disease.

NER activity was examined in the BCR/ABL-expressing cell lines K562 and BV173 of myeloid and lymphoid origin, respectively, as well as in CCRF-CEM cells, which do not express BCR/ABL.

A murine myeloid parental 32D cell line and its counterpart transfected with the BCR/ABL gene were also tested.

NER activity was assessed in the cell extracts by use of an UV-irradiated plasmid as a substrate and by a modified single-cell gel electrophoresis (comet) assay on UV-treated nucleoids.

Therefore, STI571 may overcome the drug resistance associated with increased DNA repair in BCR/ABL-positive leukemias.

[MeSH-major] DNA Repair. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Piperazines / pharmacology. Pyrimidines / pharmacology

[MeSH-minor] Animals. Benzamides. Cell Line, Tumor. Cell Survival / drug effects. Cell Survival / radiation effects. Comet Assay. Humans. Imatinib Mesylate. Mice. Polymerase Chain Reaction

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(PMID = 18602021.001).

[ISSN] 0027-5107

[Journal-full-title] Mutation research

[ISO-abbreviation] Mutat. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate

   

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[Title] PRAME mRNA levels in cases with chronic leukemia: Clinical importance and review of the literature.

The aim of this study is to determine the frequency and the clinical importance of PRAME expression in chronic myeloid leukemia (CML)/chronic myeloproliferative disorders (CMPD) and chronic lymphocytic leukemia (CLL).

PRAME mRNA was measured by real time RT-PCR in 88 cases with chronic leukemia (CL) and 42 controls.

Seventy cases had CML/CMPD (56 had chronic phase (CP)-14 had accelerated/blastic phase disease (AP/BP) and 18 cases had CLL (11 had early stage (Rai 0-I-II) and 7 had late stage (Rai III-IV).

Twenty-four of 70 (34%) cases with CML/CMPD and 5 of 18 (28%) cases with CLL showed PRAME expression.

PRAME (+) and PRAME (-) cases were not different for age, Hb, Hct, WBC count, platelet count, stage of the disease and response to therapy.

PRAME was monitorised in eight cases during follow-up: in three cases PRAME was negative at CP and expression developed at the AP/BP disease.

PRAME mRNA may be a useful marker to detect the minimal residual disease (MRD) and to determine the response to therapy in CLs.

[MeSH-major] Antigens, Neoplasm / genetics. Biomarkers, Tumor / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics. Myeloproliferative Disorders / genetics. RNA, Messenger / genetics

[MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chronic Disease. Disease Progression. Female. Follow-Up Studies. Gene Expression Profiling. Humans. Male. Middle Aged. Neoplasm Staging. Reverse Transcriptase Polymerase Chain Reaction / methods. Treatment Outcome

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(PMID = 16914202.001).

[ISSN] 0145-2126

[Journal-full-title] Leukemia research

[ISO-abbreviation] Leuk. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / PRAME protein, human; 0 / RNA, Messenger

   

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Epolactaene, a neuritogenic compound in human neuroblastoma SH-SY5Y, induces apoptosis in a human leukemia B-cell line, BALL-1.

The alpha-acyl-alpha,beta-epoxy-gamma-lactam moiety as well as the hydrophobicity derived from the long alkyl side chain are both important for activity.

[MeSH-major] Apoptosis / drug effects. Leukemia, B-Cell / drug therapy

[MeSH-minor] Cell Line, Tumor. Cell Survival / drug effects. Drug Screening Assays, Antitumor. Epoxy Compounds / chemical synthesis. Epoxy Compounds / chemistry. Epoxy Compounds / pharmacology. Humans. Hydrolysis. Molecular Structure. Polyenes / chemical synthesis. Polyenes / chemistry. Polyenes / pharmacology. Stereoisomerism. Structure-Activity Relationship

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(PMID = 16298530.001).

[ISSN] 0968-0896

[Journal-full-title] Bioorganic & medicinal chemistry

[ISO-abbreviation] Bioorg. Med. Chem.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Epoxy Compounds; 0 / Polyenes; 0 / epolactaene

   

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[Title] Gene expression profiling of B lymphocytes and plasma cells from Waldenström's macroglobulinemia: comparison with expression patterns of the same cell counterparts from chronic lymphocytic leukemia, multiple myeloma and normal individuals.

The tumoral clone of Waldenström's macroglobulinemia (WM) shows a wide morphological heterogeneity, which ranges from B lymphocytes (BL) to plasma cells (PC).

By means of genome-wide expression profiling we have been able to identify genes exclusively deregulated in BL and PC from WM, but with a similar expression pattern in their corresponding cell counterparts from chronic lymphocytic leukemia (CLL) and multiple myeloma (MM), as well as normal individuals.

The differentially expressed genes have important functions in B-cell differentiation and oncogenesis.

Thus, two of the genes downregulated in WM-BL were IL4R, which plays a relevant role in CLL B-cell survival, and BACH2, which participates in the development of class-switched PC.

A set of four genes was able to discriminate clonal BL from WM and CLL: LEF1 (WNT/beta-catenin pathway), MARCKS, ATXN1 and FMOD.

We also found deregulation of genes involved in plasma cell differentiation such as PAX5, which was overexpressed in WM-PC, and IRF4 and BLIMP1, which were underexpressed.

In summary, these results indicate that both PC and BL from WM are genetically different from the MM and CLL cell counterpart.

[MeSH-major] B-Lymphocytes / metabolism. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Multiple Myeloma / pathology. Plasma Cells / metabolism. Waldenstrom Macroglobulinemia / pathology

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(PMID = 17252022.001).

[ISSN] 0887-6924

[Journal-full-title] Leukemia

[ISO-abbreviation] Leukemia

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Neoplasm Proteins

   

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[Title] CLLU1 expression levels predict time to initiation of therapy and overall survival in chronic lymphocytic leukemia.

OBJECTIVES: Chronic lymphocytic leukemia (CLL) is an incurable disease with a highly variable clinical course.

IgV(H) mutational status, chromosomal aberrations, CD38 expression and ZAP-70 expression are prognostic markers in CLL, however, they are not exclusively confined to this disease.

We recently identified a novel CLL-specific gene (CLL upregulated gene1, CLLU1) that is exclusively upregulated in CLL cells.

Here we describe our evaluation of the prognostic significance of CLLU1 in CLL.

METHODS: A cohort of 59 previously untreated CLL patients was studied.

RESULTS: Analyzed as a continuous, quantitative parameter CLLU1 levels significantly predicted time from diagnosis to initiation of therapy (P < or = 0.0003) Analyzed as a categorical parameter, by segregation of the patients into groups with cDNA1 or CDS expression above or below the median, the CLLU1 levels significantly predicted time from diagnosis to initiation of therapy (P = 0.001) and predicted overall survival with borderline significance (P < or = 0.05).

Patient stratification according to clinical stage, cytogenetics, IgV(H) mutational status, ZAP-70 and CD38, demonstrated significantly increased CLLU1 expression in all investigated CLL poor risk groups.

CONCLUSIONS: CLLU1 is the first identified CLL specific gene.

The CLLU1 mRNA expression level can predict time to initiation of treatment and survival in CLL patients.

[MeSH-major] Biomarkers, Tumor / biosynthesis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Neoplasm Proteins / biosynthesis

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[CommentIn] Eur J Haematol. 2006 Aug;77(2):177; author reply 178 [16856913.001]

(PMID = 16529606.001).

[ISSN] 0902-4441

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Denmark

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CLLU1 protein, human; 0 / DNA, Complementary; 0 / Immunoglobulin Heavy Chains; 0 / Immunoglobulin Variable Region; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38

   

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The objective of this study was to examine the effect of ion-pair complexation with endogenous bile salts on the transport of a quarternary ammonium organic cationic (OC) drug, berberine, across the Caco-2 and LLC-PK1 cell monolayers.

Similar results were observed for the transport of berberine across the LLC-PK1 cells.

These results suggest that an efflux transporter, probably P-gp, is involved in the Caco-2 cell transport.

The apparent partition coefficient (APC) of berberine between n-octanol and a phosphate buffer (pH 7.4) was increased by the presence of an organic anion (OA), taurodeoxycholate (TDC, a bile salt), suggesting the formation of a lipophilic ion-pair complex between an OC (berberine) and an OA (TDC).

Despite the ion-pair complexation, however, the BL-AP transport of berberine across the Caco-2 and LLC-PK1 cells was not altered by the cis-presence of bile salts or the rat bile juice.

This is consistent with the reportedly unaltered secretory transport of a quarternary ammonium compound, tributylmethylammonium (TBuMA), across the Caco-2 cell monolayers in the cis-presence of bile salts or the rat bile juice, but not with our previous report in which the secretory transport of TBuMA across the LLC-PK1 cell was increased in the cis-presence of TDC.

Therefore, the effect of ion-pair formation with the bile components or bile salts on the secretory transport of OCs appears to depend on the molecular properties of OCs (e.g., molecular weight, lipophilicity and affinity to relevant transporters) and the characteristics of cell strains (e.g., expression and contribution of responsible transporters to the transport).

[MeSH-minor] Animals. Biological Transport, Active. Caco-2 Cells. Cell Membrane / metabolism. Chemistry, Physical. Chromatography, High Pressure Liquid. Data Interpretation, Statistical. Humans. LLC-PK1 Cells. P-Glycoprotein / antagonists & inhibitors. P-Glycoprotein / metabolism. Physicochemical Phenomena. Solubility. Swine. Taurodeoxycholic Acid / chemistry

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(PMID = 18277615.001).

[ISSN] 0253-6269

[Journal-full-title] Archives of pharmacal research

[ISO-abbreviation] Arch. Pharm. Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Korea (South)

[Chemical-registry-number] 0 / Bile Acids and Salts; 0 / P-Glycoprotein; 0I8Y3P32UF / Berberine; 516-50-7 / Taurodeoxycholic Acid

   

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[Title] Development of a security vulnerability assessment process for the RAMCAP chemical sector.

The Department of Homeland Security (DHS), Directorate of Information Analysis & Infrastructure Protection (IAIP), Protective Services Division (PSD), contracted the American Society of Mechanical Engineers Innovative Technologies Institute, LLC (ASME ITI, LLC) to develop guidance on Risk Analysis and Management for Critical Asset Protection (RAMCAP).

AcuTech Consulting Group (AcuTech) has been contracted by ASME ITI, LLC, to provide assistance by facilitating the development of sector-specific guidance on vulnerability analysis and management for critical asset protection for the chemical manufacturing, petroleum refining, and liquefied natural gas (LNG) sectors.

This activity involves two key tasks for these three sectors: Development of a screening to supplement DHS understanding of the assets that are important to protect against terrorist attack and to prioritize the activities.

Development of a standard security vulnerability analysis (SVA) framework for the analysis of consequences, vulnerabilities, and threats.

This project involves the cooperative effort of numerous leading industrial companies, industry trade associations, professional societies, and security and safety consultants representative of those sectors.

Jones is the chief technology officer for ASME-ITI, LLC for RAMCAP.

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(PMID = 16920260.001).

[ISSN] 0304-3894

[Journal-full-title] Journal of hazardous materials

[ISO-abbreviation] J. Hazard. Mater.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Hazardous Substances

   

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[Title] Gene expression profile and genomic changes in disease progression of early-stage chronic lymphocytic leukemia.

The biologic mechanisms involved in the clinical progression from early stages of patients with chronic lymphocytic leukemia (CLL) are not well known.

We investigated sequential samples from 16 untreated CLL patients obtained at diagnosis in early stage and after progression before treatment.

One patient had a p16 (INK4a) homozygous deletion at diagnosis and progression, and 3 patients acquired a p53 mutation, gains of 5q21-q23 and 11pter-p14, and a gain of chromosome 12 respectively, during the progression of the disease.

Gene expression profile analysis showed a significant modulation of 58 genes with a particular downregulation of genes that are inhibitors of cell adhesion and motility.

[MeSH-major] Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genome. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / pathology

[MeSH-minor] Aged. Aged, 80 and over. Cyclin-Dependent Kinase Inhibitor p16 / metabolism. Disease Progression. Female. Genes, p53 / genetics. Humans. Male. Middle Aged. Nucleic Acid Hybridization. Oligonucleotide Array Sequence Analysis

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(PMID = 18166798.001).

[ISSN] 1592-8721

[Journal-full-title] Haematologica

[ISO-abbreviation] Haematologica

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Italy

[Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16

   

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[Title] Treatment resistance in chronic lymphocytic leukemia: the role of the p53 pathway.

The importance of studying p53 pathway defects in chronic lymphocytic leukemia (CLL) has been promoted by the demonstration of the fundamentally different clinical course of patients with 17p deletion.

The observation of resistance to chemotherapy and mutation of the remaining TP53 allele explain the clinical presentation of CLL with 17p deletion.

In addition, other principal components of the DNA damage pathway reportedly are de-regulated by mutation (ATM), deletion (ATM) or potentially more complex down-regulation (miR-34a) in CLL.

Nonetheless, challenges remain because we can only explain resistance in a proportion of the cases that are resistant to first line treatment.

[MeSH-major] Drug Resistance, Neoplasm / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Tumor Suppressor Protein p53 / genetics

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(PMID = 19347737.001).

[ISSN] 1029-2403

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Tumor Suppressor Protein p53

[Number-of-references] 12

   

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[Title] [Leukaemia cutis: clinical manifestation of chronic lymphocytic leukaemia relapse].

[Transliterated title] Leucemia cutis: expresión clínica de recaída de leucemia linfocítica crónica.

We present a 71 year old male patient with previous records of Chronic Lymphocytic Leukaemia who presented with a tumoral skin lesion.

Histological and immunohistochemical studies confirmed the Leukaemia Cutis diagnosis.

[MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Leukemic Infiltration / pathology. Skin / pathology

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(PMID = 18426096.001).

[ISSN] 0014-6722

[Journal-full-title] Revista de la Facultad de Ciencias Médicas (Córdoba, Argentina)

[ISO-abbreviation] Rev Fac Cien Med Univ Nac Cordoba

[Language] spa

[Publication-type] Case Reports; English Abstract; Journal Article

[Publication-country] Argentina

[Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 18D0SL7309 / Chlorambucil

   

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[Title] Discordant results of flow cytometric ZAP-70 expression status in B-CLL samples if different gating strategies are applied.

BACKGROUND: Recent studies have identified ZAP-70 expression status as an excellent prognostic parameter in chronic lymphocytic leukemia (CLL).

METHODS: One hundred and one patients with B-CLL were analyzed employing a directly labeled alexa-fluor-488-ZAP-70-antibody.

RESULTS: Applying either T-/NK-cell isotype or healthy control analysis strategies on patient samples that were processed in parallel revealed discrepant results in 48% (12/25) of all cases.

Taken together with the 74 B-CLL patients, who were analyzed with regard to average reference values, disconcordant results were obtained in 58% of the samples.

We demonstrate that high variances in ZAP-70 T-/NK-cell staining within B-CLL patients, paired with a close proximity of ZAP-70 B-cell values to the suggested cut-off levels, may lead to interpretation difficulties of ZAP-70 status.

Further standardization is required before ZAP-70 can be used as a reliable prognostic parameter in immunophenotyping of B-CLL.

[MeSH-major] Flow Cytometry / methods. Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. ZAP-70 Protein-Tyrosine Kinase / analysis

[MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / analysis. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / immunology. Humans. Immunophenotyping. Kaplan-Meier Estimate. Killer Cells, Natural / immunology. Middle Aged. Reference Values. Reproducibility of Results. Survival Rate. T-Lymphocytes / immunology

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[Copyright] (c) 2006 International Society for Analytical Cytology.

(PMID = 16906574.001).

[ISSN] 1552-4949

[Journal-full-title] Cytometry. Part B, Clinical cytometry

[ISO-abbreviation] Cytometry B Clin Cytom

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human

   

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[Title] Increased proteasomal degradation of Bax is a common feature of poor prognosis chronic lymphocytic leukemia.

Many biologic markers are associated with poor prognosis in chronic lymphocytic leukemia (CLL), but their mechanistic role remains unclear.

Using a Bax degradation activity (BDA) assay, CLL cells were found to show variable Bax instability.

However, BDA did not correlate with Bax protein levels: BDA positive and negative cases had high and low baseline Bax levels.

Patients with BDA positive cells had a shorter median overall survival (OS; 126 months vs not reached, P = .011) and time to first treatment (16 vs 156 months, P = .029) than BDA negative cases.

Dual BDA and ZAP-70 positivity had a median OS of 84 months (P = .012).

The BDA assay measures the intrinsic ubiquitin/proteasome activity of CLL cells and dynamic changes in Bax protein levels over time.

Mechanistically, Bax instability may represent a final common pathway for disparate prognostic markers, as well as being itself an indicator of poor prognosis.

[MeSH-major] Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis. Leukemia, Lymphocytic, Chronic, B-Cell / metabolism. Proteasome Endopeptidase Complex / metabolism. Protein Processing, Post-Translational. bcl-2-Associated X Protein / metabolism

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(PMID = 18160666.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Glycoproteins; 0 / bcl-2-Associated X Protein; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human; EC 3.2.2.5 / Antigens, CD38; EC 3.2.2.5 / CD38 protein, human; EC 3.4.25.1 / Proteasome Endopeptidase Complex

   

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[Title] Occupational exposure to ethylene oxide and risk of lymphoma.

BACKGROUND: Ethylene oxide, a high-volume commodity, is an established human carcinogen, although the relevant epidemiologic evidence is limited.

METHODS: We explored the association between occupational exposure to ethylene oxide and risk of lymphoma in a case-control study, including 2347 lymphoma cases first diagnosed in 1998-2004 and 2463 controls, from 6 European countries.

The diagnosis of lymphoma was based on the 2001 World Health Organization Classification of lymphoma.

We modeled risk of lymphoma with unconditional logistic regression analysis as a function of various exposure measures, adjusting for age, sex, and participating center.

Lymphoma risk showed a 4.3-fold increase associated with medium-high frequency of exposure to ethylene oxide (95% CI = 1.4-13).

Among major subtypes, chronic lymphocytic leukemia was consistently associated with ethylene oxide exposure, related in a dose-response manner to probability, frequency, and duration of exposure, as well as to cumulative exposure and (less definitively) with exposure intensity.

[MeSH-major] Carcinogens / toxicity. Ethylene Oxide / toxicity. Lymphoma / chemically induced. Occupational Exposure

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(PMID = 20811284.001).

[ISSN] 1531-5487

[Journal-full-title] Epidemiology (Cambridge, Mass.)

[ISO-abbreviation] Epidemiology

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Carcinogens; JJH7GNN18P / Ethylene Oxide

   

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MicroRNAs are small non-coding RNAs that act at the post-transcriptional level, regulating protein expression by repressing translation or destabilizing mRNA target.

Because of their discovery, microRNAs have been associated with almost every normal cell function, including proliferation, differentiation and apoptosis.

Several lines of evidence suggest that they have an important role in normal hematopoiesis as exemplified by the role of mir-155 and mir-150 in the differentiation of B and T lymphocytes, the suppressive role of mir-221 and mir-222 in erythroid differentiation, the inhibitory effect of mir-181 on hematopoietic differentiation and the induction of myeloid differentiation by mir-223.

Their aberrant expression has been associated with solid tumors and hematopoietic malignancies as suggested by the frequent deletion of mir-15a and mir-16-1 in chronic lymphocytic leukemia, the increased levels of mir-155 in diffuse large B-cell lymphomas and the increased levels of mir-181 in acute myeloid leukemia M1 and M2.

[MeSH-minor] Animals. Cell Transformation, Neoplastic / genetics. Down-Regulation. Erythroid Precursor Cells / cytology. Gene Expression Regulation, Neoplastic / genetics. Genes, Tumor Suppressor. Humans. Invertebrates / genetics. Lymphocytes / cytology. Mice. Myeloid Cells / cytology. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Oncogenes. RNA, Neoplasm / antagonists & inhibitors. RNA, Neoplasm / genetics

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(PMID = 19744129.001).

[ISSN] 1600-0609

[Journal-full-title] European journal of haematology

[ISO-abbreviation] Eur. J. Haematol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / MicroRNAs; 0 / Neoplasm Proteins; 0 / RNA, Neoplasm

[Number-of-references] 110

   

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[Title] Cyclin E but not bcl-2, bax or mcl-1 is differentially expressed in ZAP 70-positive and ZAP 70-negative B-CLL cells.

The clinical course of chronic lymphocytic leukemia is variable.

While some patients have indolent disease, others require aggressive treatment within a short time after diagnosis.

Differences in the expression of proteins regulating cell cycle and apoptosis may be responsible for the heterogeneous course of the disease.

Recently, protein ZAP 70 [zeta-chain (T-cell receptor) associated protein kinase 70 kDa] has been found to be differentially expressed within two biologic subgroups, characterized by the presence or absence of somatic mutations in specific immunoglobulin heavy-chain variable region genes.

In the present work, we analyzed highly purified B-CLL cells from 60 patients for ZAP 70 expression and the expression of cyclin E, bcl-2, bax, and mcl-1 as well as the ratios of bcl-2/bax and mcl-1/bax.

We conclude that higher cyclin E expression in samples of ZAP 70-positive patients may reflect a larger proliferating compartment in vivo compared to ZAP 70-negative patients and that cyclin E may add prognostic information in this context for patients with B-CLL.

[MeSH-major] Cyclin E / genetics. Leukemia, Lymphocytic, Chronic, B-Cell / genetics. Neoplasm Proteins / genetics. Proto-Oncogene Proteins c-bcl-2 / genetics. ZAP-70 Protein-Tyrosine Kinase / metabolism. bcl-2-Associated X Protein / genetics

[MeSH-minor] Adult. Aged. Aged, 80 and over. Antibodies, Monoclonal. Gene Expression Regulation, Neoplastic. Humans. Middle Aged. Myeloid Cell Leukemia Sequence 1 Protein. Neoplasm Staging. Tumor Cells, Cultured

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(PMID = 16538501.001).

[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 / Antibodies, Monoclonal; 0 / Cyclin E; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 2.7.10.2 / ZAP-70 Protein-Tyrosine Kinase; EC 2.7.10.2 / ZAP70 protein, human