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1. Zang RY, Zhang ZY, Cai SM, Tang MQ, Chen J, Li ZT: Epithelial ovarian cancer presenting initially with extraabdominal or intrahepatic metastases: a preliminary report of 25 cases and literature review. Am J Clin Oncol; 2000 Aug;23(4):416-9
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  • Twenty-five patients with EOC, who were treated in the Cancer Hospital of Shanghai Medical University from January 1986 to December 1997, and manifesting as extraperitoneal or liver parenchyma metastases at the time of presentation without detectable ovarian tumors, were retrospectively studied.
  • When compared with 52 other women with stage IV EOC, 20 patients who initially sought treatment for extraabdominal metastases experienced a better prognosis, with an estimated median survival of 24 months versus 10 months (p = 0.0427).
  • The median survival was 30 months in patients with pleural effusion or supraclavicular lymph node metastases versus 19 months in those with spread to other sites (p = 0.0264).
  • The prognosis of such cases, mainly for those with supraclavicular lymphadenopathy or malignant pleural effusion, is better than that for other stage IV EOC patients, probably because most of the patients who initially had distant metastases were generally in condition that permitted aggressive surgery or multicycle chemotherapy.
  • [MeSH-major] Carcinoma / diagnosis. Liver Neoplasms / secondary. Lymphatic Metastasis / pathology. Ovarian Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / secondary. Adult. Aged. CA-125 Antigen / analysis. Diagnosis, Differential. Female. Follow-Up Studies. Humans. Linear Models. Middle Aged. Neoadjuvant Therapy. Neoplasm Staging. Pleural Effusion, Malignant / diagnosis. Prognosis. Remission Induction. Retrospective Studies. Survival Rate


2. Sher T, Miller KC, Deeb G, Lee K, Chanan-Khan A: Plasma cell leukaemia and other aggressive plasma cell malignancies. Br J Haematol; 2010 Aug;150(4):418-27
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  • [Title] Plasma cell leukaemia and other aggressive plasma cell malignancies.
  • These can be primary (de-novo) or secondary due to progressive prior multiple myeloma (MM).
  • Compared to MM, organ invasion is common in PCL, while soft tissue tumors involving the head, neck or paraspinal area are common sites for MEP.
  • Even high dose chemotherapy with autologous stem cell rescue has not been able to demonstrate consistent improvement in survival outcome.
  • Although not specifically evaluated, novel anti-plasma cell agents, such as the proteasome inhibitor bortezomib, and immunomodulatory drugs, such as lenalidomide, appear to be active against these aggressive cancers.
  • Clinical and translational research directed at improved understanding of disease biology and development of novel therapeutics is urgently needed.
  • [MeSH-major] Multiple Myeloma / drug therapy
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Bortezomib. Female. Humans. Leukemia, Plasma Cell / diagnosis. Leukemia, Plasma Cell / drug therapy. Leukemia, Plasma Cell / etiology. Male. Middle Aged. Prognosis. Pyrazines / therapeutic use. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use

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  • [Cites] Rinsho Ketsueki. 1987 Mar;28(3):428-33 [3613131.001]
  • [Cites] Clin Lymphoma Myeloma. 2009 Aug;9(4):328-30 [19717386.001]
  • [Cites] Eur J Haematol Suppl. 1989;51:76-83 [2697596.001]
  • [Cites] Rinsho Ketsueki. 1991 Apr;32(4):399-403 [2067085.001]
  • [Cites] Dtsch Med Wochenschr. 1992 Jun 5;117(23):900-4 [1597118.001]
  • [Cites] Anticancer Res. 1993 Jul-Aug;13(4):1091-5 [8352531.001]
  • [Cites] Am J Hematol. 1994 Mar;45(3):262-4 [8296801.001]
  • [Cites] Rinsho Ketsueki. 1994 Aug;35(8):756-60 [7933562.001]
  • [Cites] J Clin Oncol. 1994 Nov;12(11):2398-404 [7964956.001]
  • [Cites] Br J Haematol. 1994 Dec;88(4):754-9 [7819100.001]
  • [Cites] Br J Haematol. 1995 Apr;89(4):914-6 [7772534.001]
  • [Cites] Br J Haematol. 1996 May;93(2):345-51 [8639427.001]
  • [Cites] Leuk Lymphoma. 1997 May;25(5-6):545-54 [9250826.001]
  • [Cites] Am J Hematol. 1998 Jan;57(1):51-6 [9423817.001]
  • [Cites] Leukemia. 1998 Dec;12(12):1977-82 [9844928.001]
  • [Cites] Blood. 1999 Feb 1;93(3):1032-7 [9920853.001]
  • [Cites] Br J Haematol. 1999 Jan;104(1):138-43 [10027726.001]
  • [Cites] Br J Haematol. 1999 Jul;106(1):28-34 [10444159.001]
  • [Cites] Blood. 1953 Jun;8(6):519-23 [13059037.001]
  • [Cites] Leukemia. 2005 Mar;19(3):449-55 [15674420.001]
  • [Cites] Am J Hematol. 2005 Apr;78(4):288-94 [15795922.001]
  • [Cites] Ann Hematol. 2006 Apr;85(4):263-7 [16416115.001]
  • [Cites] Leukemia. 2006 Mar;20(3):542-5 [16408097.001]
  • [Cites] Ann Hematol. 2006 Jul;85(7):487-8 [16570151.001]
  • [Cites] Leuk Lymphoma. 2006 Aug;47(8):1670-3 [16966282.001]
  • [Cites] Leuk Res. 2006 Dec;30(12):1581-3 [16540168.001]
  • [Cites] Haematologica. 2007 Jan;92(1):143-4 [17229655.001]
  • [Cites] Leuk Lymphoma. 2007 Jan;48(1):180-2 [17325863.001]
  • [Cites] Cancer. 2007 Jun 1;109(11):2285-90 [17469169.001]
  • [Cites] Leuk Lymphoma. 2007 Jul;48(7):1423-5 [17613775.001]
  • [Cites] Leuk Lymphoma. 2007 Jul;48(7):1426-8 [17613776.001]
  • [Cites] Blood. 2008 Mar 1;111(5):2516-20 [17975015.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Gan To Kagaku Ryoho. 2008 Mar;35(3):533-7 [18347412.001]
  • [Cites] J Clin Oncol. 2008 Mar 20;26(9):1544-52 [18285605.001]
  • [Cites] Leuk Res. 2008 Jul;32(7):1153-6 [18083228.001]
  • [Cites] Bone Marrow Transplant. 2008 May;41(9):779-84 [18195681.001]
  • [Cites] Leukemia. 2008 May;22(5):1044-52 [18216867.001]
  • [Cites] Med Oncol. 2008;25(2):154-60 [18488157.001]
  • [Cites] Leuk Res. 2008 Oct;32(10):1637-8 [18433866.001]
  • [Cites] Ann Oncol. 1999 Oct;10(10):1249-50 [10586345.001]
  • [Cites] Lancet. 2000 Jan 22;355(9200):248-50 [10675068.001]
  • [Cites] Blood. 2001 Feb 1;97(3):822-5 [11157506.001]
  • [Cites] Ann Hematol. 2002 Feb;81(2):119-23 [11907796.001]
  • [Cites] Leuk Lymphoma. 2002 Feb;43(2):351-4 [11999568.001]
  • [Cites] Br J Haematol. 2002 Jun;117(4):882-5 [12060125.001]
  • [Cites] Ann Hematol. 2002 Jul;81(7):362-7 [12185504.001]
  • [Cites] J Bone Miner Res. 2002 Nov;17(11):1921-5 [12412796.001]
  • [Cites] Blood. 2003 Mar 15;101(6):2377-80 [12424198.001]
  • [Cites] Leuk Lymphoma. 2003 Feb;44(2):379-80 [12688365.001]
  • [Cites] Arch Pathol Lab Med. 2003 Aug;127(8):1026-7 [12873179.001]
  • [Cites] Nihon Naika Gakkai Zasshi. 2004 Jan 10;93(1):139-41 [14968586.001]
  • [Cites] Cancer Res. 2004 Feb 15;64(4):1546-58 [14989251.001]
  • [Cites] Leuk Lymphoma. 2004 Apr;45(4):735-8 [15160948.001]
  • [Cites] Leuk Lymphoma. 2004 Apr;45(4):821-4 [15160964.001]
  • [Cites] Can Med Assoc J. 1977 Oct 8;117(7):788-9 [907952.001]
  • [Cites] N Engl J Med. 2008 Aug 28;359(9):906-17 [18753647.001]
  • [Cites] Cancer Causes Control. 2008 Oct;19(8):841-58 [18365759.001]
  • [Cites] Leuk Res. 2009 Feb;33(2):259-62 [18676019.001]
  • [Cites] Acta Haematol. 2009;121(1):47-51 [19339770.001]
  • [Cites] Int J Lab Hematol. 2009 Jun;31(3):338-43 [18284415.001]
  • [Cites] Leuk Res. 2009 Aug;33(8):1137-40 [19250676.001]
  • [Cites] Ann Oncol. 2010 Feb;21(2):325-30 [19633044.001]
  • [Cites] Am J Med. 1987 Dec;83(6):1062-8 [3503574.001]
  • (PMID = 20701603.001).
  • [ISSN] 1365-2141
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA121044
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 4Z8R6ORS6L / Thalidomide; 69G8BD63PP / Bortezomib; F0P408N6V4 / lenalidomide
  • [Number-of-references] 69
  • [Other-IDs] NLM/ NIHMS585047; NLM/ PMC4044724
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3. Shukla GS, Krag DN: Developing bifunctional beta-lactamase molecules with built-in target-recognizing module for prodrug therapy: identification of Enterobacter Cloacae P99 cephalosporinase loops suitable for randomization and phage-display selection. J Mol Recognit; 2009 Nov-Dec;22(6):425-36
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  • [Title] Developing bifunctional beta-lactamase molecules with built-in target-recognizing module for prodrug therapy: identification of Enterobacter Cloacae P99 cephalosporinase loops suitable for randomization and phage-display selection.
  • This study was focused on developing catalytically active beta-lactamase enzyme molecules that have target-recognizing sites built within their scaffold.
  • The complexity of the loop-2 linear library, as determined by the frequency and diversity of amino acid distributions in the randomized region, appears consistent with the standards of other types of phage display library systems.
  • This is an enabling step in our long-term goal of developing bifunctional beta-lactamase molecules against cancer-specific targets for enzyme prodrug therapy of cancer.

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  • [Cites] Cancer Res. 1995 Aug 15;55(16):3558-63 [7627964.001]
  • [Cites] Nature. 1990 Jan 18;343(6255):284-8 [2300174.001]
  • [Cites] Cancer Chemother Pharmacol. 1997;40(3):189-201 [9219501.001]
  • [Cites] Bioconjug Chem. 1997 Jul-Aug;8(4):510-9 [9258449.001]
  • [Cites] J Biol Chem. 1997 Nov 14;272(46):29144-50 [9360991.001]
  • [Cites] Immunotechnology. 1996 Feb;2(1):47-57 [9373327.001]
  • [Cites] J Pharm Pharmacol. 1998 Apr;50(4):387-94 [9625483.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 Aug;87(16):6378-82 [2201029.001]
  • [Cites] J Bacteriol. 1993 Mar;175(6):1856-9 [8449893.001]
  • [Cites] Cancer Res. 1993 Sep 1;53(17):3956-63 [8358723.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Dec 1;90(23):11257-61 [8248237.001]
  • [Cites] Bioconjug Chem. 1993 Sep-Oct;4(5):334-40 [8274516.001]
  • [Cites] Biochemistry. 1994 Jun 7;33(22):6762-72 [8204611.001]
  • [Cites] J Med Chem. 1995 Apr 14;38(8):1380-5 [7731023.001]
  • [Cites] J Natl Cancer Inst. 1996 Feb 21;88(3-4):153-65 [8632489.001]
  • [Cites] Bioinformatics. 1998;14(1):55-67 [9520502.001]
  • [Cites] Can J Microbiol. 1998 Apr;44(4):313-29 [9674105.001]
  • [Cites] Fold Des. 1998;3(5):321-8 [9806934.001]
  • [Cites] Nat Biotechnol. 1999 Jan;17(1):67-72 [9920272.001]
  • [Cites] Bioinformatics. 2004 Dec 12;20(18):3481-9 [15284106.001]
  • [Cites] N Engl J Med. 2005 Jan 27;352(4):380-91 [15673804.001]
  • [Cites] Mol Cancer Ther. 2005 Nov;4(11):1791-800 [16276001.001]
  • [Cites] Expert Opin Biol Ther. 2006 Jan;6(1):39-54 [16370913.001]
  • [Cites] Protein Sci. 2006 Jan;15(1):14-27 [16373474.001]
  • [Cites] Nat Biotechnol. 2006 Jul;24(7):823-31 [16823375.001]
  • [Cites] Expert Rev Anticancer Ther. 2006 Oct;6(10):1421-31 [17069527.001]
  • [Cites] Int J Cancer. 2007 May 15;120(10):2233-42 [17285581.001]
  • [Cites] Nature. 2007 Aug 16;448(7155):828-31 [17700701.001]
  • [Cites] Curr Med Chem. 2008;15(18):1802-26 [18691040.001]
  • [Cites] Int J Cancer. 2000 Feb 15;85(4):571-7 [10699932.001]
  • [Cites] J Mol Recognit. 2000 Jul-Aug;13(4):167-87 [10931555.001]
  • [Cites] Adv Drug Deliv Rev. 2001 Dec 31;53(3):247-64 [11744170.001]
  • [Cites] Br J Cancer. 2002 Mar 4;86(5):811-8 [11875747.001]
  • [Cites] J Biol Chem. 2002 Aug 16;277(33):30382-7 [12048201.001]
  • [Cites] Int J Med Microbiol. 2002 Jul;292(2):127-37 [12195735.001]
  • [Cites] J Mol Biol. 2002 Oct 4;322(5):1039-52 [12367527.001]
  • [Cites] Bioorg Med Chem Lett. 2003 Feb 10;13(3):539-42 [12565967.001]
  • [Cites] Bioconjug Chem. 2003 Jul-Aug;14(4):797-804 [12862433.001]
  • [Cites] Pharmacol Rev. 2004 Mar;56(1):53-102 [15001663.001]
  • [Cites] Cancer Res. 2004 Apr 15;64(8):2853-7 [15087403.001]
  • [Cites] Proteomics. 2004 May;4(5):1439-60 [15188413.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:2605-17 [15358584.001]
  • [Cites] Biochem J. 1984 Jul 15;221(2):505-12 [6332621.001]
  • [Cites] Cancer Res. 1995 Jun 1;55(11):2357-65 [7757987.001]
  • (PMID = 19437416.001).
  • [ISSN] 1099-1352
  • [Journal-full-title] Journal of molecular recognition : JMR
  • [ISO-abbreviation] J. Mol. Recognit.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA112091-03; United States / NCI NIH HHS / CA / R01 CA112091; United States / NCI NIH HHS / CA / R01 CA112091-03; United States / NCI NIH HHS / CA / R01CA112091
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Peptide Library; 0 / Peptides; 0 / Prodrugs; EC 3.5.2.- / Cephalosporinase; EC 3.5.2.6 / beta-Lactamases
  • [Other-IDs] NLM/ NIHMS174379; NLM/ PMC2824592
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4. Kushner BH, Cheung NK, Barker CA, Kramer K, Modak S, Yataghene K, Wolden SL: Hyperfractionated low-dose (21 Gy) radiotherapy for cranial skeletal metastases in patients with high-risk neuroblastoma. Int J Radiat Oncol Biol Phys; 2009 Nov 15;75(4):1181-6
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  • [Title] Hyperfractionated low-dose (21 Gy) radiotherapy for cranial skeletal metastases in patients with high-risk neuroblastoma.
  • PURPOSE: To present a large experience (73 patients) using a standard radiotherapy (RT) protocol to prevent relapse in cranial sites where measurable metastatic neuroblastoma (NB), an adverse prognostic marker, is common.
  • METHODS AND MATERIALS: High-risk NB patients with measurable cranial disease at diagnosis or residual cranial disease after induction therapy had those sites irradiated with hyperfractionated 21 Gy; a brain-sparing technique was used for an extensive field.
  • The patients were grouped according to the response to systemic therapy.
  • Two relapses involved irradiated cranial sites.
  • Two other patients relapsed in the irradiated cranial sites 6 and 12 months after a systemic relapse.
  • The cranial sites showed major (n = 13), minor (n = 2), or no response (n = 4) to RT.
  • Group 2 also included 15 patients who had persistent NB in extracranial, but not cranial, sites.
  • Of these 15 patients, 2 relapsed in the irradiated cranial sites and elsewhere at 8 and 14 months.
  • CONCLUSION: Hyperfractionated 21-Gy cranial RT might help control NB and is feasible without significant toxicity in children.
  • [MeSH-major] Neuroblastoma / radiotherapy. Neuroblastoma / secondary. Skull Neoplasms / radiotherapy. Skull Neoplasms / secondary
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Cranial Irradiation / adverse effects. Cranial Irradiation / methods. Disease-Free Survival. Dose Fractionation. Female. Humans. Infant. Male. Neoplasm Recurrence, Local / radiotherapy. Neoplasm, Residual. Orbital Neoplasms / drug therapy. Orbital Neoplasms / mortality. Orbital Neoplasms / radiotherapy. Orbital Neoplasms / secondary. Remission Induction. Survival Rate. Young Adult

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  • [Cites] Biometrics. 1978 Dec;34(4):541-54 [373811.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 May-Jun;21(3):181-9 [10363850.001]
  • [Cites] Cancer. 1997 Nov 15;80(10):1997-2004 [9366304.001]
  • [Cites] J Clin Oncol. 1993 Nov;11(11):2226-33 [8229138.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1466-77 [8336186.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1986 Oct;12(10):1829-37 [2428788.001]
  • [Cites] J Clin Oncol. 2001 Jun 1;19(11):2821-8 [11387353.001]
  • [Cites] S Afr Med J. 1984 Jul 14;66(2):62-3 [6740426.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):1082-6 [12637474.001]
  • [Cites] Eur J Cancer. 1992;28A(10):1654-9 [1389481.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Jan 1;28(1):85-92 [8270462.001]
  • [Cites] Pediatr Blood Cancer. 2008 Jun;50(6):1163-8 [17973314.001]
  • [Cites] J Clin Oncol. 1998 Dec;16(12):3880-9 [9850034.001]
  • [Cites] Cancer. 2006 Jul 15;107(2):417-22 [16779793.001]
  • [Cites] Radiother Oncol. 1986 Aug;6(4):317-26 [3534967.001]
  • [Cites] Pediatr Blood Cancer. 2006 Mar;46(3):278-84 [16124002.001]
  • [Cites] J Clin Oncol. 2001 Nov 15;19(22):4189-94 [11709561.001]
  • [Cites] Gan To Kagaku Ryoho. 1987 May;14(5 Pt 2):1723-8 [3036015.001]
  • [Cites] J Clin Oncol. 1998 Sep;16(9):3053-60 [9738575.001]
  • [Cites] Eur J Cancer. 1997 Oct;33(12):2117-20 [9516865.001]
  • [Cites] J Pediatr Hematol Oncol. 2004 Jan;26(1):35-9 [14707711.001]
  • [Cites] J Clin Oncol. 1984 Jul;2(7):719-32 [6737018.001]
  • [Cites] Med Pediatr Oncol. 2001 Jan;36(1):227-30 [11464891.001]
  • [Cites] Cancer. 1983 Sep 1;52(5):915-25 [6871832.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1995 Jul 15;32(4):1127-35 [7607934.001]
  • [Cites] Radiother Oncol. 1985 Apr;3(3):201-9 [4001442.001]
  • [Cites] Pediatr Hematol Oncol. 2003 Jan-Feb;20(1):23-30 [12687750.001]
  • [Cites] N Engl J Med. 1999 Oct 14;341(16):1165-73 [10519894.001]
  • [Cites] J Clin Oncol. 2004 Dec 15;22(24):4888-92 [15611504.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 May 1;56(1):28-39 [12694821.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1982 Feb;8(2):219-26 [7085377.001]
  • [Cites] Pediatr Blood Cancer. 2005 Sep;45(3):324-32 [15714447.001]
  • (PMID = 19427746.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / CA61017; United States / NCI NIH HHS / CA / CA72868
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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5. Yu EW, McDermott G, Zgurskaya HI, Nikaido H, Koshland DE Jr: Structural basis of multiple drug-binding capacity of the AcrB multidrug efflux pump. Science; 2003 May 9;300(5621):976-80
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  • [Title] Structural basis of multiple drug-binding capacity of the AcrB multidrug efflux pump.
  • Multidrug efflux pumps cause serious problems in cancer chemotherapy and treatment of bacterial infections.
  • The bound ligand molecules often interact with each other, stabilizing the binding.
  • [MeSH-minor] Anti-Infective Agents / chemistry. Anti-Infective Agents / metabolism. Anti-Infective Agents, Local / chemistry. Anti-Infective Agents, Local / metabolism. Binding Sites. Cell Membrane / chemistry. Chemistry, Physical. Ciprofloxacin / chemistry. Ciprofloxacin / metabolism. Crystallization. Crystallography, X-Ray. Dequalinium / chemistry. Dequalinium / metabolism. Ethidium / chemistry. Ethidium / metabolism. Hydrogen Bonding. Hydrophobic and Hydrophilic Interactions. Ligands. Models, Molecular. Multidrug Resistance-Associated Proteins. Physicochemical Phenomena. Protein Binding. Protein Conformation. Protein Structure, Quaternary. Protein Structure, Secondary. Protein Structure, Tertiary. Rhodamines / chemistry. Rhodamines / metabolism. Static Electricity

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  • (PMID = 12738864.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] eng
  • [Databank-accession-numbers] PDB/ 1OY6/ 1OY8/ 1OY9/ 1OYD/ 1OYE
  • [Grant] United States / NIAID NIH HHS / AI / AI 09644
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AcrB protein, E coli; 0 / Anti-Infective Agents; 0 / Anti-Infective Agents, Local; 0 / Carrier Proteins; 0 / Escherichia coli Proteins; 0 / Ligands; 0 / Membrane Proteins; 0 / Multidrug Resistance-Associated Proteins; 0 / Rhodamines; 5E8K9I0O4U / Ciprofloxacin; E7QC7V26B8 / Dequalinium; EN464416SI / Ethidium
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6. Friedberg JW, Neuberg D, Monson E, Jallow H, Nadler LM, Freedman AS: The impact of external beam radiation therapy prior to autologous bone marrow transplantation in patients with non-Hodgkin's lymphoma. Biol Blood Marrow Transplant; 2001;7(8):446-53
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  • [Title] The impact of external beam radiation therapy prior to autologous bone marrow transplantation in patients with non-Hodgkin's lymphoma.
  • External beam radiation therapy (XRT) is frequently used to treat refractory disease sites or consolidate remission in patients with relapsed non-Hodgkin's lymphoma (NHL) prior to autologous bone marrow transplantation (ABMT).
  • We report the long-term outcome and toxicities associated with this therapy.
  • We uniformly treated 552 patients with NHL with total body irradiation, high-dose chemotherapy, and anti-B-cell monoclonal antibody-purged ABMT.
  • Of these patients, 152 received XRT to the mediastinum, abdomen, or pelvis (n = 102) or other sites (n = 50) prior to ABMT.
  • For patients with aggressive histology, the median overall survival time was 64 months in the XRT patients and 79 months in the patients not treated with XRT (P= .09).
  • Of patients who received XRT, 12.5% developed secondary myelodysplasia compared with 5.8% of patients not receiving XRT (P = .01).
  • [MeSH-minor] Adult. Aged. Cause of Death. Cohort Studies. Combined Modality Therapy / adverse effects. Combined Modality Therapy / standards. Disease-Free Survival. Female. Follow-Up Studies. Humans. Lymphoma, B-Cell / mortality. Lymphoma, B-Cell / radiotherapy. Lymphoma, B-Cell / therapy. Male. Middle Aged. Prognosis. Retrospective Studies. Survival Rate. Transplantation, Autologous / methods. Transplantation, Autologous / mortality

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  • (PMID = 11569890.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA66996
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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7. Wiseman CL, Kharazi A: Objective clinical regression of metastatic breast cancer in disparate sites after use of whole-cell vaccine genetically modified to release sargramostim. Breast J; 2006 Sep-Oct;12(5):475-80
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  • [Title] Objective clinical regression of metastatic breast cancer in disparate sites after use of whole-cell vaccine genetically modified to release sargramostim.
  • A patient with recurrent breast cancer metastases following initial response to chemotherapy and hormonal maintenance was treated with a whole-cell tumor vaccine, resulting in a prompt objective complete remission of a lung lesion on computed tomography (CT) scans and near-complete regression of multiple breast lesions on magnetic resonance imaging (MRI).
  • Reinstitution of vaccine inoculation resulted in major regression of the brain and breast lesions, improvement in all other areas, and no indication of new lesions.
  • Therapy consisted of inoculation of 20 x 10(6) SV-BR-1-GM cells, a unique breast cancer cell line transfected to release sargramostim (granulocyte macrophage colony-stimulating factor [GM-CSF]).
  • Each treatment was preceded 48 hours earlier with low-dose cyclophosphamide 300 mg/m2 to abrogate regulatory T-cell activity.
  • The patient developed positive delayed-type hypersensitivity responses and also antibody reactivity to the vaccine cells.
  • [MeSH-major] Breast Neoplasms / therapy. Cancer Vaccines / genetics. Cancer Vaccines / therapeutic use. Carcinoma, Ductal, Breast / therapy. Granulocyte-Macrophage Colony-Stimulating Factor / immunology. Immunologic Factors / immunology
  • [MeSH-minor] Antibodies, Neoplasm / immunology. Brain Neoplasms / immunology. Brain Neoplasms / secondary. Female. Humans. Liver Neoplasms / immunology. Liver Neoplasms / secondary. Lung Neoplasms / immunology. Lung Neoplasms / secondary. Magnetic Resonance Imaging. Middle Aged. Postmenopause. Recombinant Proteins. Tomography, X-Ray Computed


8. Germanov E, Berman JN, Guernsey DL: Current and future approaches for the therapeutic targeting of metastasis (review). Int J Mol Med; 2006 Dec;18(6):1025-36
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  • [Title] Current and future approaches for the therapeutic targeting of metastasis (review).
  • Metastasis is the process whereby cancer cells disseminate and establish secondary tumors at distant sites from the primary tumor and is estimated to be responsible for approximately 90% of all cancer deaths.
  • Cancers with metastatic spread are frequently resistant to conventional chemotherapeutic approaches, underlining the urgent need for novel treatments in these diseases.
  • Recent advances in understanding the mechanisms underlining both the intrinsic cellular and extrinsic micro-environmental factors contributing to the metastatic process have resulted in the identification of a number of molecular targets for the development of specific anti-metastatic therapeutic strategies.
  • Many of these pathways interact with each other, with the possibility of multiple downstream antineoplastic consequences as well as the potential for synergistic effects by targeting more than one of these factors.
  • This review outlines several of the promising targets, and provides examples, of how these targets are being exploited as anti-metastatic therapies in conjunction with conventional treatments.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasm Metastasis / drug therapy. Neoplasms / therapy
  • [MeSH-minor] Animals. Chemokines / therapeutic use. Humans. Matrix Metalloproteinases / therapeutic use. Neovascularization, Pathologic / drug therapy. Neurotransmitter Agents / therapeutic use. Polysaccharides / therapeutic use. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / genetics. Protein-Tyrosine Kinases / metabolism. Receptors, G-Protein-Coupled / therapeutic use. Signal Transduction / drug effects

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  • (PMID = 17089005.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chemokines; 0 / Neurotransmitter Agents; 0 / Polysaccharides; 0 / Protein Kinase Inhibitors; 0 / Receptors, G-Protein-Coupled; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.4.24.- / Matrix Metalloproteinases
  • [Number-of-references] 111
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9. Alexandre J, Bleuzen P, Bonneterre J, Sutherland W, Misset JL, Guastalla J, Viens P, Faivre S, Chahine A, Spielman M, Bensmaïne A, Marty M, Mahjoubi M, Cvitkovic E: Factors predicting for efficacy and safety of docetaxel in a compassionate-use cohort of 825 heavily pretreated advanced breast cancer patients. J Clin Oncol; 2000 Feb;18(3):562-73
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  • PATIENTS AND METHODS: A total of 825 ABC patients treated with docetaxel (100 mg/m(2) every 3 weeks) were source-reviewed and analyzed for prognostic factors associated with overall response rate (ORR), time to treatment failure (TTF), overall survival (OS), febrile neutropenia, mucositis, and severe fluid retention syndrome by univariate and multivariate analysis.
  • By multivariate analysis, secondary anthracycline-resistant disease was significantly associated (P <.
  • Liver dysfunction (transaminase levels > 1.5 times the upper limit of normal [ULN] and alkaline phosphatase [AP] level > three times ULN) and time since first relapse less than 24 months were associated with shorter TTF and OS.
  • Other significant correlations included the following: elevated CA 15-3 serum level with lower ORR; more than two involved sites, and minor transaminase and AP level abnormalities with shorter OS; and no previous chemotherapy for ABC with shorter TTF.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / adverse effects. Antineoplastic Agents, Phytogenic / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms, Male / drug therapy. Paclitaxel / analogs & derivatives. Taxoids
  • [MeSH-minor] Anthracyclines / therapeutic use. Chemical and Drug Induced Liver Injury. Drug Resistance, Neoplasm. Female. Fever / chemically induced. Humans. Liver Neoplasms / secondary. Male. Middle Aged. Multivariate Analysis. Neutropenia / chemically induced. Prognosis. Risk Factors. Stomatitis / chemically induced. Treatment Outcome

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  • (PMID = 10653871.001).
  • [ISSN] 0732-183X
  • [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; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents, Phytogenic; 0 / Taxoids; 15H5577CQD / docetaxel; P88XT4IS4D / Paclitaxel
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10. Ganesh SK, Skelding KA, Mehta L, O'Neill K, Joo J, Zheng G, Goldstein J, Simari R, Billings E, Geller NL, Holmes D, O'Neill WW, Nabel EG: Rationale and study design of the CardioGene Study: genomics of in-stent restenosis. Pharmacogenomics; 2004 Oct;5(7):952-1004
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  • BACKGROUND AND AIMS: in-stent restenosis is a major limitation of stent therapy for atherosclerosis coronary artery disease.
  • The CardioGene Study is an ongoing study of restenosis in bare mental stents (BMS) for the treatment of coronary artery disease.
  • Furthermore, the delineation of genetic biomarkers would be of value in the clinical setting of risk-stratify patients prior to stent therapy.
  • Prospective risk stratification would allow for the rational selection of specialized treatments against the development of in-stent restenosis (ISR), such as drug-eluting stents.
  • SETTING: Patients are enrolled at two sites in the US with high-volume cardiac catheterization facilities: the William Beaumont Hospital in Royal Oak, MI, USA, and the Mayo Clinic in Rochester, MN, USA.
  • First, 350 patients are enrolled prospectively at the time of stent implantation.
  • The major secondary outcome is clinical restenosis at 12 months.
  • Second, a corollary case-control analysis will be carried out with the enrollment of an additional 250 cases with a history of recurrent restenosis after treatment with BMS.
  • A standardized questionnaire is used to collect clinical data primarily through direct patient interview to assess medical history, medication use, functional status, family history, environmental factors, and social history.
  • Per individual in the prospective cohort, high-quality transcript profiles of peripheral blood mononuclear cells at each time of blood sampling are obtained using Affymetrix U133A microarrays (Affymetrix, Santa Clara, CA, USA).
  • Per chip, this yields 495,930 features per individual per time of sampling.
  • This represents expression levels for 22,283 genes per patients oer time of blood sampling, including 14,500 well-characterized human genes.
  • These genes are finely investigated for candidate SNPs and other gene variants.
  • These include determining blood gene and protein expression in patients with ISR, investigating the genetic basis of ISR, developing predictive gene and protein biomarkers, and the identification of new targets for treatment.
  • [MeSH-minor] Gene Expression Profiling / methods. Genotype. Humans. Multicenter Studies as Topic / methods. Patient Selection. Phenotype. Polymorphism, Single Nucleotide. Predictive Value of Tests. Prospective Studies. Proteomics / methods. RNA, Messenger / biosynthesis. Research Design. Risk Factors. Treatment Outcome

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  • (PMID = 15469413.001).
  • [ISSN] 1462-2416
  • [Journal-full-title] Pharmacogenomics
  • [ISO-abbreviation] Pharmacogenomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger
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11. Lokeshwar BL, Selzer MG, Zhu BQ, Block NL, Golub LM: Inhibition of cell proliferation, invasion, tumor growth and metastasis by an oral non-antimicrobial tetracycline analog (COL-3) in a metastatic prostate cancer model. Int J Cancer; 2002 Mar 10;98(2):297-309
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  • However, their low in vivo efficacy and associated morbidity limit their long-term application in cancer therapy.
  • One of the CMTs, 6-deoxy, 6-demethyl, 4-de-dimethylamino tetracycline (CMT-3, COL-3), was the most potent inhibitor (50% inhibition dose [GI(50)] < or = 5.0 ,microg/ml).
  • CMT-3 and DC decreased matrix metalloproteinase (MMP)-2, tissue inhibitor of MMP (TIMP)-1 and TIMP-2 secretion in treated cultures and inhibited activity of secreted MMPs, CMT-3 was a stronger inhibitor.
  • Decreases in tumor growth (27-35%) and lung metastases were observed (28.9 +/- 15.4 sites/animal [CMT-3-treated] versus 43.6 +/- 18.8 sites/animal [DC-treated] versus 59.5 +/- 13.9 [control]; p < 0.01].
  • No significant drug-induced morbidity was observed in any of the animals.
  • These results, along with a recently concluded clinical trial, suggest a potential use of CMT-3 as an oral, nontoxic drug to treat metastatic prostate and other cancers.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Matrix Metalloproteinase Inhibitors. Prostatic Neoplasms / drug therapy. Protease Inhibitors / pharmacology. Tetracyclines / pharmacology
  • [MeSH-minor] Administration, Oral. Animals. Apoptosis. Cell Cycle / drug effects. Cell Division / drug effects. Dose-Response Relationship, Drug. Doxycycline / adverse effects. Doxycycline / pharmacology. Hydroxyl Radical / metabolism. Lung Neoplasms / secondary. Male. Matrix Metalloproteinases / biosynthesis. Neoplasm Invasiveness. Neoplasm Transplantation. Rats. Tissue Inhibitor of Metalloproteinases / metabolism. Tumor Cells, Cultured

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  • [Copyright] Copyright 2001 Wiley‐Liss, Inc.
  • (PMID = 11857423.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R29-CA 63108; United States / NCI NIH HHS / CA / 5R01 CA 63108
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Matrix Metalloproteinase Inhibitors; 0 / Protease Inhibitors; 0 / Tetracyclines; 0 / Tissue Inhibitor of Metalloproteinases; 0 / tetracycline CMT-3; 3352-57-6 / Hydroxyl Radical; EC 3.4.24.- / Matrix Metalloproteinases; N12000U13O / Doxycycline
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12. Brell JM, Krishnamurthi SS, Javle M, Saltzman J, Wollner I, Pelley R, Dowlati A, Kantharaj BN, Schluchter MD, Rath L, Ivy SP, Remick SC: A multi-center phase II study of oxaliplatin, irinotecan, and capecitabine in advanced gastric/gastroesophageal junction carcinoma. Cancer Chemother Pharmacol; 2009 Apr;63(5):851-7
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  • [Title] A multi-center phase II study of oxaliplatin, irinotecan, and capecitabine in advanced gastric/gastroesophageal junction carcinoma.
  • BACKGROUND: There is no standard first-line therapy for advanced gastric and gastroesophageal junction (GEJ) adenocarcinoma and the prognosis remains poor.
  • The regimen was tolerated; pharmacodynamic studies revealed no drug interactions, and there was one confirmed response in a gastric cancer patient.
  • METHODS: This was a multi-center single treatment arm study involving six sites.
  • Only prior adjuvant therapy was allowed.
  • Patients had ECOG performance status of 0-2, adequate organ function, and were able to tolerate oral medications.
  • All patients received oxaliplatin 60 mg/m(2) intravenously (IV) and irinotecan 50 mg/m(2) IV weekly times 4 weeks with a 2-week rest period.
  • There were no grade 5 treatment related events, with all deaths secondary to disease progression.
  • However, the total response rate is modest and not an improvement over other regimens.

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  • (PMID = 18670776.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA062502; United States / NCI NIH HHS / CA / U01 CA62502
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 04ZR38536J / oxaliplatin; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; 7673326042 / irinotecan; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin
  • [Other-IDs] NLM/ NIHMS634366; NLM/ PMC4209292
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13. Lindrud S, Orlick M, Barnard N, Hait WN, Toppmeyer DL: Central nervous system progression during systemic response to trastuzumab, humanized anti-HER-2/neu antibody, plus paclitaxel in a woman with refractory metastatic breast cancer. Breast J; 2003 Mar-Apr;9(2):116-9
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  • Treatment of selected patients with anti-HER-2/neu antibodies alone (1) or in combination with chemotherapy (2) may be of benefit to patients with refractory breast cancer.
  • These patients may have a poorer overall prognosis (3) due to relative resistance to both hormonal therapy and chemotherapy (4-6).
  • While on combination treatment she developed cerebellar metastases.
  • Follow-up computed tomography (CT) scan revealed that her disease continued to respond in the liver, lungs, and bone.
  • This case suggests that failure of trastuzumab to cross the blood-brain barrier may compromise its overall effectiveness and raises the possibility that the central nervous system (CNS), or other sanctuary sites, may become clinically more significant in patients with breast cancer in the era of antibody-based therapies.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cerebellar Neoplasms / secondary. Paclitaxel / administration & dosage
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Agents, Phytogenic / administration & dosage. Blood-Brain Barrier. Central Nervous System Neoplasms / secondary. Fatal Outcome. Female. Humans. Middle Aged. Receptor, ErbB-2 / drug effects. Time Factors. Tomography, X-Ray Computed. Trastuzumab


14. Hauck ML, LaRue SM, Petros WP, Poulson JM, Yu D, Spasojevic I, Pruitt AF, Klein A, Case B, Thrall DE, Needham D, Dewhirst MW: Phase I trial of doxorubicin-containing low temperature sensitive liposomes in spontaneous canine tumors. Clin Cancer Res; 2006 Jul 1;12(13):4004-10
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  • The tumors did not involve bone and were located at sites amenable to local hyperthermia.
  • Three treatments, given 3 weeks apart, were scheduled.
  • Pharmacokinetics were evaluated during the first treatment cycle.
  • Grade 4 neutropenia and acute death secondary to liver failure, possibly drug related, were the dose-limiting toxicities.
  • Other toxicities, with the possible exception of renal damage, were consistent with those observed following free doxorubicin administration.
  • Of the 20 dogs that received > or = 2 doses of LTSL-doxorubicin, 12 had stable disease, and 6 had a partial response to treatment.
  • Tumor drug concentrations at a dose of 1.0 mg/kg averaged 9.12 +/- 6.17 ng/mg tissue.
  • CONCLUSION: LTSL-doxorubicin offers a novel approach to improving drug delivery to solid tumors.

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  • (PMID = 16818699.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA042745; United States / NCI NIH HHS / CA / P01CA42745
  • [Publication-type] Clinical Trial, Phase I; 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 / Liposomes; 80168379AG / Doxorubicin
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15. Hirao M, Onai N, Hiroishi K, Watkins SC, Matsushima K, Robbins PD, Lotze MT, Tahara H: CC chemokine receptor-7 on dendritic cells is induced after interaction with apoptotic tumor cells: critical role in migration from the tumor site to draining lymph nodes. Cancer Res; 2000 Apr 15;60(8):2209-17
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  • Coculture of DCs and apoptotic tumor cells resulted in decreased expression of CC chemokine receptor (CCR) 1 and increased CCR7 expression at mRNA level without alteration in other phenotypical markers on DCs.
  • Chemotaxis assay showed that CCR7 ligands, macrophage inflammatory protein 3beta and secondary lymphoid-tissue chemokine significantly (P < 0.05) induced the migration of DCs when cocultured with apoptotic tumor cells.
  • The means to promote DC delivery to tumor and to nodal sites represent novel targets for the biological therapy of cancer.
  • [MeSH-minor] Animals. Chemokine CCL4. Chemokines, CC / pharmacology. Coculture Techniques. Female. Flow Cytometry. Lymph Nodes / drug effects. Lymph Nodes / immunology. Macrophage Inflammatory Proteins / pharmacology. Mice. Mice, Inbred C57BL. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptors, CCR1. Receptors, CCR7. Th1 Cells / immunology. Transduction, Genetic. Tumor Cells, Cultured. Ultraviolet Rays

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  • (PMID = 10786686.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1PO1 CA73743-01; United States / NCI NIH HHS / CA / P01 CA59371
  • [Publication-type] 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 / Ccr1 protein, mouse; 0 / Ccr7 protein, mouse; 0 / Chemokine CCL4; 0 / Chemokines, CC; 0 / Macrophage Inflammatory Proteins; 0 / RNA, Messenger; 0 / Receptors, CCR1; 0 / Receptors, CCR7; 0 / Receptors, Chemokine
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16. Allison AC, Eugui EM: Mycophenolate mofetil and its mechanisms of action. Immunopharmacology; 2000 May;47(2-3):85-118
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  • This is the rate-limiting enzyme in de novo synthesis of guanosine nucleotides.
  • T- and B-lymphocytes are more dependent on this pathway than other cell types are.
  • Moreover, MPA is a fivefold more potent inhibitor of the type II isoform of IMPDH, which is expressed in activated lymphocytes, than of the type I isoform of IMPDH, which is expressed in most cell types.
  • MPA has therefore a more potent cytostatic effect on lymphocytes than on other cell types.
  • Three other mechanisms may also contribute to the efficacy of MPA in preventing allograft rejection and other applications.
  • Second, by depleting guanosine nucleotides, MPA suppresses glycosylation and the expression of some adhesion molecules, thereby decreasing the recruitment of lymphocytes and monocytes into sites of inflammation and graft rejection.
  • MPA therefore suppresses the production by iNOS of NO, and consequent tissue damage mediated by peroxynitrite.
  • CellCept(R) suppresses T-lymphocytic responses to allogeneic cells and other antigens.
  • The drug also suppresses primary, but not secondary, antibody responses.
  • The efficacy of regimes including CellCept(R) in preventing allograft rejection, and in the treatment of rejection, is now firmly established.
  • CellCept(R) is also efficacious in several experimental animal models of chronic rejection, and it is hoped that the drug will have the same effect in humans.
  • [MeSH-major] Immunosuppressive Agents / pharmacology. Mycophenolic Acid / analogs & derivatives. Nitric Oxide Synthase / antagonists & inhibitors. Purines / antagonists & inhibitors. T-Lymphocytes / drug effects
  • [MeSH-minor] Animals. Autoimmune Diseases / drug therapy. Cell Adhesion Molecules / drug effects. Glycosylation / drug effects. Graft Rejection / drug therapy. Graft Rejection / prevention & control. Guanosine Monophosphate / biosynthesis. Humans. IMP Dehydrogenase / antagonists & inhibitors. Nitric Oxide Synthase Type II. Prodrugs / pharmacology. Prodrugs / therapeutic use

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  • (PMID = 10878285.001).
  • [ISSN] 0162-3109
  • [Journal-full-title] Immunopharmacology
  • [ISO-abbreviation] Immunopharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Immunosuppressive Agents; 0 / Prodrugs; 0 / Purines; 85-32-5 / Guanosine Monophosphate; 9242ECW6R0 / mycophenolate mofetil; EC 1.1.1.205 / IMP Dehydrogenase; EC 1.14.13.39 / NOS2 protein, human; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; HU9DX48N0T / Mycophenolic Acid
  • [Number-of-references] 150
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17. Black DM, Schwartz AV, Ensrud KE, Cauley JA, Levis S, Quandt SA, Satterfield S, Wallace RB, Bauer DC, Palermo L, Wehren LE, Lombardi A, Santora AC, Cummings SR, FLEX Research Group: Effects of continuing or stopping alendronate after 5 years of treatment: the Fracture Intervention Trial Long-term Extension (FLEX): a randomized trial. JAMA; 2006 Dec 27;296(24):2927-38
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  • [Title] Effects of continuing or stopping alendronate after 5 years of treatment: the Fracture Intervention Trial Long-term Extension (FLEX): a randomized trial.
  • CONTEXT: The optimal duration of treatment of women with postmenopausal osteoporosis is uncertain.
  • OBJECTIVE: To compare the effects of discontinuing alendronate treatment after 5 years vs continuing for 10 years.
  • PARTICIPANTS: One thousand ninety-nine postmenopausal women who had been randomized to alendronate in FIT, with a mean of 5 years of prior alendronate treatment.
  • MAIN OUTCOME MEASURES: The primary outcome measure was total hip bone mineral density (BMD); secondary measures were BMD at other sites and biochemical markers of bone remodeling.
  • Similarly, those discontinuing alendronate had increased serum markers of bone turnover compared with continuing alendronate: 55.6% (P<.001) for C-telopeptide of type 1 collagen, 59.5% (P < .001) for serum n = propeptide of type 1 collagen, and 28.1% (P<.001) for bone-specific alkaline phosphatase, but after 5 years without therapy, bone marker levels remained somewhat below pretreatment levels 10 years earlier.
  • CONCLUSIONS: Women who discontinued alendronate after 5 years showed a moderate decline in BMD and a gradual rise in biochemical markers but no higher fracture risk other than for clinical vertebral fractures compared with those who continued alendronate.


18. Minzenberg MJ, Carter CS: Modafinil: a review of neurochemical actions and effects on cognition. Neuropsychopharmacology; 2008 Jun;33(7):1477-502
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  • Modafinil (2-[(Diphenylmethyl) sulfinyl] acetamide, Provigil) is an FDA-approved medication with wake-promoting properties.
  • In addition, modafinil shows initial promise for a variety of off-label indications in psychiatry, including treatment-resistant depression, attention-deficit/hyperactivity disorder, and schizophrenia.
  • Cognitive dysfunction may be a particularly important emerging treatment target for modafinil, across these and other neuropsychiatric disorders.
  • Many of these effects may be secondary to catecholamine effects, with some selectivity for cortical over subcortical sites of action.
  • In addition, modafinil (at well-tolerated doses) improves function in several cognitive domains, including working memory and episodic memory, and other processes dependent on prefrontal cortex and cognitive control.
  • [MeSH-major] Benzhydryl Compounds / pharmacology. Brain Chemistry / drug effects. Cognition / drug effects. Neuroprotective Agents / pharmacology
  • [MeSH-minor] Animals. Humans. Mental Disorders / drug therapy


19. Zhou Q, Sherwin RP, Parrish C, Richters V, Groshen SG, Tsao-Wei D, Markland FS: Contortrostatin, a dimeric disintegrin from Agkistrodon contortrix contortrix, inhibits breast cancer progression. Breast Cancer Res Treat; 2000 Jun;61(3):249-60
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  • However, contortrostatin inhibits angiogenesis induced by the breast cancer, as shown by immunohistochemical quantitation of the vascular endothelial cells in tumor tissue removed from the nude mice.
  • We have identified alpha(v)beta3, an important integrin mediating cell motility and tumor invasion, as one of the binding sites of contortrostatin on MDA-MB-435 cells.
  • We conclude that contortrostatin blocks alpha(v)beta3, and perhaps other integrins, and thus inhibits in vivo progression.
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Division / drug effects. Disease Progression. Extracellular Matrix / metabolism. Extracellular Matrix Proteins / metabolism. Female. Humans. Lung Neoplasms / prevention & control. Lung Neoplasms / secondary. Mice. Mice, Inbred BALB C. Mice, Nude. Neovascularization, Pathologic / drug therapy. Tumor Cells, Cultured

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  • (PMID = 10966001.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA14089
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] NETHERLANDS
  • [Chemical-registry-number] 0 / Crotalid Venoms; 0 / Disintegrins; 0 / Extracellular Matrix Proteins; 0 / Receptors, Vitronectin; 0 / contortrostatin
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20. Nickerson HJ, Matthay KK, Seeger RC, Brodeur GM, Shimada H, Perez C, Atkinson JB, Selch M, Gerbing RB, Stram DO, Lukens J: Favorable biology and outcome of stage IV-S neuroblastoma with supportive care or minimal therapy: a Children's Cancer Group study. J Clin Oncol; 2000 Feb;18(3):477-86
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  • [Title] Favorable biology and outcome of stage IV-S neuroblastoma with supportive care or minimal therapy: a Children's Cancer Group study.
  • The purpose of this study was to evaluate outcome and prognostic factors in infants with stage IV-S neuroblastoma treated prospectively with supportive care only or, in symptomatic patients, with low-dose cytotoxic therapy.
  • PATIENTS AND METHODS: Eighty eligible infants were studied for response and survival with supportive care or, for symptomatic patients, cyclophosphamide 5 mg/kg/d for 5 days with or without hepatic radiation of 4.5 Gy over 3 days.
  • Supportive care was the only treatment provided for 44 (55%) of 80 infants, and their 5-year survival rate was 100%, compared with 81% survival for those requiring cytotoxic therapy for symptoms (P =.005).
  • The only other significant factor predictive for improved survival was favorable Shimada histopathologic classification.
  • Sites of metastatic involvement (liver, skin, or bone marrow) and surgical resection of the primary tumor were not significant for survival.
  • CONCLUSION: This study confirms the favorable biologic features and excellent survival of infants with stage IV-S neuroblastoma with minimal therapy.
  • Infants younger than 2 months old at diagnosis with rapidly progressive abdominal disease may benefit from earlier and more intensive treatment.
  • [MeSH-major] Neuroblastoma / pathology. Neuroblastoma / therapy. Palliative Care
  • [MeSH-minor] Adrenal Gland Neoplasms / pathology. Adrenal Gland Neoplasms / secondary. Adrenal Gland Neoplasms / therapy. Bone Marrow Neoplasms / secondary. Disease-Free Survival. Dose-Response Relationship, Drug. Humans. Infant. Liver Neoplasms / secondary. Neoplasm Staging. Prognosis. Prospective Studies. Skin Neoplasms / secondary. Treatment Outcome

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  • (PMID = 10653863.001).
  • [ISSN] 0732-183X
  • [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 / CA02649; United States / NCI NIH HHS / CA / CA13539; United States / NCI NIH HHS / CA / CA22794; etc
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
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21. Lee J, Dibble S, Dodd M, Abrams D, Burns B: The relationship of chemotherapy-induced nausea to the frequency of pericardium 6 digital acupressure. Oncol Nurs Forum; 2010 Nov;37(6):E419-25
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  • [Title] The relationship of chemotherapy-induced nausea to the frequency of pericardium 6 digital acupressure.
  • PURPOSE/OBJECTIVES: To explain the relationship between the intensity of chemotherapy-induced nausea (CIN) and the frequency of pericardium 6 (P6) digital acupressure.
  • DESIGN: Secondary data analysis of a multicenter, longitudinal, randomized, clinical trial.
  • SETTING: Nine community clinical oncology programs and six independent sites in the United States.
  • SAMPLE: 53 patients with breast cancer who received moderate to highly emetogenic chemotherapy and applied P6 digital acupressure in addition to antiemetics to control CIN.
  • METHODS: A daily log measuring nausea intensity and the frequency of acupressure for 11 days after the administration of chemotherapy.
  • Hierarchical generalized linear modeling procedure (multilevel negative binomial regression) was used for analyzing the data.
  • FINDINGS: Participants used acupressure an average of two times per day (SD = 1.84, range 0-10).
  • Women who used acupressure more frequently after the peak of nausea (on day 4) were predicted to have a 0.97-point higher nausea intensity in the acute phase than women who used acupressure less frequently, controlling for the effects of other variables in the model (incidence rate ratio = 1.52, p < 0.01).
  • CONCLUSIONS: Patients with breast cancer whose nausea intensity started higher from the acute phase continued to experience higher symptom intensity during the 11 days after chemotherapy administration and required more frequent acupressure even after the peak of nausea.
  • IMPLICATIONS FOR NURSING: Careful assessment and management of acute CIN with continuous monitoring and care of CIN in the delayed phase are important nursing issues in caring for patients receiving chemotherapy.
  • [MeSH-major] Acupressure / methods. Antineoplastic Agents / adverse effects. Breast Neoplasms / drug therapy. Nausea / chemically induced. Nausea / therapy
  • [MeSH-minor] Adult. Aged. Antiemetics / therapeutic use. Combined Modality Therapy. Female. Humans. Longitudinal Studies. Middle Aged. Oncology Nursing / methods. Pericardium

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  • (PMID = 21059575.001).
  • [ISSN] 1538-0688
  • [Journal-full-title] Oncology nursing forum
  • [ISO-abbreviation] Oncol Nurs Forum
  • [Language] eng
  • [Grant] United States / PHS HHS / / R01-84014; United States / NCI NIH HHS / CA / U10 CA 045809-15
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiemetics; 0 / Antineoplastic Agents
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22. Kaluza V, Rao DS, Said JW, de Vos S: Primary extranodal nasal-type natural killer/T-cell lymphoma of the brain: a case report. Hum Pathol; 2006 Jun;37(6):769-72
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  • [Title] Primary extranodal nasal-type natural killer/T-cell lymphoma of the brain: a case report.
  • Natural killer (NK)/T-cell lymphomas represent a rare type of lymphoma derived from either activated NK cells or, rarely, cytotoxic T cells.
  • Other than the nasal cavity and paranasal sinuses, several other extranodal sites of involvement have been reported, including the pharynx, gastrointestinal tract, and testis.
  • Although secondary involvement of the central nervous system has been reported, a convincing case of primary brain NK/T-cell lymphoma has not been previously reported.
  • Here, we report a case of primary brain lymphoma of NK/T-cell type with a characteristic phenotype expressing CD3epsilon, CD56, granzyme B, Epstein-Barr virus-encoded small nuclear RNAs, with germline T-cell receptor gene configuration, and showing an unusual intravascular component.
  • The lymphoma failed to respond to therapy and the patient eventually died after transfer to a hospice facility.
  • This unusual case highlights an unusual presentation of a rare disease entity and highlights the need for a better understanding of the biology and treatment of T-cell lymphomas.
  • [MeSH-minor] Antigens, CD3 / genetics. Antigens, CD3 / metabolism. Antigens, CD56 / genetics. Antigens, CD56 / metabolism. Antimetabolites, Antineoplastic / therapeutic use. DNA, Neoplasm / analysis. Enoxaparin / therapeutic use. Fatal Outcome. Fibrinolytic Agents / therapeutic use. Genes, T-Cell Receptor gamma / genetics. Granzymes. Humans. Magnetic Resonance Imaging. Male. Methotrexate / therapeutic use. Middle Aged. Pulmonary Embolism / complications. Pulmonary Embolism / drug therapy. RNA, Viral / metabolism. Serine Endopeptidases / genetics. Serine Endopeptidases / metabolism. Tomography, X-Ray Computed. Tumor Virus Infections / pathology

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  • (PMID = 16733220.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD3; 0 / Antigens, CD56; 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / Enoxaparin; 0 / Epstein-Barr virus encoded RNA 1; 0 / Fibrinolytic Agents; 0 / RNA, Viral; EC 3.4.21.- / GZMB protein, human; EC 3.4.21.- / Granzymes; EC 3.4.21.- / Serine Endopeptidases; YL5FZ2Y5U1 / Methotrexate
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23. Mustra DJ, Warren AJ, Wilcox DE, Hamilton JW: Preferential binding of human XPA to the mitomycin C-DNA interstrand crosslink and modulation by arsenic and cadmium. Chem Biol Interact; 2007 Jun 30;168(2):159-68
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  • DNA interstrand crosslinks are of particular interest as a form of DNA damage, since these lesions involve both strands of duplex DNA and present special challenges to the repair machinery, and mitomycin C (MMC) is one of several useful cancer chemotherapy drugs that induce these lesions.
  • Purified XPA and the minimal DNA-binding domain of XPA are both fully capable of preferentially binding to MMC-DNA interstrand crosslinks in the absence of other proteins from the NER complex.
  • Circular dichroism (CD) and gel shift assays were used to investigate XPA-DNA binding and to assess changes in secondary structure induced as a consequence of the interaction of XPA with model MMC-crosslinked and unmodified DNAs.
  • This change in conformation may be more important in recruiting other proteins into a competent NER complex at damaged sites than preferential binding per se.
  • [MeSH-minor] Circular Dichroism. Drug Interactions. Electrophoretic Mobility Shift Assay. Humans. Zinc Fingers

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  • (PMID = 17512921.001).
  • [ISSN] 0009-2797
  • [Journal-full-title] Chemico-biological interactions
  • [ISO-abbreviation] Chem. Biol. Interact.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / P42 ES07373; United States / NCI NIH HHS / CA / T32 CA09658
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / DNA Adducts; 0 / Xeroderma Pigmentosum Group A Protein; 00BH33GNGH / Cadmium; 50SG953SK6 / Mitomycin; N712M78A8G / Arsenic
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24. Reuter S, Prasad S, Phromnoi K, Kannappan R, Yadav VR, Aggarwal BB: Embelin suppresses osteoclastogenesis induced by receptor activator of NF-κB ligand and tumor cells in vitro through inhibition of the NF-κB cell signaling pathway. Mol Cancer Res; 2010 Oct;8(10):1425-36
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  • Most patients with cancer die not because of the tumor in the primary site, but because it has spread to other sites.
  • Receptor activator of NF-κB ligand (RANKL), a member of the tumor necrosis factor superfamily and an activator of the NF-κB signaling pathway, has emerged as a major mediator of bone loss, commonly associated with cancer and other chronic inflammatory diseases.
  • Thus, embelin, an inhibitor of RANKL-induced NF-κB activation has great potential as a therapeutic agent for osteoporosis and cancer-linked bone loss.

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  • [Cites] Endocrinology. 2001 Mar;142(3):1290-5 [11181547.001]
  • [Cites] Cancer. 2000 Jun 15;88(12 Suppl):2989-94 [10898342.001]
  • [Cites] Br J Cancer. 2001 Jul 6;85(1):78-84 [11437406.001]
  • [Cites] J Biol Chem. 2001 Aug 10;276(32):30499-503 [11408488.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11581-6 [11562486.001]
  • [Cites] Blood. 2001 Dec 15;98(13):3527-33 [11739153.001]
  • [Cites] Blood. 2002 Dec 15;100(13):4615-21 [12393684.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1436-40 [12684416.001]
  • [Cites] Nature. 2003 May 15;423(6937):337-42 [12748652.001]
  • [Cites] Nat Rev Genet. 2003 Aug;4(8):638-49 [12897775.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5438-45 [14500379.001]
  • [Cites] J Immunol. 2003 Nov 15;171(10):5547-53 [14607962.001]
  • [Cites] Blood. 2004 Apr 15;103(8):3175-84 [15070700.001]
  • [Cites] N Engl J Med. 2004 Apr 15;350(16):1655-64 [15084698.001]
  • [Cites] Nat Med. 2004 Jun;10(6):617-24 [15156202.001]
  • [Cites] Br J Haematol. 2004 Jul;126(2):192-201 [15238139.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10137-42 [15220474.001]
  • [Cites] J Biol Chem. 2004 Sep 3;279(36):37219-22 [15252035.001]
  • [Cites] Cancer Cell. 2004 Sep;6(3):203-8 [15380510.001]
  • [Cites] Apoptosis. 2004 Nov;9(6):677-90 [15505411.001]
  • [Cites] Chem Ber. 1972;105(2):614-24 [4645596.001]
  • [Cites] Indian J Physiol Pharmacol. 1977 Jan-Mar;21(1):31-9 [873589.001]
  • [Cites] Chemotherapy. 1994 Mar-Apr;40(2):109-13 [7510605.001]
  • [Cites] J Bone Miner Res. 1996 Feb;11(2):150-9 [8822338.001]
  • [Cites] Mol Pathol. 1997 Jun;50(3):132-7 [9292147.001]
  • [Cites] Genes Dev. 1997 Dec 15;11(24):3482-96 [9407039.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3540-5 [10097072.001]
  • [Cites] Yao Xue Xue Bao. 1963 Sep;10:578-80 [14082600.001]
  • [Cites] J Biol Chem. 2004 Dec 24;279(52):54841-8 [15485831.001]
  • [Cites] Clin Cancer Res. 2005 Jan 1;11(1):162-5 [15671541.001]
  • [Cites] J Exp Med. 2005 May 16;201(10):1677-87 [15897281.001]
  • [Cites] Int J Cancer. 2005 Aug 20;116(2):253-62 [15800904.001]
  • [Cites] J Mammary Gland Biol Neoplasia. 2005 Apr;10(2):169-80 [16025223.001]
  • [Cites] Immunol Rev. 2005 Dec;208:30-49 [16313339.001]
  • [Cites] Clin Cancer Res. 2006 Feb 15;12(4):1221-8 [16489077.001]
  • [Cites] J Biol Chem. 2006 Jun 9;281(23):15809-20 [16613848.001]
  • [Cites] Mol Pharmacol. 2007 Jan;71(1):209-19 [17028156.001]
  • [Cites] Nat Med. 2007 Jan;13(1):62-9 [17159986.001]
  • [Cites] Mol Pharmacol. 2007 Jun;71(6):1703-14 [17387141.001]
  • [Cites] J Biol Chem. 2007 Jun 15;282(24):17340-50 [17439942.001]
  • [Cites] J Am Dent Assoc. 2008 Jan;139(1):23-30 [18167381.001]
  • [Cites] Clin Exp Metastasis. 2008;25(2):119-29 [18064531.001]
  • [Cites] J Bone Miner Res. 2008 Jun;23(6):826-36 [18558816.001]
  • [Cites] Curr Opin Otolaryngol Head Neck Surg. 2008 Aug;16(4):325-30 [18626250.001]
  • [Cites] J Dent Educ. 2008 Aug;72(8):919-29 [18676801.001]
  • [Cites] J Musculoskelet Neuronal Interact. 2008 Jul-Sep;8(3):204-16 [18799853.001]
  • [Cites] Morphologie. 2008 Dec;92(299):162-70 [19019718.001]
  • [Cites] Mol Cancer Ther. 2009 Aug;8(8):2339-47 [19671767.001]
  • [Cites] J Cell Biol. 2000 Jan 24;148(2):333-42 [10648566.001]
  • [Cites] Cancer Treat Rev. 2001 Jun;27(3):165-76 [11417967.001]
  • (PMID = 20826545.001).
  • [ISSN] 1557-3125
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA091844; United States / NCI NIH HHS / CA / P01 CA124787; United States / NCI NIH HHS / CA / CA-124787-01A2; United States / NCI NIH HHS / CA / CA-16 672
  • [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 / Benzoquinones; 0 / Bone Density Conservation Agents; 0 / NF-kappa B; 0 / RANK Ligand; 0 / TNFSF11 protein, human; SHC6U8F5ER / embelin
  • [Other-IDs] NLM/ NIHMS233648; NLM/ PMC2974017
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25. Studeny M, Marini FC, Champlin RE, Zompetta C, Fidler IJ, Andreeff M: Bone marrow-derived mesenchymal stem cells as vehicles for interferon-beta delivery into tumors. Cancer Res; 2002 Jul 1;62(13):3603-8
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  • Molecules that physiologically control cell proliferation are often produced locally in tissues and are rapidly destroyed when they enter circulation.
  • This allows local effects while avoiding interference with other systems.
  • Unfortunately, it also limits the therapeutic use of these molecules via systemic delivery.
  • We here demonstrate that, for the purpose of anticancer therapy, bone marrow-derived mesenchymal stem cells (MSCs) can produce biological agents locally at tumor sites.
  • We show that the tumor microenvironment preferentially promotes the engraftment of MSCs as compared with other tissues.
  • [MeSH-major] Interferon-beta / physiology. Melanoma / therapy. Stem Cells / physiology
  • [MeSH-minor] Adenoviridae / genetics. Animals. Bone Marrow Cells / cytology. Bone Marrow Cells / metabolism. Bone Marrow Cells / physiology. Cell Communication / physiology. Cell Division / physiology. Coculture Techniques. Drug Carriers. Humans. Lung Neoplasms / pathology. Lung Neoplasms / secondary. Lung Neoplasms / therapy. Male. Mice. Mice, Nude. Transduction, Genetic. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12097260.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA49639; United States / NCI NIH HHS / CA / CA55164
  • [Publication-type] 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 / Drug Carriers; 77238-31-4 / Interferon-beta
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