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1. Knight LA, Di Nicolantonio F, Whitehouse P, Mercer S, Sharma S, Glaysher S, Johnson P, Cree IA: The in vitro effect of gefitinib ('Iressa') alone and in combination with cytotoxic chemotherapy on human solid tumours. BMC Cancer; 2004 Nov 23;4:83
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  • [Title] The in vitro effect of gefitinib ('Iressa') alone and in combination with cytotoxic chemotherapy on human solid tumours.
  • METHODS: In this study we have used a standardised ATP-based tumour chemosensitivity assay (ATP-TCA) to measure the activity of gefitinib alone or in combination with different cytotoxic drugs (cisplatin, gemcitabine, oxaliplatin and treosulfan) against a variety of solid tumours (n = 86), including breast, colorectal, oesophageal and ovarian cancer, carcinoma of unknown primary site, cutaneous and uveal melanoma, non-small cell lung cancer (NSCLC) and sarcoma.
  • To allow comparison between samples the IndexSUM was calculated based on the percentage tumour growth inhibition (TGI) at each test drug concentration (TDC).
  • CONCLUSION: The in vitro model suggests that gefitinib may have differential effects in response to concomitant cytotoxic chemotherapy with the agents tested during this study.
  • The mechanism involved may relate to the effect of TKIs on growth rate versus their effect on the ability of the cell to survive the stimulus to apoptosis produced by chemotherapy.
  • [MeSH-major] Busulfan / analogs & derivatives. Deoxycytidine / analogs & derivatives. Neoplasms / drug therapy. Quinazolines / pharmacology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenosine Triphosphate / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Squamous Cell / drug therapy. Cisplatin / administration & dosage. Colorectal Neoplasms / drug therapy. Drug Screening Assays, Antitumor / methods. Female. Humans. Melanoma / drug therapy. Neoplasms, Unknown Primary / drug therapy. Organoplatinum Compounds / administration & dosage. Ovarian Neoplasms / drug therapy. Sarcoma / drug therapy. Skin Neoplasms / drug therapy. Stomach Neoplasms / drug therapy. Uveal Neoplasms / drug therapy

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  • [Cites] Eur J Surg Oncol. 1993 Jun;19(3):242-9 [8314382.001]
  • [Cites] Pharmacol Ther. 1999 May-Jun;82(2-3):241-50 [10454201.001]
  • [Cites] Lancet. 1996 Apr 20;347(9008):1066-71 [8602056.001]
  • [Cites] Anticancer Drugs. 1996 Aug;7(6):630-5 [8913430.001]
  • [Cites] Anticancer Drugs. 1998 Jan;9(1):51-7 [9491792.001]
  • [Cites] Gynecol Oncol. 2000 May;77(2):258-63 [10785475.001]
  • [Cites] Biochem J. 2000 Oct 15;351 Pt 2:289-305 [11023813.001]
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4885-92 [11156248.001]
  • [Cites] Melanoma Res. 2001 Dec;11(6):601-9 [11725206.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2240-50 [11980995.001]
  • [Cites] Anticancer Drugs. 2002 Jul;13(6):625-30 [12172508.001]
  • [Cites] Oncologist. 2002;7 Suppl 4:16-24 [12202784.001]
  • [Cites] Oncologist. 2002;7 Suppl 4:31-9 [12202786.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5749-54 [12384534.001]
  • [Cites] J Clin Oncol. 2003 Jun 15;21(12):2237-46 [12748244.001]
  • [Cites] J Clin Oncol. 2003 Jul 15;21(14):2658-63 [12860941.001]
  • [Cites] JAMA. 2003 Oct 22;290(16):2149-58 [14570950.001]
  • [Cites] J Cell Physiol. 2004 Feb;198(2):259-68 [14603528.001]
  • [Cites] J Clin Oncol. 2004 Mar 1;22(5):777-84 [14990632.001]
  • [Cites] J Clin Oncol. 2004 Mar 1;22(5):785-94 [14990633.001]
  • [Cites] BMC Cancer. 2003 Jul 3;3:19 [12841853.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Nov 10;95(23):13513-8 [9811831.001]
  • [Cites] Br J Cancer. 1999 Mar;79(9-10):1487-93 [10188895.001]
  • [Cites] Cancer Res. 1995 Nov 15;55(22):5276-82 [7585588.001]
  • (PMID = 15560844.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 0 / Quinazolines; 04ZR38536J / oxaliplatin; 0W860991D6 / Deoxycytidine; 8L70Q75FXE / Adenosine Triphosphate; B76N6SBZ8R / gemcitabine; CO61ER3EPI / treosulfan; G1LN9045DK / Busulfan; Q20Q21Q62J / Cisplatin; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC535559
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2. Arora S, Gonzales IM, Hagelstrom RT, Beaudry C, Choudhary A, Sima C, Tibes R, Mousses S, Azorsa DO: RNAi phenotype profiling of kinases identifies potential therapeutic targets in Ewing's sarcoma. Mol Cancer; 2010;9:218
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  • [Title] RNAi phenotype profiling of kinases identifies potential therapeutic targets in Ewing's sarcoma.
  • With current treatments, significant number of patients relapse and survival is poor for those with metastatic disease.
  • As part of novel target discovery in Ewing's sarcoma, we applied RNAi mediated phenotypic profiling to identify kinase targets involved in growth and survival of Ewing's sarcoma cells.
  • RESULTS: Four Ewing's sarcoma cell lines TC-32, TC-71, SK-ES-1 and RD-ES were tested in high throughput-RNAi screens using a siRNA library targeting 572 kinases.
  • Knockdown of 25 siRNAs reduced the growth of all four Ewing's sarcoma cell lines in replicate screens.
  • Of these, 16 siRNA were specific and reduced proliferation of Ewing's sarcoma cells as compared to normal fibroblasts.
  • Secondary validation and preliminary mechanistic studies highlighted the kinases STK10 and TNK2 as having important roles in growth and survival of Ewing's sarcoma cells.
  • CONCLUSION: In summary, RNAi-based phenotypic profiling proved to be a powerful gene target discovery strategy, leading to successful identification and validation of STK10 and TNK2 as two novel potential therapeutic targets for Ewing's sarcoma.
  • [MeSH-major] RNA Interference. Sarcoma, Ewing / drug therapy
  • [MeSH-minor] Cell Division. Cell Line, Tumor. Humans. Phenotype. RNA, Small Interfering

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  • [Cites] Cancer Res. 2005 Oct 15;65(20):9226-35 [16230383.001]
  • [Cites] Adv Anat Pathol. 2005 Jul;12(4):212-20 [16096383.001]
  • [Cites] Curr Oncol Rep. 2006 Jul;8(4):310-5 [17254532.001]
  • [Cites] Nature. 2007 Apr 12;446(7137):815-9 [17429401.001]
  • [Cites] Cancer Lett. 2007 Aug 28;254(1):1-10 [17250957.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2366-74 [18381444.001]
  • [Cites] Anticancer Res. 2008 Mar-Apr;28(2A):825-32 [18507025.001]
  • [Cites] Breast Cancer Res. 2008;10(2):R36 [18435854.001]
  • [Cites] Curr Opin Oncol. 2008 Jul;20(4):412-8 [18525337.001]
  • [Cites] Oncology. 2008;74(3-4):198-206 [18714168.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16472-7 [18948591.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16484-9 [18948595.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16490-5 [18948597.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16478-83 [18948598.001]
  • [Cites] Mol Cancer Res. 2008 Dec;6(12):1937-45 [19074838.001]
  • [Cites] Ann Clin Lab Sci. 2009 Spring;39(2):160-6 [19429803.001]
  • [Cites] J Transl Med. 2009;7:43 [19519883.001]
  • [Cites] Mol Cancer Ther. 2009 Oct;8(10):2811-20 [19825801.001]
  • [Cites] PLoS One. 2009;4(10):e7608 [19859563.001]
  • [Cites] Mol Cancer Ther. 2009 Nov;8(11):3024-35 [19887553.001]
  • [Cites] Oncogene. 2009 Nov 19;28(46):4126-32 [19718047.001]
  • [Cites] Cancer Sci. 2009 Dec;100(12):2268-74 [19725836.001]
  • [Cites] J Clin Oncol. 1999 Jun;17(6):1809-14 [10561219.001]
  • [Cites] Nat Cell Biol. 1999 Dec;1(8):507-13 [10587647.001]
  • [Cites] Genes Cells. 2000 Jun;5(6):491-8 [10886374.001]
  • [Cites] Cancer Res. 2000 Sep 15;60(18):5134-42 [11016640.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Jun 8;284(2):470-7 [11394904.001]
  • [Cites] Oncogene. 2001 Jul 19;20(32):4365-72 [11466617.001]
  • [Cites] Br J Cancer. 2009 Jul 7;101(1):80-90 [19491900.001]
  • [Cites] Nat Methods. 2009 Aug;6(8):569-75 [19644458.001]
  • [Cites] Curr Treat Options Oncol. 2009 Apr;10(1-2):126-40 [19533369.001]
  • [Cites] World J Gastroenterol. 2009 Sep 7;15(33):4177-82 [19725153.001]
  • [Cites] Leukemia. 2009 Sep;23(9):1564-76 [19421227.001]
  • [Cites] Cancer Res. 2009 Sep 15;69(18):7140-50 [19738075.001]
  • [Cites] Appl Immunohistochem Mol Morphol. 2001 Sep;9(3):255-60 [11556754.001]
  • [Cites] Oncogene. 2002 May 9;21(20):3162-71 [12082631.001]
  • [Cites] N Engl J Med. 2003 Feb 20;348(8):694-701 [12594313.001]
  • [Cites] J Biol Chem. 2003 May 16;278(20):18221-8 [12639966.001]
  • [Cites] Mol Cell. 2003 Sep;12(3):627-37 [14527409.001]
  • [Cites] Curr Opin Mol Ther. 2004 Apr;6(2):136-40 [15195924.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2873-6 [15254055.001]
  • [Cites] Assay Drug Dev Technol. 2004 Aug;2(4):363-72 [15357917.001]
  • [Cites] J Biol Chem. 1993 May 5;268(13):9194-7 [8486620.001]
  • [Cites] FEBS Lett. 1996 May 20;386(2-3):230-4 [8647288.001]
  • [Cites] J Biol Chem. 1997 Sep 5;272(36):22679-84 [9278426.001]
  • [Cites] Trends Biochem Sci. 1998 Aug;23(8):301-6 [9757831.001]
  • [Cites] Immunogenetics. 1999 May;49(5):369-75 [10199912.001]
  • [Cites] Oncogene. 2005 Jan 10;24(2):287-91 [15640844.001]
  • [Cites] Curr Opin Pediatr. 2005 Feb;17(1):14-9 [15659957.001]
  • [Cites] Br J Cancer. 2005 Feb 28;92(4):705-10 [15685229.001]
  • [Cites] Oncogene. 2005 Apr 7;24(15):2512-24 [15735734.001]
  • [Cites] Nat Cell Biol. 2005 Jun;7(6):591-600 [15864305.001]
  • [Cites] Pharmacol Ther. 2006 Sep;111(3):974-84 [16603252.001]
  • (PMID = 20718987.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Small Interfering
  • [Other-IDs] NLM/ PMC2933621
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3. Davies AM, Ho C, Metzger AS, Beckett LA, Christensen S, Tanaka M, Lara PN, Lau DH, Gandara DR: Phase I study of two different schedules of bortezomib and pemetrexed in advanced solid tumors with emphasis on non-small cell lung cancer. J Thorac Oncol; 2007 Dec;2(12):1112-6
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  • [Title] Phase I study of two different schedules of bortezomib and pemetrexed in advanced solid tumors with emphasis on non-small cell lung cancer.
  • Tumor types included lung (n = 16), adenoid cystic carcinoma (n = 2), prostate (n = 2), sarcoma (n = 2), breast (n = 1), thymus (n = 1), head and neck (n = 1), and gastrointestinal(n = 2).
  • Of the 16 patients with non-small cell lung cancer, 2 (12.5%) had partial response and 9 had stable disease, for a disease control rate of 68.8%.
  • Based on the observed efficacy, a phase II study in non-small cell lung cancer is warranted.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / mortality. Lung Neoplasms / drug therapy. Lung Neoplasms / mortality
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Boronic Acids / administration & dosage. Boronic Acids / adverse effects. Bortezomib. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Glutamates / administration & dosage. Glutamates / adverse effects. Guanine / administration & dosage. Guanine / adverse effects. Guanine / analogs & derivatives. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Staging. Neoplasms / drug therapy. Neoplasms / mortality. Neoplasms / pathology. Pemetrexed. Pyrazines / administration & dosage. Pyrazines / adverse effects. Survival Analysis

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  • (PMID = 18090584.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Glutamates; 0 / Pyrazines; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; 69G8BD63PP / Bortezomib
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4. Rosti G, Ferrante P, Ledermann J, Leyvraz S, Ladenstein R, Koscileniak E, Crown J, Dazzi C, Cariello A, Marangolo M: High-dose chemotherapy for solid tumors: results of the EBMT. Crit Rev Oncol Hematol; 2002 Feb;41(2):129-40
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  • [Title] High-dose chemotherapy for solid tumors: results of the EBMT.
  • The European Group for Blood and Marrow Transplantation (EBMT), formerly known as European Group for Bone Marrow Transplantation, was established in 1974 in the Netherlands to share experiences, to promote research and clinical studies and to set up registries in the field of hematopoietic tissue transplantation.
  • At the present time more 400 European and non-European centers are members of the EBMT group.
  • In 1984 a new Working Party was created (Solid Tumors) with the aim to investigate the role of high-dose chemotherapy and stem cell support in the fields of adult and pediatric solid tumors.
  • By January 2000 more than 14000 patients were registered, and at the present time this Registry is the world largest database on this subject.
  • Several phase III randomized clinical trials have recently started on behalf of the Group in different diseases (breast carcinoma, small cell lung cancer, ovarian carcinoma, germ cell tumors and Ewing's family sarcoma).
  • Hundreds of randomized patients will finally produce clearer information on this still experimental therapeutic modality.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Neoplasms / drug therapy

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  • (PMID = 11856589.001).
  • [ISSN] 1040-8428
  • [Journal-full-title] Critical reviews in oncology/hematology
  • [ISO-abbreviation] Crit. Rev. Oncol. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 38
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5. Pedrazzoli P, Ledermann JA, Lotz JP, Leyvraz S, Aglietta M, Rosti G, Champion KM, Secondino S, Selle F, Ketterer N, Grignani G, Siena S, Demirer T, European Group for Blood and Marrow Transplantation (EBMT) Solid Tumors Working Party: High dose chemotherapy with autologous hematopoietic stem cell support for solid tumors other than breast cancer in adults. Ann Oncol; 2006 Oct;17(10):1479-88
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  • [Title] High dose chemotherapy with autologous hematopoietic stem cell support for solid tumors other than breast cancer in adults.
  • Since the early 1980s high dose chemotherapy with autologous hematopoietic stem cell support was adopted by many oncologists as a potentially curative option for solid tumors, supported by a strong rationale from laboratory studies and apparently convincing results of early phase II studies.
  • As a result, the number and size of randomized trials comparing this approach with conventional chemotherapy initiated (and often abandoned before completion) to prove or disprove its value was largely insufficient.
  • In fact, with the possible exception of breast carcinoma, the benefit of a greater escalation of dose of chemotherapy with stem cell support in solid tumors is still unsettled and many oncologists believe that this approach should cease.
  • In this article, we critically review and comment on the data from studies of high dose chemotherapy so far reported in adult patients with small cell lung cancer, ovarian cancer, germ cell tumors and sarcomas.

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  • (PMID = 16547069.001).
  • [ISSN] 0923-7534
  • [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; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 96
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6. Nieboer P, de Vries EG, Mulder NH, van der Graaf WT: Relevance of high-dose chemotherapy in solid tumours. Cancer Treat Rev; 2005 May;31(3):210-25
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  • [Title] Relevance of high-dose chemotherapy in solid tumours.
  • Drug resistance is a major problem in the treatment of solid tumours.
  • Based on a steep dose-response relationship for especially alkylating agents on tumour cell survival, high-dose chemotherapy was considered of interest for the treatment of solid tumours.
  • Results of phase 1 and 2 studies with high-dose chemotherapy in a variety of tumour types showed good response rates.
  • Nowadays, several phase 3 studies are available especially in metastatic and high-risk breast cancer patients.
  • The high expectations of high-dose chemotherapy did not come true.
  • This review analyses results of randomised studies and comments on the discrepancy between findings in patients versus those in tissue culture.
  • Potential factors involved are the presence of tumour stem cells with different characteristics from more mature tumour cells, limitations in drug escalation in the clinic, transplant mortality, trial design and tumour cell contamination of the haematopoietic stem cell transplant.
  • Maturation of the results from recent studies indicating a more modest benefit in, e.g., adjuvant breast cancer balanced versus long-term side effects will ultimately determine the role of high-dose chemotherapy in certain solid tumours.
  • In case of well-defined indications for high-dose chemotherapy, further selection of patients based on patient and tumour characteristics as well as the introduction of new agents will most likely play a role.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / adverse effects. Neoplasms / drug therapy
  • [MeSH-minor] Bone Neoplasms / drug therapy. Breast Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Small Cell / drug therapy. Drug Administration Schedule. Female. Germinoma / drug therapy. Humans. Lung Neoplasms / drug therapy. Ovarian Neoplasms / drug therapy. Randomized Controlled Trials as Topic. Salvage Therapy / methods. Sarcoma / drug therapy. Sarcoma, Ewing / drug therapy. Treatment Outcome

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  • (PMID = 15944050.001).
  • [ISSN] 0305-7372
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 101
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7. Maki RG: Small is beautiful: insulin-like growth factors and their role in growth, development, and cancer. J Clin Oncol; 2010 Nov 20;28(33):4985-95
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  • [Title] Small is beautiful: insulin-like growth factors and their role in growth, development, and cancer.
  • Interest of the role of insulin-like growth factors in cancer reached a peak in the 1990s, and then waned until the availability in the past 5 years of monoclonal antibodies and small molecules that block the insulin-like growth factor 1 receptor.
  • Recent developments regarding phase I to II clinical trials of such agents are discussed, as well as potential studies to consider in the future, given the lack of efficacy of one such monoclonal antibody in combination with cytotoxic chemotherapy in a first-line study in metastatic non-small-cell lung adenocarcinoma.
  • Greater success with these agents clinically is expected when combining the agents with inhibitors of other cell signaling pathways in which cross-resistance has been observed.
  • [MeSH-minor] Animals. Clinical Trials as Topic. Humans. Insulin / physiology. Insulin-Like Growth Factor Binding Proteins / physiology. Longevity. Receptor, IGF Type 1 / antagonists & inhibitors. Receptor, IGF Type 1 / physiology. Sarcoma / etiology. Signal Transduction

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  • [Cites] Eur J Endocrinol. 2010 Feb;162(2):249-57 [19917654.001]
  • [Cites] Sci Signal. 2010;3(108):ra10 [20145208.001]
  • [Cites] Breast Cancer Res Treat. 2010 Apr;120(2):327-35 [19337828.001]
  • [Cites] Cell. 2010 Apr 2;141(1):69-80 [20371346.001]
  • [Cites] Mol Cancer Ther. 2010 May;9(5):1286-97 [20457621.001]
  • [Cites] J Pathol. 2010 Jul;221(3):300-7 [20527023.001]
  • [Cites] Proc Natl Acad Sci U S A. 2010 Jun 15;107(24):11122-7 [20534466.001]
  • [Cites] Cancer Res. 2010 Aug 15;70(16):6412-9 [20710042.001]
  • [Cites] Clin Cancer Res. 2010 Sep 15;16(18):4654-65 [20670944.001]
  • [Cites] Cell Res. 2001 Jun;11(2):107-15 [11453542.001]
  • [Cites] Growth Horm IGF Res. 2001 Oct;11(5):289-97 [11735247.001]
  • [Cites] Cancer. 2001 Dec 1;92(11):2941-7 [11753970.001]
  • [Cites] J Natl Cancer Inst. 2001 Dec 19;93(24):1852-7 [11752009.001]
  • [Cites] J Natl Cancer Inst. 2002 Mar 20;94(6):454-60 [11904318.001]
  • [Cites] J Natl Cancer Inst. 2002 Jul 17;94(14):1099-106 [12122101.001]
  • [Cites] J Endocrinol. 2002 Oct;175(1):33-40 [12379488.001]
  • [Cites] Cancer Res. 2002 Nov 1;62(21):6035-8 [12414625.001]
  • [Cites] Nature. 2003 Jan 9;421(6919):182-7 [12483226.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):3299-304 [12843179.001]
  • [Cites] Hum Pathol. 2003 Aug;34(8):803-8 [14506643.001]
  • [Cites] N Engl J Med. 2003 Dec 4;349(23):2211-22 [14657428.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Jan 30;314(1):83-8 [14715249.001]
  • [Cites] Nat Genet. 2004 Sep;36(9):958-60 [15314640.001]
  • [Cites] Biochem Biophys Res Commun. 2004 Aug 27;321(3):524-30 [15358139.001]
  • [Cites] Clin Cancer Res. 2004 Sep 15;10(18 Pt 1):6134-42 [15448000.001]
  • [Cites] Nature. 1976 Dec 9;264(5586):542-5 [1004590.001]
  • [Cites] J Biol Chem. 1978 Apr 25;253(8):2769-76 [632300.001]
  • [Cites] Acta Paediatr Scand Suppl. 1977;(270):15-25 [356516.001]
  • [Cites] FEBS Lett. 1983 Sep 5;161(1):117-21 [6350044.001]
  • [Cites] Am J Gastroenterol. 1985 Apr;80(4):266-9 [3984995.001]
  • [Cites] Annu Rev Physiol. 1985;47:443-67 [2986538.001]
  • [Cites] FEBS Lett. 1985 Sep 9;189(1):115-8 [3896851.001]
  • [Cites] N Engl J Med. 1988 Dec 1;319(22):1434-40 [3185662.001]
  • [Cites] Clin Endocrinol (Oxf). 1990 Jan;32(1):65-71 [2331812.001]
  • [Cites] Clin Endocrinol (Oxf). 1990 Nov;33(5):593-603 [1701371.001]
  • [Cites] J Clin Invest. 1990 Dec;86(6):1806-14 [2174908.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Aug 30;179(1):579-85 [1715698.001]
  • [Cites] Cancer. 1991 Oct 15;68(8):1673-7 [1913507.001]
  • [Cites] J Biol Chem. 2005 May 20;280(20):19665-72 [15757893.001]
  • [Cites] Science. 2005 Sep 16;309(5742):1829-33 [16123266.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):11118-28 [16322262.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1500-8 [16452206.001]
  • [Cites] Genes Dev. 2006 Feb 1;20(3):267-75 [16452501.001]
  • [Cites] J Biol Chem. 2006 May 5;281(18):12743-50 [16517595.001]
  • [Cites] Mutat Res. 2006 Mar 20;595(1-2):117-24 [16448675.001]
  • [Cites] Mod Pathol. 2006 Jun;19(6):788-96 [16575403.001]
  • [Cites] Clin Cancer Res. 2006 Jun 1;12(11 Pt 1):3532-40 [16740780.001]
  • [Cites] Cancer Sci. 2006 Jul;97(7):597-604 [16827799.001]
  • [Cites] Nat Clin Pract Endocrinol Metab. 2006 Jul;2(7):395-407 [16932322.001]
  • [Cites] Cancer. 2006 Oct 15;107(8):1898-908 [16986125.001]
  • [Cites] Cancer Lett. 2007 Jan 8;245(1-2):69-74 [16458427.001]
  • [Cites] Nucleic Acids Res. 2007 Jan;35(Database issue):D237-40 [17135202.001]
  • [Cites] Mol Cancer Ther. 2007 Feb;6(2):667-74 [17308062.001]
  • [Cites] Clin Cancer Res. 2007 Mar 1;13(5):1438-44 [17332286.001]
  • [Cites] Growth Horm IGF Res. 2007 Feb;17(1):54-7 [17166755.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Apr 13;355(3):700-6 [17320820.001]
  • [Cites] J Pathol. 2007 Apr;211(5):550-4 [17299733.001]
  • [Cites] BMC Genomics. 2007;8:73 [17359542.001]
  • [Cites] Cancer Res. 2007 Apr 1;67(7):3431-40 [17409454.001]
  • [Cites] Science. 2007 Apr 6;316(5821):112-5 [17412960.001]
  • [Cites] Nat Med. 2007 Jun;13(6):748-53 [17496901.001]
  • [Cites] Arch Biochem Biophys. 2007 Sep 15;465(2):359-69 [17644060.001]
  • [Cites] Clin Cancer Res. 2007 Oct 1;13(19):5834-40 [17908976.001]
  • [Cites] Adv Exp Med Biol. 2007;612:104-18 [18161484.001]
  • [Cites] J Intern Med. 2008 Feb;263(2):179-91 [18226095.001]
  • [Cites] Endocrinology. 2008 Mar;149(3):1214-26 [18039785.001]
  • [Cites] FASEB J. 2008 Mar;22(3):807-18 [17928362.001]
  • [Cites] Cancer Res. 2008 Mar 1;68(5):1538-45 [18316619.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2007;72:483-8 [18419308.001]
  • [Cites] Clin Cancer Res. 2008 May 15;14(10):3204-15 [18483389.001]
  • [Cites] Front Biosci. 2008;13:3906-12 [18508484.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jun 17;105(24):8387-92 [18550829.001]
  • [Cites] Ann Oncol. 2008 Jul;19(7):1293-8 [18372285.001]
  • [Cites] Cell. 1992 Apr 3;69(1):119-28 [1555236.001]
  • [Cites] Nature. 1992 Oct 8;359(6395):554-6 [1406976.001]
  • [Cites] Cell. 1993 Oct 8;75(1):59-72 [8402901.001]
  • [Cites] J Intern Med. 1993 Dec;234(6):543-52 [7505031.001]
  • [Cites] J Endocrinol. 1993 Sep;138(3):545-54 [7506292.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2803-7 [8168113.001]
  • [Cites] Mol Cell Biol. 1994 Jul;14(7):4588-95 [8007963.001]
  • [Cites] EMBO J. 1994 Jul 15;13(14):3286-95 [8045259.001]
  • [Cites] Endocrinology. 1995 Apr;136(4):1635-41 [7895674.001]
  • [Cites] J Biol Chem. 1995 Jun 9;270(23):13589-92 [7539790.001]
  • [Cites] Nat Genet. 1995 Jun;10(2):196-201 [7663515.001]
  • [Cites] Cancer Res. 1996 Apr 1;56(7):1545-50 [8603400.001]
  • [Cites] J Biol Chem. 1996 Aug 9;271(32):19304-9 [8702614.001]
  • [Cites] Pediatr Res. 1996 Jun;39(6):992-8 [8725260.001]
  • [Cites] J Neurosurg. 1996 Oct;85(4):634-41 [8814167.001]
  • [Cites] J Clin Invest. 1996 Dec 1;98(11):2612-5 [8958225.001]
  • [Cites] Semin Oncol. 1997 Aug;24(4 Suppl 10):S10-3-S10-10 [9275000.001]
  • [Cites] Science. 1998 Jan 23;279(5350):563-6 [9438850.001]
  • [Cites] Lancet. 1998 May 9;351(9113):1393-6 [9593409.001]
  • [Cites] Blood Press. 1998 May;7(2):89-95 [9657535.001]
  • [Cites] Int Rev Cytol. 1998;183:1-94 [9666565.001]
  • [Cites] Clin Cancer Res. 1998 Oct;4(10):2383-90 [9796969.001]
  • [Cites] J Natl Cancer Inst. 1999 Apr 7;91(7):620-5 [10203281.001]
  • [Cites] J Lab Clin Med. 1957 Jun;49(6):825-36 [13429201.001]
  • [Cites] Mol Cell Endocrinol. 2005 Jan 14;229(1-2):149-60 [15607539.001]
  • [Cites] Endocrinology. 2005 Feb;146(2):851-60 [15498882.001]
  • [Cites] Clin Cancer Res. 2005 Feb 15;11(4):1563-71 [15746061.001]
  • [Cites] J Clin Oncol. 2005 Mar 20;23(9):1803-10 [15677699.001]
  • [Cites] Cancer Res. 2005 May 1;65(9):3868-76 [15867386.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3196-203 [18474873.001]
  • [Cites] PLoS One. 2008;3(7):e2578 [18596909.001]
  • [Cites] Nature. 2008 Jul 17;454(7202):345-9 [18528331.001]
  • [Cites] Cell. 2008 Aug 8;134(3):405-15 [18674809.001]
  • [Cites] Mol Cancer Ther. 2008 Sep;7(9):2589-98 [18765823.001]
  • [Cites] J Endocrinol. 2008 Oct;199(1):69-80 [18653623.001]
  • [Cites] Cancer Res. 2008 Oct 1;68(19):8039-48 [18829562.001]
  • [Cites] Cell Cycle. 2008 Oct;7(19):3098-103 [18802403.001]
  • [Cites] Ann Oncol. 2008 Nov;19(11):1860-9 [18641009.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2008 Aug;22(4):639-57 [18971124.001]
  • [Cites] J Pathol. 2008 Dec;216(4):428-39 [18855347.001]
  • [Cites] Cancer Cell. 2008 Dec 9;14(6):447-57 [19061836.001]
  • [Cites] J Pathol. 2009 Mar;217(4):469-82 [19148905.001]
  • [Cites] FEBS J. 2009 Mar;276(5):1221-32 [19175674.001]
  • [Cites] Pediatr Dev Pathol. 2009 Mar-Apr;12(2):127-35 [18788888.001]
  • [Cites] Nature. 2009 Apr 9;458(7239):725-31 [19279572.001]
  • [Cites] Nature. 2009 Apr 23;458(7241):1056-60 [19262508.001]
  • [Cites] Anticancer Res. 2009 Apr;29(4):1131-5 [19414355.001]
  • [Cites] Curr Oncol Rep. 2009 Jul;11(4):307-13 [19508836.001]
  • [Cites] Nat Rev Endocrinol. 2009 Jul;5(7):367-73 [19455179.001]
  • [Cites] Mod Pathol. 2009 Jul;22(7):914-21 [19407853.001]
  • [Cites] Nature. 2009 Jul 16;460(7253):392-5 [19587680.001]
  • [Cites] Semin Oncol. 2009 Aug;36(4):338-46 [19664494.001]
  • [Cites] Science. 2009 Oct 2;326(5949):140-4 [19797661.001]
  • [Cites] Lancet. 2009 Oct 3;374(9696):1196-208 [19801098.001]
  • [Cites] PLoS One. 2009;4(10):e7273 [19806209.001]
  • [Cites] Endocr Regul. 2009 Oct;43(4):149-55 [19908933.001]
  • [Cites] Eur J Hum Genet. 2009 Dec;17(12):1668-75 [19491931.001]
  • [Cites] J Clin Oncol. 2009 Dec 1;27(34):5800-7 [19786654.001]
  • [Cites] Hum Pathol. 1999 Oct;30(10):1128-33 [10534157.001]
  • [Cites] J Cell Physiol. 2000 Apr;183(1):1-9 [10699960.001]
  • [Cites] J Clin Endocrinol Metab. 2000 Apr;85(4):1598-600 [10770203.001]
  • [Cites] Biochem Pharmacol. 2000 Oct 15;60(8):1101-7 [11007947.001]
  • [Cites] J Biol Chem. 2000 Oct 27;275(43):33607-13 [10874028.001]
  • [Cites] J Clin Oncol. 2001 Jun 15;19(12):3091-102 [11408506.001]
  • (PMID = 20975071.001).
  • [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 / CA148260; United States / NCI NIH HHS / CA / RC2 CA148260; United States / NCI NIH HHS / CM / CM62202; United States / NCI NIH HHS / CA / CA47179; United States / NCI NIH HHS / CA / N01CM62202; United States / NCI NIH HHS / CA / P01 CA047179
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Insulin; 0 / Insulin-Like Growth Factor Binding Proteins; 0 / Somatomedins; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Other-IDs] NLM/ PMC3039924
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8. Sabbatini P, Rowand JL, Groy A, Korenchuk S, Liu Q, Atkins C, Dumble M, Yang J, Anderson K, Wilson BJ, Emmitte KA, Rabindran SK, Kumar R: Antitumor activity of GSK1904529A, a small-molecule inhibitor of the insulin-like growth factor-I receptor tyrosine kinase. Clin Cancer Res; 2009 May 1;15(9):3058-67
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  • [Title] Antitumor activity of GSK1904529A, a small-molecule inhibitor of the insulin-like growth factor-I receptor tyrosine kinase.
  • PURPOSE: Dysregulation of the insulin-like growth factor-I receptor (IGF-IR) signaling pathway has been implicated in the development of many types of tumors, including prostate, colon, breast, pancreatic, ovarian, and sarcomas.
  • Agents that inhibit IGF-IR activity may be useful in treatment of patients with various cancers.
  • EXPERIMENTAL DESIGN: Kinase assays were used to identify a selective small-molecule inhibitor of IGF-IR activity.
  • The effects of this compound on IGF-IR signaling, cell proliferation, and the cell cycle were determined using a panel of cell lines.
  • GSK1904529A blocks receptor autophosphorylation and downstream signaling, leading to cell cycle arrest.
  • It inhibits the proliferation of cell lines derived from solid and hematologic malignancies, with multiple myeloma and Ewing's sarcoma cell lines being most sensitive.
  • CONCLUSION: GSK1904529A is a promising candidate for therapeutic use in IGF-IR-dependent tumors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Imidazoles / pharmacology. Protein Kinase Inhibitors / pharmacology. Pyridines / pharmacology. Receptor, IGF Type 1 / antagonists & inhibitors
  • [MeSH-minor] 3-Hydroxybutyric Acid / metabolism. Animals. Apoptosis / drug effects. Blood Glucose / metabolism. Blotting, Western. Cell Cycle / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Enzyme-Linked Immunosorbent Assay. Female. Flow Cytometry. Humans. Male. Mice. Mice, Nude. Neoplasms / drug therapy. Neoplasms / metabolism. Neoplasms / pathology. Phosphorylation / drug effects. Receptor, Insulin / antagonists & inhibitors. Receptor, Insulin / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 19383820.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Blood Glucose; 0 / GSK1904529A; 0 / Imidazoles; 0 / Protein Kinase Inhibitors; 0 / Pyridines; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptor, Insulin; TZP1275679 / 3-Hydroxybutyric Acid
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9. Fizazi K, Zelek L: Is òne cycle every three or four weeks' obsolete? A critical review of dose-dense chemotherapy in solid neoplasms. Ann Oncol; 2000 Feb;11(2):133-49
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  • [Title] Is òne cycle every three or four weeks' obsolete? A critical review of dose-dense chemotherapy in solid neoplasms.
  • BACKGROUND: Shortening the interval between cycles is one means of increasing the dose intensity of chemotherapy, and can be supported by biological and mathematical rationales.
  • Our objective was to assess the clinical relevance of the rapid repetition of regimens (so-called 'dose-dense chemotherapy') in various solid neoplasms.
  • Randomised studies comparing frequently-repeated chemotherapy to standard regimens as well as open studies are described and critically examined.
  • In small-cell lung cancer, survival of patients receiving dose-dense regimens was better than that of patients treated by standard chemotherapy in three trials, two of which reached significance, when these intensive regimens allowed better dose intensity.
  • In poor-prognosis germ-cell tumors, a dose-dense regimen was not better than standard therapy, perhaps because of an excessively high toxicity-related death rate.
  • In early breast cancer, the one published randomized study in the adjuvant setting showed only a trend towards better disease-free survival in node-positive women receiving a weekly-repeated regimen.
  • No evidence of a benefit was provided in metastatic breast cancer.
  • In advanced colorectal cancer, evidence of an improvement in survival with weekly or bi-weekly 5-FU-leucovorin compared to a classic monthly schedule has recently been shown in two randomized trials, and dose-dense regimens are recognized as standard therapy in many countries.
  • Phase II studies of dose-dense regimens have also shown high response rates and long survival in many neoplasms, including Ewing's sarcoma, gestational trophoblastic disease, ovarian carcinoma and gastric cancer.
  • A few randomized trials have demonstrated a benefit for survival on standard chemotherapy in small-cell lung cancer and advanced colorectal cancer.
  • The combination of dose-dense chemotherapy regimens with new anti-cancer strategies based on our insights into the mechanisms of oncogenesis is a challenge on the eve of the millennium.

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  • (PMID = 10761747.001).
  • [ISSN] 0923-7534
  • [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; Review
  • [Publication-country] England
  • [Number-of-references] 139
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10. Balasubramanian L, Evens AM: Targeting angiogenesis for the treatment of sarcoma. Curr Opin Oncol; 2006 Jul;18(4):354-9
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  • [Title] Targeting angiogenesis for the treatment of sarcoma.
  • PURPOSE OF REVIEW: More therapeutic options are needed for bone and soft tissue sarcomas, especially for patients with metastatic disease.
  • Recent randomized clinical trials conducted in colon, breast and lung cancer have shown the anti-vascular endothelial growth factor agent, bevacizumab, alone or in combination with chemotherapy, improves response and survival.
  • Preclinical studies have demonstrated the anti-tumor effects of varied anti-angiogenic agents in sarcoma cell lines and tumor models.
  • RECENT FINDINGS: Preclinical studies in sarcomas have evaluated the role of targeted agents including platelet-derived growth factor, matrix metalloproteinases, urokinase receptor and varied small-molecule tyrosine kinase inhibitors.
  • Novel angiogenesis inhibitors are being studied in the treatment of sarcoma, including monoclonal antibodies against vascular endothelial growth factor, cis- and trans-retinoic acids, thalidomide, and tyrosine kinase inhibitors.
  • Phase I, II and III clinical trials continue to evaluate these agents alone, in combinations together and combined with standard chemotherapy.
  • We review herein the preclinical rationale and clinical trial results of anti-angiogenesis therapy in the treatment of soft tissue and bone sarcoma.
  • SUMMARY: Preclinical mechanistic study and clinical trials are continuing in order to evaluate the therapeutic role and ultimately validate the efficacy of the varied anti-angiogenesis agents in soft tissue and bone sarcoma.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neovascularization, Pathologic. Sarcoma / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / chemistry. Clinical Trials as Topic. Humans. Protein-Tyrosine Kinases / antagonists & inhibitors. Sarcoma, Kaposi / metabolism. Thalidomide / metabolism. Tretinoin / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 16721130.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Vascular Endothelial Growth Factor A; 4Z8R6ORS6L / Thalidomide; 5688UTC01R / Tretinoin; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 63
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11. Cattel L, Ceruti M, Dosio F: From conventional to stealth liposomes: a new frontier in cancer chemotherapy. Tumori; 2003 May-Jun;89(3):237-49
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] From conventional to stealth liposomes: a new frontier in cancer chemotherapy.
  • Many attempts have been made to achieve good selectivity to targeted tumor cells by preparing specialized carrier agents that are therapeutically profitable for anticancer therapy.
  • Among these, liposomes are the most studied colloidal particles thus far applied in medicine and in particular in antitumor therapy.
  • Although they were first described in the 1960s, only at the beginning of 1990s did the first therapeutic liposomes appear on the market.
  • The first-generation liposomes (conventional liposomes) comprised a liposome-containing amphotericin B, Ambisome (Nexstar, Boulder, CO, USA), used as an antifungal drug, and Myocet (Elan Pharma Int, Princeton, NJ, USA), a doxorubicin-containing liposome, used in clinical trials to treat metastatic breast cancer.
  • The second-generation liposomes ("pure lipid approach") were long-circulating liposomes, such as Daunoxome, a daunorubicin-containing liposome approved in the US and Europe to treat AIDS-related Kaposi's sarcoma.
  • Actually, the only stealth liposome on the market is Caelyx/Doxil (Schering-Plough, Madison NJ, USA), used to cure AIDS-related Kaposi's sarcoma, resistant ovarian cancer and metastatic breast cancer.
  • Pegylated liposomal doxorubicin is characterized by a very long-circulation half-life, favorable pharmacokinetic behavior and specific accumulation in tumor tissues.
  • Active and cell targeted liposomes can be obtained by attaching some antigen-directed monoclonal antibodies (Moab or Moab fragments) or small proteins and molecules (folate, epidermal growth factor, transferrin) to the distal end of polyethylene glycol in pegylated liposomal doxorubicin.
  • The most promising therapeutic application of liposomes is as non-viral vector agents in gene therapy, characterized by the use of cationic phospholipids complexed with the negatively charged DNA plasmid.
  • The use of liposome formulations in local-regional anticancer therapy is also discussed.
  • Finally, pegylated liposomal doxorubicin containing radionuclides are used in clinical trials as tumor-imaging agents or in positron emission tomography.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Delivery Systems. Neoplasms / drug therapy

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  • (PMID = 12908776.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Liposomes; 30IQX730WE / Polyethylene Glycols
  • [Number-of-references] 121
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12. Tejada-Berges T, Granai CO, Gordinier M, Gajewski W: Caelyx/Doxil for the treatment of metastatic ovarian and breast cancer. Expert Rev Anticancer Ther; 2002 Apr;2(2):143-50
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  • [Title] Caelyx/Doxil for the treatment of metastatic ovarian and breast cancer.
  • This, coupled with a small vesicular size, uniquely promotes the localization of Caelyx/Doxil at tumor sites and explains its altered toxicity profile.
  • The FDA and EMEA have approved its use for the treatment of AIDS-related Kaposi's sarcoma and, more recently, for recurrent epithelial ovarian cancer (EOC).
  • Numerous investigations have focused on its use in the treatment of metastatic breast cancer, as well as recurrent squamous cell cervical carcinoma, soft tissue sarcoma, squamous head and neck cancers, prostate cancers and malignant gliomas.
  • Ongoing clinical studies of combination regimens incorporating Caelyx/Doxil will further clarify its role in the treatment of advanced solid tumors.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Breast Neoplasms / drug therapy. Doxorubicin / administration & dosage. Ovarian Neoplasms / drug therapy
  • [MeSH-minor] Animals. Clinical Trials as Topic / methods. Clinical Trials as Topic / statistics & numerical data. Female. Humans. Neoplasm Recurrence, Local / drug therapy


13. Ferrucci PF, Martinoni A, Cocorocchio E, Civelli M, Cinieri S, Cardinale D, Peccatori FA, Lamantia G, Agazzi A, Corsini C, Tealdo F, Fiorentini C, Cipolla CM, Martinelli G: Evaluation of acute toxicities associated with autologous peripheral blood progenitor cell reinfusion in patients undergoing high-dose chemotherapy. Bone Marrow Transplant; 2000 Jan;25(2):173-7

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of acute toxicities associated with autologous peripheral blood progenitor cell reinfusion in patients undergoing high-dose chemotherapy.
  • Peripheral blood progenitor cell reinfusion (PBPC) in patients undergoing high-dose chemotherapy (HDC) for poor prognosis malignancies, has been described as causing possible acute gastrointestinal (nausea, vomiting), allergic (oedema, bronchospasm, anaphyl- axis), renal (proteinuria, haematuria) and/or cardiovascular (hypotension, arrhythmia, conduction disturbances, transient ischaemic phenomena) toxicities.
  • To establish the clinical relevance of these observations and the possible relationship with different HDC regimens used, we performed a clinical and instrumental evaluation on 33 patients with advanced breast cancer, non-Hodgkin's lymphoma, Hodgkin's disease, relapsed ovarian cancer, Ewing's sarcoma, extragonadal germinal tumour and small cell lung cancer.
  • To evaluate cardiovascular function, we continuously monitored 12-lead ECGs, with arterial pressure (AP) measurements every 5 min from the beginning of the procedure to 15 min after the reinfusion ended.
  • We did not observe any significant differences between basal and subsequent steps in AP, heart rate, PQ and QTc time, P wave and QRS complex duration or P wave and QRS electrical axes.
  • No patient showed any ST-T tract pathological abnormality, but one patient developed a transient ectopic atrial rhythm, without any haemodynamic disfunction and with spontaneous reversion to sinus rhythm.
  • In one patient a tonic-clonic seizure occurred during a vomiting episode, but no patient developed allergic or renal toxicities.
  • We conclude that PBPC reinfusion, if managed according to the procedure we propose in patients without organic impairment, is a safe procedure not associated either with increased risk of acute arrhythmias or ischaemic or significant systemic acute toxicities.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Hematopoietic Stem Cell Transplantation / adverse effects. Neoplasms / therapy

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  • [CommentIn] Bone Marrow Transplant. 2002 Mar;29(6):544 [11960281.001]
  • (PMID = 10673676.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
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14. Samantas E, Kalofonos H, Linardou H, Nicolaides C, Mylonakis N, Fountzilas G, Kosmidis P, Skarlos D: Phase II study of pegylated liposomal doxorubicin: inactive in recurrent small-cell lung cancer. A Hellenic Cooperative Oncology Group Study. Ann Oncol; 2000 Nov;11(11):1395-7
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  • [Title] Phase II study of pegylated liposomal doxorubicin: inactive in recurrent small-cell lung cancer. A Hellenic Cooperative Oncology Group Study.
  • PURPOSE: Although clinical experience with liposomal doxorubicin is still limited in solid tumours, single agent Caelyx (pegylated liposomal doxorubicin) treatment has shown promising results in AIDS-related Kaposi's sarcoma, metastatic breast and ovarian cancer and anecdotally in other solid tumours.
  • This is the first report of its use in small-cell lung cancer (SCLC).
  • PATIENTS AND METHODS: A total of 14 patients with recurrent SCLC who had not received prior treatment with doxorubicin, were accrued into this phase II study.
  • All patients had progressed or relapsed after first-line chemotherapy.
  • All but one had achieved objective responses to first-line treatment with median duration of five months (range 2-18 months) but half of them had experienced 'refractory' relapses (within 3-4 months).
  • Study treatment consisted of Caelyx 50 mg/m2 (1-hour i.v infusion every 4 weeks for 6 cycles).
  • The median number of cycles was 2 per patient, with 11 of 14 patients not completing 6 cycles of Caelyx treatment.
  • Overall, treatment was well tolerated with no episodes of grade 4 toxicity and only two episodes of grade 3 toxicities: one of thrombocytopenia and one of prolonged palmar-plantar erythrodysesthesia (PPE).

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  • (PMID = 11142478.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 80168379AG / Doxorubicin
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15. Hoogendoorn WE, Hollema H, van Boven HH, Bergman E, de Leeuw-Mantel G, Platteel I, Fles R, Nederlof PM, Mourits MJ, van Leeuwen FE, Comprehensive Cancer Centers TAMARISK-group: Prognosis of uterine corpus cancer after tamoxifen treatment for breast cancer. Breast Cancer Res Treat; 2008 Nov;112(1):99-108
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  • [Title] Prognosis of uterine corpus cancer after tamoxifen treatment for breast cancer.
  • Since only few, mostly small, studies have examined prognosis of uterine corpus cancer following tamoxifen, we conducted a large retrospective cohort study to further investigate this.
  • We examined histopathologic and immunohistochemical characteristics of 332 patients with uterine corpus cancer following breast cancer, according to tamoxifen use.
  • Our results can be applied when weighing risks and benefits of tamoxifen versus other hormonal agents used in the prevention and treatment of breast cancer.
  • [MeSH-major] Antineoplastic Agents, Hormonal / therapeutic use. Breast Neoplasms / drug therapy. Tamoxifen / therapeutic use. Uterine Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma, Clear Cell / chemically induced. Adenocarcinoma, Clear Cell / diagnosis. Adenocarcinoma, Clear Cell / mortality. Aged. Cohort Studies. Cystadenocarcinoma, Serous / chemically induced. Cystadenocarcinoma, Serous / diagnosis. Cystadenocarcinoma, Serous / mortality. Endometrial Neoplasms / chemically induced. Endometrial Neoplasms / diagnosis. Endometrial Neoplasms / mortality. Female. Follow-Up Studies. Humans. Immunoenzyme Techniques. Middle Aged. Neoplasm Staging. Neoplasms, Second Primary / chemically induced. Neoplasms, Second Primary / diagnosis. Prognosis. Retrospective Studies. Risk Factors. Sarcoma / chemically induced. Sarcoma / diagnosis. Sarcoma / mortality. Survival Rate

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  • (PMID = 18064567.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 094ZI81Y45 / Tamoxifen
  • [Investigator] Visser O; Damhuis RA; Louwman WJ; van Dijck JA; Westerman Y; Dirx MJ; Jansen-Landheer ML; de Munck L; Siesling S
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16. Susa M, Choy E, Yang C, Schwab J, Mankin H, Hornicek F, Duan Z: Multidrug resistance reversal agent, NSC77037, identified with a cell-based screening assay. J Biomol Screen; 2010 Mar;15(3):287-96
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  • [Title] Multidrug resistance reversal agent, NSC77037, identified with a cell-based screening assay.
  • The development of multidrug resistance (MDR) remains a significant obstacle in treating cancer patients with chemotherapy.
  • To identify small-molecule compounds that can reverse MDR, the authors used a cell-based screening assay with an MDR ovarian cancer cell line.
  • Incubating MDR cells with a sublethal concentration of paclitaxel in combination with each of 2000 small-molecule compounds from the National Cancer Institute Diversity Set Library, they identified NSC77037.
  • The cytotoxic activity of NSC77037 and the duration of its effect were evaluated in vitro using a panel of cancer cell lines expressing permeability glycoprotein (Pgp), multiple drug resistance protein 1 (MRP 1), and breast cancer resistance protein (BCRP).
  • NSC77037, at a concentration of >10 microM, moderately inhibited the proliferation of both sensitive and resistant cell lines, but the inhibitory effect of NSC77037 was not altered by coincubation with the Pgp inhibitor verapamil, suggesting that NSC77037 itself is not a substrate of Pgp.
  • The use of NSC77037 to restore sensitivity to chemotherapy or to prevent resistance could be a potential treatment strategy for cancer patients.
  • [MeSH-major] Benzylisoquinolines / analysis. Benzylisoquinolines / pharmacology. Drug Resistance, Multiple / drug effects. Drug Resistance, Neoplasm / drug effects. Drug Screening Assays, Antitumor / methods
  • [MeSH-minor] Adenosine Triphosphatases / metabolism. Cell Line, Tumor. Fluoresceins / metabolism. Humans. P-Glycoprotein / metabolism. Paclitaxel / pharmacology. Substrate Specificity / drug effects. Time Factors. Verapamil / pharmacology

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  • (PMID = 20150589.001).
  • [ISSN] 1552-454X
  • [Journal-full-title] Journal of biomolecular screening
  • [ISO-abbreviation] J Biomol Screen
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01-CA119617
  • [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 / Benzylisoquinolines; 0 / Fluoresceins; 0 / P-Glycoprotein; 148504-34-1 / calcein AM; 29EX23D5AJ / tetrandrine; CJ0O37KU29 / Verapamil; EC 3.6.1.- / Adenosine Triphosphatases; P88XT4IS4D / Paclitaxel
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17. Korman DB, Mikaélian SG, Boronovskaia LE, Maslova IA: [Results of a phase I-II clinical trial of Emoxyl, a novel antineoplastic anthracycline]. Vopr Onkol; 2004;50(2):202-7
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  • The drug was given to 63 patients with different malignancies stages I-II.
  • Out of 55 cases evaluated for immediate effect, complete remission (breast cancer, small-cell cancer of the lung, Kaposi's sarcoma)--3; partial remission (breast cancer--2; non-Hodgkin's lymphoma--1)--3, and stabilization--26.
  • [MeSH-major] Anthracyclines / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Daunorubicin / analogs & derivatives. Daunorubicin / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Aged. Breast Neoplasms / drug therapy. Carcinoma, Small Cell / drug therapy. Drug Administration Schedule. Female. Humans. Lung Neoplasms / drug therapy. Lymphoma, Non-Hodgkin / drug therapy. Male. Middle Aged. Sarcoma, Kaposi / drug therapy. Treatment Outcome

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  • (PMID = 15176224.001).
  • [ISSN] 0507-3758
  • [Journal-full-title] Voprosy onkologii
  • [ISO-abbreviation] Vopr Onkol
  • [Language] rus
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 84412-94-2 / Emoxyl; ZS7284E0ZP / Daunorubicin
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18. Trabectedin: Ecteinascidin 743, Ecteinascidin-743, ET 743, ET-743, NSC 684766. Drugs R D; 2006;7(5):317-28
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  • The drug is being developed by PharmaMar (Zeltia) in partnership with Johnson & Johnson Pharmaceutical Research & Development LLC.
  • It was synthetically isolated and developed by the University of Illinois and licensed to PharmaMar; the company has completed the hemisynthesis of agent.
  • In this manner, it is thought that the drug affects various transcription factors involved in cell proliferation, particularly via the transcription-coupled nucleotide excision repair system.
  • Trabectedin blocks the cell cycle at the G(2) phase, while cells at the G(1 )phase are most sensitive to the drug.
  • It also inhibits overexpression of the multidrug resistance-1 gene (MDR-1) coding for the P-glycoprotein that is a major factor responsible for cells developing resistance to cancer drugs.
  • The agent is also thought to interfere with the nucleotide excision repair pathways of cancer cells, suggesting that it could be effective in the treatment of many cancer types including melanoma and sarcoma, as well as lung, breast, ovarian, endometrial and prostate cancers; clinical evaluations are underway in these indications.
  • Ortho Biotech will market the product in the US, Japan and the rest of the world; Tibotec Therapeutics (a division of Ortho Biotech) will commercialise it in the US.
  • PharmaMar will receive an initial payment from Ortho Biotech plus future milestone and royalty payments linked to development targets and sales; the upfront payment would be approximately 20 million US dollars with royalties contributing 10-20% of total sales of the drug.
  • Trabectedin is undergoing clinical trials in soft tissue sarcoma (Sarcoma in the Phase table), ovarian, breast, endometrial, prostate and non-small-cell lung cancers.
  • The US FDA granted trabectedin orphan drug status for ovarian cancer in April 2005.
  • Trabectedin also received orphan drug status from the European Commission for the treatment of ovarian cancer in October 2003.
  • Trabectedin has undergone a phase II study for the second- or third-line treatment of ovarian cancer in Europe (England and Belgium), the US and Canada.
  • A separate phase II trial evaluating the antitumour activity of trabectedin as a second-line therapy in advanced ovarian cancer was conducted by researchers at the Southern Europe New Drugs Organization (SENDO) in Milan, Italy.
  • PharmaMar and Johnson & Johnson are conducting a pivotal (STS-201) trial to compare a weekly and daily dosing regimen of trabectedin among patients with advanced or metastatic soft tissue sarcoma who are unresponsive to standard chemotherapy of doxorubicin and ifosfamide.
  • An independent data monitoring committee has found that interim data supports a positive trend in time to disease progression favouring patients receiving the daily dosing regimen.
  • PharmaMar has held a pre-submission meeting with the EMEA and has presented a formal letter of intent to file for approval of trabectedin for soft tissue sarcoma.
  • Previously, PharmaMar first filed for EU registration of trabectedin for treatment of advanced soft tissue sarcoma in November 2001, which was accepted for review by the EMEA and Swiss Health Authorities.
  • Trabectedin was granted orphan drug status in Europe for recurrent soft tissue sarcoma in 2001.
  • It was also granted orphan drug status by the FDA for the same indication in October 2004.
  • Phase I studies are being conducted to evaluate trabectedin in combination with doxorubicin and liposomal doxorubicin for the treatment of soft tissue sarcoma.
  • PharmaMar is also conducting a phase I study of sequential paclitaxel followed by trabectedin in patients with soft tissue sarcoma.
  • At additional dose levels, patients with other tumour types will be enrolled to assess the antitumour activity of the combination.
  • The US NCI has approved and is partially funding a phase I clinical programme to determine the feasibility of using trabectedin to treat children with soft tissue sarcoma and bone sarcoma who are resistant to conventional therapies.
  • Trabectedin has completed phase II studies for small round cell sarcoma and rhabdomyosarcoma, which are aggressive tumours occurring predominantly in children.
  • A phase II study evaluating two dosing schedules of trabectedin has been conducted in patients with leiomyosarcomas or liposarcomas refractory to standard doxorubicin + ifosfamide chemotherapy.
  • [MeSH-minor] Animals. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Humans. Randomized Controlled Trials as Topic. Sarcoma / drug therapy. Urochordata / chemistry

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  • (PMID = 16922593.001).
  • [ISSN] 1174-5886
  • [Journal-full-title] Drugs in R&D
  • [ISO-abbreviation] Drugs R D
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Dioxoles; 0 / Tetrahydroisoquinolines; 114899-77-3 / trabectedin
  • [Number-of-references] 56
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19. Schluep T, Hwang J, Cheng J, Heidel JD, Bartlett DW, Hollister B, Davis ME: Preclinical efficacy of the camptothecin-polymer conjugate IT-101 in multiple cancer models. Clin Cancer Res; 2006 Mar 1;12(5):1606-14
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  • Antitumor efficacy was further evaluated in mice bearing six different s.c. xenografts (LS174T and HT29 colorectal cancer, H1299 non-small-cell lung cancer, H69 small-cell lung cancer, Panc-1 pancreatic cancer, and MDA-MB-231 breast cancer) and one disseminated xenograft (TC71-luc Ewing's sarcoma).
  • In all cases, a single treatment cycle of three weekly doses of IT-101 resulted in a significant antitumor effect.
  • Complete tumor regression was observed in all animals bearing H1299 tumors and in the majority of animals with disseminated Ewing's sarcoma tumors.
  • Importantly, IT-101 is effective in a number of tumors that are resistant to treatment with irinotecan (MDA-MB-231, Panc-1, and HT29), consistent with the hypothesis that polymeric drug conjugates may be able to overcome certain kinds of multidrug resistance.
  • [MeSH-major] Camptothecin / therapeutic use. Cyclodextrins / chemistry. Disease Models, Animal. Polymers / chemistry. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Small Cell / drug therapy. Colorectal Neoplasms / drug therapy. Female. Humans. Lung Neoplasms / drug therapy. Mice. Mice, Nude. Nanotechnology. Pancreatic Neoplasms / drug therapy. Sarcoma, Ewing / drug therapy. Tumor Cells, Cultured

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  • (PMID = 16533788.001).
  • [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
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclodextrins; 0 / Polymers; XT3Z54Z28A / Camptothecin
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20. Mekhail TM, Markman M: Paclitaxel in cancer therapy. Expert Opin Pharmacother; 2002 Jun;3(6):755-66
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  • [Title] Paclitaxel in cancer therapy.
  • Paclitaxel promotes the polymerisation of tubulin, thereby causing cell death by disrupting the normal microtubule dynamics required for cell division and vital interphase processes.
  • Mechanisms of acquired resistance to paclitaxel include alterations of tubulin structure and the amplification of membrane phosphoglycoproteins that function as drug-efflux pumps.
  • Paclitaxel has activity against a broad band of tumour types, including breast, ovarian, lung, head and neck cancers.
  • Paclitaxel also has activity in other malignancies that are refractory to conventional chemotherapy, including previously-treated lymphoma and small cell lung cancers and oesophageal, gastric endometrial, bladder and germ cell tumours.
  • Paclitaxel is also active against AIDS-associated Kaposi's sarcoma.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Antineoplastic Agents, Phytogenic / therapeutic use. Paclitaxel / pharmacology. Paclitaxel / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Clinical Trials as Topic. Drug Administration Schedule. Drug Resistance, Neoplasm. Female. Head and Neck Neoplasms / drug therapy. Humans. Lung Neoplasms / drug therapy. Male. Ovarian Neoplasms / drug therapy

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  • (PMID = 12036415.001).
  • [ISSN] 1465-6566
  • [Journal-full-title] Expert opinion on pharmacotherapy
  • [ISO-abbreviation] Expert Opin Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; P88XT4IS4D / Paclitaxel
  • [Number-of-references] 106
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21. LaPlant KD, Louzon PD: Pazopanib: an oral multitargeted tyrosine kinase inhibitor for use in renal cell carcinoma. Ann Pharmacother; 2010 Jun;44(6):1054-60
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  • [Title] Pazopanib: an oral multitargeted tyrosine kinase inhibitor for use in renal cell carcinoma.
  • OBJECTIVE: To summarize the currently available clinical data on pazopanib, as well as review the merits and adverse effects of pazopanib in the treatment of renal cell carcinoma (RCC).
  • Phase 2 and 3 studies have shown promising activity in RCC, including treatment naïve or cytokine-pretreated patients, demonstrating a greater rate of total disease control with pazopanib compared to placebo.
  • Activity has also been shown in a variety of other cancers, including ovarian cancer, non-small-cell lung cancer, breast cancer, and soft tissue sarcoma.
  • Other Phase 3 trials are ongoing in RCC, including a comparison to sunitinib, another TKI used in RCC, as well as trials in other tumor types.
  • CONCLUSIONS: Current data suggest pazopanib to be a viable treatment option as first-line therapy for advanced RCC.
  • Until results of head-to-head trials conducted of the various agents are available, it cannot be said whether pazopanib is more tolerable or efficacious than currently available therapies.
  • [MeSH-major] Carcinoma, Renal Cell / drug therapy. Drug Delivery Systems / methods. Kidney Neoplasms / drug therapy. Protein Kinase Inhibitors / administration & dosage. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / administration & dosage. Sulfonamides / administration & dosage

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  • (PMID = 20407031.001).
  • [ISSN] 1542-6270
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Sulfonamides; 7RN5DR86CK / pazopanib; EC 2.7.10.1 / Protein-Tyrosine Kinases
  • [Number-of-references] 36
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22. Duan Z, Weinstein EJ, Ji D, Ames RY, Choy E, Mankin H, Hornicek FJ: Lentiviral short hairpin RNA screen of genes associated with multidrug resistance identifies PRP-4 as a new regulator of chemoresistance in human ovarian cancer. Mol Cancer Ther; 2008 Aug;7(8):2377-85
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  • Published reports implicate a variety of mechanisms that may contribute to drug resistance in ovarian cancer.
  • The chief aim of this study is to understand the relationship between overexpression of drug resistance associated genes and multidrug resistance in ovarian cancer.
  • Using lentiviral short hairpin RNA collections targeting 132 genes identified from transcriptional profiling of drug-resistant cancer cell lines, individual knockdown experiments were done in the presence of sublethal doses of paclitaxel.
  • These genes, when repressed, can reverse paclitaxel resistance in the multidrug-resistant cell line SKOV-3(TR) and OVCAR8(TR).
  • Both MDR1 and survivin have been reported previously to play a role in multidrug resistance and chemotherapy-induced apoptosis; however, the effect of PRP-4 expression on drug sensitivity is currently unrecognized.
  • PRP-4 belongs to the serine/threonine protein kinase family, plays a role in pre-mRNA splicing and cell mitosis, and interacts with CLK1.
  • Northern analysis shows that PRP-4 is overexpressed in several paclitaxel-resistant cell lines and confirms that PRP-4 expression could be significantly repressed by PRP-4 lentiviral short hairpin RNA.
  • Finally, overexpression of PRP-4 in drug-sensitive cells could induce a modest level of drug resistance to paclitaxel, doxorubicin, and vincristine.

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  • [Cites] Cancer Res. 1991 Nov 1;51(21):5903-9 [1657373.001]
  • [Cites] J Biol. 2003;2(4):27 [14527345.001]
  • [Cites] Cancer Res. 1993 Jan 1;53(1):16-8 [8416741.001]
  • [Cites] EMBO J. 1993 Feb;12(2):461-8 [8440237.001]
  • [Cites] Breast Cancer Res Treat. 1992;24(2):85-95 [8095168.001]
  • [Cites] Cancer Res. 1994 Feb 1;54(3):794-9 [8306343.001]
  • [Cites] J Cell Biol. 1994 Nov;127(3):609-22 [7525595.001]
  • [Cites] Biochemistry. 1995 Jan 10;34(1):32-9 [7819214.001]
  • [Cites] Br J Cancer. 1996 Oct;74(8):1263-8 [8883415.001]
  • [Cites] Nucleic Acids Res. 1997 Mar 1;25(5):1028-35 [9102632.001]
  • [Cites] Gene. 2004 Sep 29;340(1):53-9 [15556294.001]
  • [Cites] Cancer Chemother Pharmacol. 2005 Mar;55(3):277-85 [15565326.001]
  • [Cites] Cell. 2006 Mar 24;124(6):1283-98 [16564017.001]
  • [Cites] Trends Mol Med. 2007 Jan;13(1):4-11 [17118707.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):1988-96 [17332326.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4843-50 [17510414.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5831-9 [17575151.001]
  • [Cites] Cancer Res. 2007 Jul 15;67(14):6657-64 [17638875.001]
  • [Cites] Am J Clin Pathol. 2007 Sep;128(3):389-97 [17709312.001]
  • [Cites] Transgenic Res. 2007 Oct;16(5):571-80 [17682833.001]
  • [Cites] Genes Chromosomes Cancer. 2007 Dec;46(12):1069-79 [17726699.001]
  • [Cites] J Cell Biol. 2007 Nov 19;179(4):601-9 [17998396.001]
  • [Cites] Nat Rev Cancer. 2004 Sep;4(9):677-87 [15343274.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3445-53 [10589757.001]
  • [Cites] Biochem Biophys Res Commun. 1999 Dec 20;266(2):291-5 [10600495.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):E31-6 [10655601.001]
  • [Cites] Cell Mol Life Sci. 2001 Jun;58(7):931-59 [11497241.001]
  • [Cites] J Biol Chem. 2001 Aug 24;276(34):32247-56 [11418604.001]
  • [Cites] Cytokine. 2002 Mar 7;17(5):234-42 [12027404.001]
  • [Cites] Drug Resist Updat. 2002 Apr;5(2):65-72 [12135582.001]
  • [Cites] Anticancer Res. 2002 Jul-Aug;22(4):1933-41 [12174867.001]
  • [Cites] Curr Cancer Drug Targets. 2003 Feb;3(1):1-19 [12570657.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2200-5 [12727840.001]
  • [Cites] Mod Pathol. 2003 Jun;16(6):574-83 [12808063.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2778-85 [12855658.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7280-95 [14576838.001]
  • [Cites] Int J Gynecol Cancer. 2003 Nov-Dec;13(6):701-34 [14675307.001]
  • [Cites] Curr Drug Metab. 2004 Feb;5(1):21-53 [14965249.001]
  • [Cites] Mol Cancer Ther. 2004 Jul;3(7):833-8 [15252144.001]
  • [Cites] Nat Rev Drug Discov. 2006 Mar;5(3):219-34 [16518375.001]
  • [Cites] Gene Ther. 2006 Mar;13(6):503-8 [16195700.001]
  • [Cites] Cancer Res. 1987 Feb 15;47(4):936-42 [3802100.001]
  • [Cites] Mol Gen Genet. 1991 Apr;226(1-2):305-9 [2034223.001]
  • [Cites] Cancer Res. 1992 Oct 1;52(19):5407-11 [1394146.001]
  • (PMID = 18687998.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA119617-01; United States / NCI NIH HHS / CA / R01 CA119617; United States / NCI NIH HHS / CA / R01 CA 119617; United States / NCI NIH HHS / CA / R01 CA119617-01
  • [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, Phytogenic; 0 / DNA Primers; 0 / PRPF4 protein, human; 0 / RNA, Viral; 0 / Ribonucleoprotein, U4-U6 Small Nuclear; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ NIHMS66400; NLM/ PMC2597512
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23. Singhal S, Mehta J: Thalidomide in cancer. Biomed Pharmacother; 2002 Feb;56(1):4-12
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  • After its success in myeloma, it has been investigated in other plasma cell dyscrasias, myelodysplastic syndromes, gliomas, Kaposi's sarcoma, renal cell carcinoma, advanced breast cancer, and colon cancer.
  • Thalidomide causes responses in 30-50% of myeloma patients as a single agent, and acts synergistically with corticosteroids and chemotherapy.
  • Responses have also been seen in one-third of patients with Kaposi's sarcoma, in a small proportion of patients with renal cell carcinoma and high-grade glioma, and in some patients with colon cancer in combination with irinotecan.
  • The drug is being investigated currently in a number of clinical trials for cancer.
  • Thrombotic phenomena are especially common when thalidomide is combined with chemotherapy.
  • Adverse effects severe enough to necessitate cessation of therapy are seen in around 20% of patients.
  • A therapeutic trial of thalidomide is essential in all patients with relapsed or refractory myeloma.
  • In other cancers, the best way to use the drug is in the setting of clinical trials.
  • In the absence of access to studies or alternative therapeutic options, thalidomide could be considered singly or in combination with standard therapy.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Neoplasms / drug therapy. Thalidomide / therapeutic use

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  • (PMID = 11905508.001).
  • [ISSN] 0753-3322
  • [Journal-full-title] Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
  • [ISO-abbreviation] Biomed. Pharmacother.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Interleukin-2; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 61
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24. Shih T, Lindley C: Bevacizumab: an angiogenesis inhibitor for the treatment of solid malignancies. Clin Ther; 2006 Nov;28(11):1779-802
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  • [Title] Bevacizumab: an angiogenesis inhibitor for the treatment of solid malignancies.
  • BACKGROUND: Bevacizumab is a recombinant humanized monoclonal antibody that was approved by the US Food and Drug Administration (FDA) in February 2004 for use as part of combination therapy with fluorouracil-based regimens for metastatic colorectal cancer (mCRC).
  • It summarizes data on the clinical efficacy and tolerability of bevacizumab from Phase II/III trials in mCRC, breast cancer, non-small-cell lung cancer, and renal cell carcinoma and preliminary data from investigational studies in pancreatic cancer and soft-tissue sarcomas.
  • METHODS: A comprehensive search of the English-language literature indexed on MEDLINE (1966-April 2006) was performed using the terms Avastin, bevacizumab, vascular endothelial growth factor, angiogenesis, and bevacizumab plus colorectal cancer, breast cancer, non-small-cell lung cancer, pancreatic cancer, and renal cell carcinoma.
  • Bevacizumab has been reported to result in changes in exposure to concomitant chemotherapy, although formal drug-interaction studies have not been performed.
  • Surrogate markers of disease progression or treatment response to bevacizumab have been studied, but no significant correlations with any outcome measure have been found.
  • When combined with standard chemotherapy regimens, bevacizumab has been associated with significant improvements compared with chemotherapy alone in the efficacy end points of overall survival, progression-free survival, and response rates in patients with mCRC (all, P < 0.05).
  • Combination bevacizumab regimens have been associated with clinical activity in breast cancer, non-small-cell lung cancer, renal cell carcinoma, pancreatic cancer, and soft-tissue sarcoma.
  • CONCLUSIONS: Bevacizumab is effective and generally well tolerated as first-line therapy for mCRC.
  • The results from clinical studies of bevacizumab as a single agent or as part of combination regimens for breast cancer, non-small-cell lung cancer, renal cell carcinoma, and other solid malignancies have been promising.
  • The most effective regimens for various malignancies and predictive markers of treatment response have not been fully determined.
  • Combining bevacizumab with chemotherapy or other novel targeted agents appears to be a rational approach that may enhance efficacy while limiting the traditional nonselective toxicities.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacokinetics. Angiogenesis Inhibitors / therapeutic use. Antibodies, Monoclonal / pharmacokinetics. Antibodies, Monoclonal / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bevacizumab. Clinical Trials, Phase II as Topic. Clinical Trials, Phase III as Topic. Disease-Free Survival. Humans. Recombinant Proteins / adverse effects. Recombinant Proteins / pharmacokinetics. Recombinant Proteins / therapeutic use. Survival Rate

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  • (PMID = 17212999.001).
  • [ISSN] 0149-2918
  • [Journal-full-title] Clinical therapeutics
  • [ISO-abbreviation] Clin Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Recombinant Proteins; 2S9ZZM9Q9V / Bevacizumab
  • [Number-of-references] 103
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25. Testori A, Tosti G, Martinoli C, Spadola G, Cataldo F, Verrecchia F, Baldini F, Mosconi M, Soteldo J, Tedeschi I, Passoni C, Pari C, Di Pietro A, Ferrucci PF: Electrochemotherapy for cutaneous and subcutaneous tumor lesions: a novel therapeutic approach. Dermatol Ther; 2010 Nov-Dec;23(6):651-61
Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Electrochemotherapy for cutaneous and subcutaneous tumor lesions: a novel therapeutic approach.
  • Electroporation uses pulsed, high-intensity electric fields to temporarily increase cell membrane permeability by creation of pores, through which small molecules, such as chemotherapeutic agents, can diffuse inside cells before they reseal.
  • The combination of electroporation with the administration of otherwise low-permeant cytotoxic drugs is known as electrochemotherapy (ECT).
  • The two most commonly used drugs are bleomycin and cisplatin.
  • ECT has already been proven to be effective in diverse tumor histotypes, including melanoma and basal and squamous cell carcinoma, Kaposi sarcoma, and breast cancer, also in those cases nonresponding to classical chemotherapies or other loco-regional treatment modalities, with a good safety profile.
  • ECT can be proposed as loco-regional therapy for disseminated cutaneous and subcutaneous tumor lesions as alternative treatment modality to conventional therapies or as palliative care, in order to improve patients' quality of life.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Electrochemotherapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Animals. Bleomycin / administration & dosage. Cisplatin / administration & dosage. Humans. Skin / pathology. Treatment Outcome

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 21054709.001).
  • [ISSN] 1529-8019
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 11056-06-7 / Bleomycin; Q20Q21Q62J / Cisplatin
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26. Cvetkovic RS, Figgitt DP, Plosker GL: ET-743. Drugs; 2002;62(8):1185-92; discussion 1193-4
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  • It has significant cytotoxic activity against soft tissue sarcomas (STS).
  • It also has in vitro activity against melanoma, breast, ovarian, colon, renal, non-small cell lung and prostate carcinomas.
  • The drug has unique mechanism of action which includes in vitro inhibition of transcription-dependent nucleotide excision repair pathways and inhibition of cell cycle progression leading to p53-independent apoptosis.
  • It also selectively inhibits transcriptional activation of multidrug-resistance (MDR1) gene in human sarcoma cells in vivo.
  • Patients receiving ET-743 as second- or third-line treatment had partial tumour response rates of 6 to 8%.
  • Patients receiving ET-743 as first-line chemotherapy had a partial response rate of 18%.
  • A pooled analysis of the three multicentre phase II trials showed the following: median overall survival time of 10.2 months, 1-year survival rate of 40% and 6-month progression-free rate of 27.2%.
  • Transient and reversible elevation of hepatic transaminases, nausea, vomiting and asthenia were common but seldom severe and never treatment-limiting.
  • [MeSH-minor] Clinical Trials as Topic. Humans. Liver / drug effects. Liver / pathology. Neoplasms / drug therapy. Neutropenia / chemically induced. Survival Analysis. Tetrahydroisoquinolines. Thrombocytopenia / chemically induced

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  • [ErratumIn] Drugs 2002;62(11):1634
  • [Cites] Ann Oncol. 1998 Sep;9(9):981-7 [9818072.001]
  • [Cites] Clin Cancer Res. 2001 Jan;7(1):185-91 [11205907.001]
  • [Cites] J Natl Cancer Inst. 2000 Feb 2;92 (3):205-16 [10655437.001]
  • [Cites] Eur J Cancer Clin Oncol. 1987 Oct;23(10):1477-83 [3479329.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12 ):6775-9 [10841572.001]
  • [Cites] Cancer. 1990 Sep 1;66(5):862-7 [2201431.001]
  • [Cites] Cancer Chemother Pharmacol. 1993;31 Suppl 2:S180-4 [8453694.001]
  • [Cites] Chem Biol. 2001 Nov;8(11):1033-49 [11731295.001]
  • [Cites] Clin Cancer Res. 2001 Feb;7(2):231-42 [11234874.001]
  • [Cites] J Clin Oncol. 1990 Apr;8(4):689-704 [1968964.001]
  • [Cites] J Clin Oncol. 1987 Jun;5(6):840-50 [3585441.001]
  • [Cites] Eur J Cancer. 2001 Jan;37(1):97-105 [11165136.001]
  • [Cites] Biochemistry. 1996 Oct 15;35(41):13303-9 [8873596.001]
  • [Cites] Eur J Cancer. 2001 May;37(7):870-7 [11313175.001]
  • [Cites] Clin Cancer Res. 1999 Nov;5(11):3352-6 [10589744.001]
  • [Cites] Ann Oncol. 1998 Sep;9(9):989-93 [9818073.001]
  • [Cites] Ann Surg Oncol. 1995 Jan;2(1):26-31 [7834450.001]
  • [Cites] Clin Cancer Res. 1998 Aug;4(8):1977-83 [9717828.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jun 6;97(12 ):6780-4 [10841573.001]
  • [Cites] Anticancer Drugs. 2001 Sep;12 (8):653-66 [11604552.001]
  • [Cites] Clin Cancer Res. 2000 Dec;6(12 ):4725-32 [11156226.001]
  • [Cites] N Engl J Med. 1995 Nov 23;333(21):1380-5 [7477118.001]
  • [Cites] Cancer. 1981 Jan 1;47(1):207-14 [7459811.001]
  • [Cites] Int J Cancer. 2001 May 15;92 (4):583-8 [11304695.001]
  • [Cites] Hematol Oncol Clin North Am. 1995 Aug;9(4):765-85 [7490240.001]
  • [Cites] Ann Oncol. 1999 Oct;10 (10 ):1233-40 [10586342.001]
  • [Cites] J Clin Oncol. 1995 Jul;13(7):1537-45 [7602342.001]
  • [Cites] Nat Med. 2001 Aug;7(8):961-6 [11479630.001]
  • [Cites] J Clin Oncol. 1993 Jul;11(7):1269-75 [8315424.001]
  • [Cites] Clin Cancer Res. 2001 Sep;7(9):2908-11 [11555609.001]
  • [Cites] J Med Chem. 1999 Jul 15;42(14 ):2493-7 [10411470.001]
  • [Cites] Clin Cancer Res. 2001 Oct;7(10 ):3251-7 [11595721.001]
  • (PMID = 12010079.001).
  • [ISSN] 0012-6667
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Dioxoles; 0 / Isoquinolines; 0 / Tetrahydroisoquinolines; ID0YZQ2TCP / trabectedin
  • [Number-of-references] 64
  •  go-up   go-down


27. Yuan R, Kay A, Berg WJ, Lebwohl D: Targeting tumorigenesis: development and use of mTOR inhibitors in cancer therapy. J Hematol Oncol; 2009 Oct 27;2:45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting tumorigenesis: development and use of mTOR inhibitors in cancer therapy.
  • Consequently, inhibitors of mTOR, including temsirolimus, everolimus, and ridaforolimus (formerly deforolimus) have been developed and assessed for their safety and efficacy in patients with cancer.
  • Temsirolimus is an intravenously administered agent approved by the US Food and Drug Administration (FDA) and the European Medicines Agency (EMEA) for the treatment of advanced renal cell carcinoma (RCC).
  • Everolimus is an oral agent that has recently obtained US FDA and EMEA approval for the treatment of advanced RCC after failure of treatment with sunitinib or sorafenib.
  • The use of mTOR inhibitors, either alone or in combination with other anticancer agents, has the potential to provide anticancer activity in numerous tumor types.
  • Cancer types in which these agents are under evaluation include neuroendocrine tumors, breast cancer, leukemia, lymphoma, hepatocellular carcinoma, gastric cancer, pancreatic cancer, sarcoma, endometrial cancer, and non-small-cell lung cancer.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Cell Transformation, Neoplastic / drug effects. Drug Delivery Systems / methods. Drug Discovery. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Neoplasms / drug therapy. Protein-Serine-Threonine Kinases / antagonists & inhibitors

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  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1588-95 [18332470.001]
  • [Cites] Clin Cancer Res. 2008 May 1;14(9):2756-62 [18451242.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1596-602 [18332467.001]
  • [Cites] J Clin Oncol. 2008 Jun 20;26(18):3063-72 [18565894.001]
  • [Cites] Cancer. 2008 Aug 1;113(3):508-14 [18543327.001]
  • [Cites] Lancet. 2008 Aug 9;372(9637):449-56 [18653228.001]
  • [Cites] J Clin Oncol. 2008 Sep 10;26(26):4311-8 [18779618.001]
  • [Cites] BJU Int. 2009 Mar;103(5):572-7 [19154471.001]
  • [Cites] Eur J Cancer. 2009 Mar;45(5):765-73 [19157861.001]
  • [Cites] Cancer. 2009 Jun 1;115(11):2438-46 [19306412.001]
  • [Cites] J Clin Oncol. 2009 Jun 1;27(16):2630-7 [19380449.001]
  • [Cites] J Clin Oncol. 2009 Aug 10;27(23):3822-9 [19581539.001]
  • [Cites] Ann Oncol. 2009 Oct;20(10):1674-81 [19549709.001]
  • [Cites] J Clin Oncol. 2010 Jan 1;28(1):69-76 [19933912.001]
  • [Cites] J Clin Oncol. 2010 Apr 10;28(11):1904-10 [20231677.001]
  • [Cites] Cancer. 2010 Dec 1;116(23):5415-9 [20681032.001]
  • [Cites] J Biol Chem. 1999 Nov 12;274(46):33085-91 [10551878.001]
  • [Cites] Gut. 2000 Aug;47(2):272-6 [10896921.001]
  • [Cites] Breast Cancer Res. 2000;2(5):335-44 [11250726.001]
  • [Cites] J Clin Oncol. 2002 Jan 1;20(1):289-96 [11773181.001]
  • [Cites] Nat Rev Cancer. 2002 Jul;2(7):489-501 [12094235.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3659-62 [12097271.001]
  • [Cites] Microbiol Mol Biol Rev. 2002 Dec;66(4):579-91, table of contents [12456783.001]
  • [Cites] J Urol. 2003 Aug;170(2 Pt 1):420-4 [12853790.001]
  • [Cites] N Engl J Med. 2003 Aug 28;349(9):847-58 [12944570.001]
  • [Cites] Trends Biochem Sci. 2003 Nov;28(11):573-6 [14607085.001]
  • [Cites] Clin Cancer Res. 2003 Nov 1;9(14):5078-84 [14613984.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7652-6 [14633685.001]
  • [Cites] J Clin Oncol. 2004 Mar 1;22(5):909-18 [14990647.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):335-48 [15122205.001]
  • [Cites] J Clin Oncol. 2004 Jun 15;22(12):2336-47 [15136596.001]
  • [Cites] Nature. 2006 May 25;441(7092):424-30 [16724053.001]
  • [Cites] Expert Opin Emerg Drugs. 2007 Nov;12(4):605-18 [17979602.001]
  • [Cites] Eur J Cancer. 2008 Jan;44(1):84-91 [18039566.001]
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):361-7 [18202410.001]
  • [Cites] Mod Pathol. 2008 Mar;21(3):231-7 [18157089.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1576-8 [18332465.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1603-10 [18332469.001]
  • [Cites] J Clin Oncol. 2004 Jul 15;22(14):2954-63 [15254063.001]
  • [Cites] Cancer Cell. 2004 Jul;6(1):91-9 [15261145.001]
  • [Cites] Genes Dev. 2004 Aug 15;18(16):1926-45 [15314020.001]
  • [Cites] Ann Oncol. 2004 Oct;15(10):1510-6 [15367412.001]
  • [Cites] J Antibiot (Tokyo). 1975 Oct;28(10):727-32 [1102509.001]
  • [Cites] Cancer Treat Rev. 1981 Mar;8(1):63-87 [7248995.001]
  • [Cites] Crit Rev Oncol Hematol. 1995 Jul;19(3):183-232 [7612182.001]
  • [Cites] Cancer Res. 1999 Aug 1;59(15):3581-7 [10446965.001]
  • [Cites] Am J Clin Pathol. 2004 Dec;122(6):931-7 [15539386.001]
  • [Cites] J Clin Oncol. 2004 Dec 15;22(24):4991-5004 [15611513.001]
  • [Cites] Cancer Res. 2005 Mar 15;65(6):2047-53 [15781610.001]
  • [Cites] Biochim Biophys Acta. 2005 Nov 25;1756(2):127-44 [16139957.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2028-37 [16489002.001]
  • [Cites] Nephrol Dial Transplant. 2006 Jul;21 Suppl 3:iii18-23 [16815852.001]
  • [Cites] Nat Rev Drug Discov. 2006 Aug;5(8):671-88 [16883305.001]
  • [Cites] Clin Cancer Res. 2006 Oct 1;12(19):5755-63 [17020981.001]
  • [Cites] Br J Cancer. 2006 Nov 6;95(9):1148-54 [17031397.001]
  • [Cites] Kidney Int. 2006 Nov;70(10):1777-82 [17003820.001]
  • [Cites] Clin Cancer Res. 2006 Dec 15;12(24):7215-20 [17189392.001]
  • [Cites] Endocr Relat Cancer. 2006 Dec;13 Suppl 1:S15-24 [17259554.001]
  • [Cites] Best Pract Res Clin Endocrinol Metab. 2007 Mar;21(1):163-72 [17382271.001]
  • [Cites] N Engl J Med. 2007 May 31;356(22):2271-81 [17538086.001]
  • [Cites] Cancer Cell. 2007 Jul;12(1):9-22 [17613433.001]
  • [Cites] Cancer. 2007 Aug 1;110(3):599-605 [17577220.001]
  • [Cites] Pathology. 2007 Oct;39(5):482-5 [17886097.001]
  • [Cites] Crit Rev Oncol Hematol. 2007 Nov;64(2):115-28 [17702596.001]
  • (PMID = 19860903.001).
  • [ISSN] 1756-8722
  • [Journal-full-title] Journal of hematology & oncology
  • [ISO-abbreviation] J Hematol Oncol
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Intracellular Signaling Peptides and Proteins; 0 / Protein Kinase Inhibitors; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
  • [Number-of-references] 103
  • [Other-IDs] NLM/ PMC2775749
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28. Health Quality Ontario: KRAS Testing for Anti-EGFR Therapy in Advanced Colorectal Cancer: An Evidence-Based and Economic Analysis. Ont Health Technol Assess Ser; 2010;10(25):1-49
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  • [Title] KRAS Testing for Anti-EGFR Therapy in Advanced Colorectal Cancer: An Evidence-Based and Economic Analysis.
  • Within the PEPP, subgroup committees were developed for each disease area.
  • For each technology, an economic analysis was also completed by the Toronto Health Economics and Technology Assessment Collaborative (THETA) and is summarized within the reports.THE FOLLOWING REPORTS CAN BE PUBLICLY ACCESSED AT THE MAS WEBSITE AT: www.health.gov.on.ca/mas or at www.health.gov.on.ca/english/providers/program/mas/mas_about.htmlGENE EXPRESSION PROFILING FOR GUIDING ADJUVANT CHEMOTHERAPY DECISIONS IN WOMEN WITH EARLY BREAST CANCER: An Evidence-Based and Economic AnalysisEpidermal Growth Factor Receptor Mutation (EGFR) Testing for Prediction of Response to EGFR-Targeting Tyrosine Kinase Inhibitor (TKI) Drugs in Patients with Advanced Non-Small-Cell Lung Cancer: an Evidence-Based and Economic AnalysisK-RAS testing in Treatment Decisions for Advanced Colorectal Cancer: an Evidence-Based and Economic Analysis.
  • OBJECTIVE: The objective of this systematic review is to determine the predictive value of KRAS testing in the treatment of metastatic colorectal cancer (mCRC) with two anti-EGFR agents, cetuximab and panitumumab.
  • KRAS (Kristen-RAS, a member of the rat sarcoma virus (ras) gene family of oncogenes) is frequently mutated in epithelial cancers such as colorectal cancer, with mutations occurring in mutational hotspots (codons 12 and 13) of the KRAS protein.
  • Involved in EGFR-mediated signalling of cellular processes such as cell proliferation, resistance to apoptosis, enhanced cell motility and neoangiogenesis, a mutation in the KRAS gene is believed to be involved in cancer pathogenesis.
  • Such a mutation is also hypothesized to be involved in resistance to targeted anti-EGFR (epidermal growth factor receptor with tyrosine kinase activity) treatments such as cetuximab and panitumumab, hence, the important in evaluating the evidence on the predictive value of KRAS testing in this context.
  • KRAS MUTATION TESTING IN ADVANCED COLORECTAL CANCER: Both cetuximab and panitumumab are indicated by Health Canada in the treatment of patients with metastatic colorectal cancer whose tumours are WT for the KRAS gene.
  • Cetuximab may be offered as monotherapy in patients intolerant to irinotecan-based chemotherapy or in patients who have failed both irinotecan and oxaliplatin-based regimens and who received a fluoropyrimidine.
  • It can also be administered in combination with irinotecan in patients refractory to other irinotecan-based chemotherapy regimens.
  • Panitumumab is only indicated as a single agent after failure of fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy regimens.
  • In Ontario, patients with advanced colorectal cancer who are refractory to chemotherapy may be offered the targeted anti-EGFR treatments cetuximab or panitumumab.
  • Eligibility for these treatments is based on the KRAS status of their tumour, derived from tissue collected from surgical or biopsy specimens.
  • It is believed that KRAS status is not affected by treatments, therefore, for patients for whom surgical tissue is available for KRAS testing, additional biopsies prior to treatment with these targeted agents is not necessary.
  • For patients that have not undergone surgery or for whom surgical tissue is not available, a biopsy of either the primary or metastatic site is required to determine their KRAS status.
  • RESEARCH QUESTION: To determine if there is predictive value of KRAS testing in guiding treatment decisions with anti-EGFR targeted therapies in advanced colorectal cancer patients refractory to chemotherapy.
  • In total, 14 observational studies were identified for inclusion in this EBA: 4 for cetuximab monotherapy, 7 for the cetuximab-irinotecan combination therapy, and 3 to be included in the review for panitumumab monotherapy INCLUSION CRITERIA: English-language articles, and English or French-language HTAs published from January 2005 to May 2010, inclusive.Randomized controlled trials (RCTs) or observational studies, including single arm treatment studies that include KRAS testing.Studies with data on main outcomes of interest, overall and progression-free survival.Studies of third line treatment with cetuximab or panitumumab in patients with advanced colorectal cancer refractory to chemotherapy.For the cetuximab-irinotecan evaluation, studies in which at least 70% of patients in the study received this combination therapy.
  • CETUXIMAB-IRINOTECAN COMBINATION THERAPY: There is low GRADE evidence that testing for KRAS may optimize survival benefits in patients without the KRAS mutation (KRAS wildtype, or KRAS WT) compared to those with the mutation.
  • However, cetuximab-irinotecan combination treatments based on KRAS status discount any effect of cetuximab in possibly reversing resistance to irinotecan in patients with the mutation, as observed effects were lower than for patients without the mutation.
  • Evaluation of relative cost-effectiveness, based on a decision-analytic cost-utility analysis, assessed testing for KRAS genetic mutations versus no testing in the context of treatment with cetuximab monotherapy, panitumumab monotherapy, cetuximab in combination with irinotecan, and best supportive care.
  • Of importance to note is that the cost-effectiveness analysis focused on the impact of testing for KRAS mutations compared to no testing in the context of different treatment options, and does not assess the cost-effectiveness of the drug treatments alone.
  • CONCLUSIONS: KRAS status is predictive of outcomes in cetuximab and panitumumab monotherapy, and in cetuximab-irinotecan combination therapy.
  • While KRAS testing is cost-effective for all strategies considered, it is not equally cost-effective for all treatment options.

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  • [Cites] Br J Cancer. 2008 Jul 8;99(1):83-9 [18577988.001]
  • [Cites] J Clin Oncol. 2008 Sep 1;26(25):4217-9 [18757341.001]
  • [Cites] N Engl J Med. 2008 Oct 23;359(17):1757-65 [18946061.001]
  • [Cites] J Clin Oncol. 2009 Mar 1;27(7):1122-9 [19164213.001]
  • [Cites] Ann Oncol. 2009 May;20(5):879-84 [19179548.001]
  • [Cites] J Clin Oncol. 2009 Apr 20;27(12):2091-6 [19188670.001]
  • [Cites] Clin Cancer Res. 2009 May 1;15(9):3184-8 [19366826.001]
  • [Cites] Br J Cancer. 2009 Apr 21;100(8):1330-5 [19367287.001]
  • [Cites] J Clin Oncol. 2009 Jun 1;27(16):2622-9 [19398573.001]
  • [Cites] Br J Cancer. 2009 Aug 18;101(4):715-21 [19603018.001]
  • [Cites] Curr Oncol. 2010 Jul;17 Suppl 1:S31-40 [20680106.001]
  • [Cites] Clin Colorectal Cancer. 2008 May;7(3):184-90 [18621636.001]
  • [Cites] Clin Cancer Res. 2008 Dec 1;14(23):7884-95 [19047118.001]
  • [Cites] Jpn J Clin Oncol. 2009 May;39(5):321-6 [19287023.001]
  • [Cites] J Natl Cancer Inst. 2009 Sep 2;101(17):1182-92 [19666851.001]
  • [Cites] Int J Technol Assess Health Care. 1994 Fall;10(4):714-5 [7843894.001]
  • [Cites] BMJ. 2004 Jun 19;328(7454):1490 [15205295.001]
  • [Cites] N Engl J Med. 2004 Jul 22;351(4):337-45 [15269313.001]
  • [Cites] BMC Med Res Methodol. 2005;5:13 [15840177.001]
  • [Cites] J Clin Oncol. 2007 May 1;25(13):1658-64 [17470858.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3230-7 [17664471.001]
  • [Cites] Ann Oncol. 2008 Jan;19(1):92-8 [17785764.001]
  • [Cites] N Engl J Med. 2007 Nov 15;357(20):2040-8 [18003960.001]
  • [Cites] Br J Cancer. 2007 Dec 3;97(11):1469-74 [18040272.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1626-34 [18316791.001]
  • [Cites] BMC Cancer. 2008;8:169 [18544172.001]
  • (PMID = 23074403.001).
  • [ISSN] 1915-7398
  • [Journal-full-title] Ontario health technology assessment series
  • [ISO-abbreviation] Ont Health Technol Assess Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC3377508
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29. Feng SS, Mu L, Win KY, Huang G: Nanoparticles of biodegradable polymers for clinical administration of paclitaxel. Curr Med Chem; 2004 Feb;11(4):413-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Paclitaxel is one of the best antineoplastic drugs found from nature in the past decades, which has been found effective against a wide spectrum of cancers including ovarian cancer, breast cancer, small and non small cell lung cancer, colon cancer, head and neck cancer, multiple myeloma, melanoma, and Kaposi's sarcoma.
  • Like many other anticancer drugs, it has difficulties in clinical administration due to its poor solubility in water and most pharmaceutical reagents.
  • Nanoparticles of biodegradable polymers can provide an ideal solution to such an adjuvant problem and realize a controlled and targeted delivery of the drug with better efficacy and less side effects.
  • With further development, such as particle size optimization and surface coating, nanoparticle formulation of paclitaxel can promote a new concept of chemotherapy to realize its full efficacy and to improve quality of life of the patients, which includes personalized chemotherapy, local chemotherapy, sustained chemotherapy, oral chemotherapy, chemotherapy across the blood-brain barrier, chemotherapy across the microcirculation barrier, etc.
  • The present research proposes a novel formulation for fabrication of nanoparticles of poly(lactic-co-glycolic acid) (PLGA) by a modified solvent extraction/evaporation technique, in which natural emulsifiers, such as phospholipids, cholesterol and vitamin E TPGS are creatively applied to achieve high drug encapsulation efficiency, desired drug released kinetics, high cell uptake and high cytotoxicity.
  • The drug encapsulation efficiency and the drug release kinetics under in vitro conditions were measured by high performance liquid chromatography (HPLC).
  • Nanoparticles of desired small size and narrow size distribution can be obtained.
  • The drug encapsulation efficiency can be achieved as high as 100 %.
  • The HT-29 cancer cell line experiment showed that after 24 hours of incubation, the cell mortality caused by the drug administered by such nanoparticle formulation could be more than 13 times higher than that caused by the free drug under similar conditions.
  • [MeSH-minor] Calorimetry, Differential Scanning / methods. Cell Division / drug effects. Cell Survival / drug effects. Drug Carriers / administration & dosage. Drug Carriers / chemistry. Drug Carriers / pharmacokinetics. HT29 Cells. Humans. Kinetics. Particle Size. Surface Properties. Vitamin E / analogs & derivatives. Vitamin E / chemistry. Vitamin E / pharmacokinetics

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  • (PMID = 14965222.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drug Carriers; 0 / Polymers; 1406-18-4 / Vitamin E; P88XT4IS4D / Paclitaxel
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30. André T, Wislez M, Goncalves A, de La Motte Rouge T, Blay JY, Massard C, Bay JO, comité de rédaction du Bulletin du Cancer: [Following communications made at American Society of Clinical Oncology 2010, what will change our practice? The point of view of the editorial board of Bulletin du Cancer]. Bull Cancer; 2010 Dec;97(12):1551-62

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Suite aux communications faites au congrès de l'American Society of Clinical Oncology 2010, qu'est ce qui va changer nos pratiques ? Le point de vue du comité de rédaction du Bulletin du cancer.
  • Best understanding of biological mechanisms and new molecules to inhibit targets allow in certain case, to use therapeutic targeting in the true sense.
  • In Advanced non-small cell lung cancer, myeloma and advanced lymphoma, maintenance therapy by monoclonal anti-body or inhibitors of tyrosines kinases showed the proof of their effectiveness.
  • Biological personalization of cancer treatments is on the road run but the road is still long.
  • [MeSH-major] Medical Oncology / standards. Neoplasms / therapy. Practice Patterns, Physicians' / standards. Societies, Medical / standards
  • [MeSH-minor] Breast Neoplasms / therapy. Digestive System Neoplasms / therapy. Female. Gastrointestinal Stromal Tumors / drug therapy. Genital Neoplasms, Female / drug therapy. Hematologic Neoplasms / therapy. Humans. Lung Neoplasms / drug therapy. Male. Melanoma / drug therapy. Prostatic Neoplasms / drug therapy. Sarcoma / drug therapy. Testicular Neoplasms / drug therapy. Thyroid Neoplasms / drug therapy. United States

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  • (PMID = 21220230.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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31. Strumberg D: Preclinical and clinical development of the oral multikinase inhibitor sorafenib in cancer treatment. Drugs Today (Barc); 2005 Dec;41(12):773-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Preclinical and clinical development of the oral multikinase inhibitor sorafenib in cancer treatment.
  • Tumor survival, growth and metastasis depend on efficient tumor cell proliferation and tumor angiogenesis, and targeting both of these processes simultaneously could prove to be therapeutically relevant.
  • The RAS/RAF signaling pathway is an important mediator of tumor cell proliferation, and angiogenesis and is often aberrantly activated in human tumors due to the presence of activated Ras or mutant B-Raf, or elevation of growth factor receptors.
  • Sorafenib, which belongs chemically to a class that can be described as bis-aryl ureas, was selected for further pharmacologic characterization based on potent inhibition of Raf-1 and its favorable kinase selectivity profile.
  • Further characterization showed that sorafenib suppresses both wild-type and V599E mutant B-Raf activity in vitro.
  • Preclinically, sorafenib showed broad-spectrum antitumor activity in colon, breast and non-small-cell lung cancer xenograft models.
  • A total of four phase I studies using oral sorafenib as a single agent have been completed, and the compound showed a favorable safety profile with mild to moderate diarrhea being the most common treatment-related adverse event.
  • Single-agent phase II trials reported so far demonstrated antitumor activity of sorafenib in patients with hepatocellular carcinoma, sarcoma and renal cell cancer (RCC).
  • Food and Drug Administration for this indication is pending.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Benzenesulfonates / therapeutic use. Pyridines / therapeutic use
  • [MeSH-minor] Administration, Oral. Animals. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Renal Cell / drug therapy. Clinical Trials as Topic. Drug Evaluation, Preclinical. Humans. Kidney Neoplasms / drug therapy. Liver Neoplasms / drug therapy. Niacinamide / analogs & derivatives. Phenylurea Compounds. Protein Kinase Inhibitors / therapeutic use. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors. Sarcoma / drug therapy

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  • [Copyright] Copyright 2005 Prous Science
  • (PMID = 16474853.001).
  • [ISSN] 1699-3993
  • [Journal-full-title] Drugs of today (Barcelona, Spain : 1998)
  • [ISO-abbreviation] Drugs Today
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzenesulfonates; 0 / Phenylurea Compounds; 0 / Protein Kinase Inhibitors; 0 / Pyridines; 25X51I8RD4 / Niacinamide; 9ZOQ3TZI87 / sorafenib; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 78
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32. Green AM, Steinmetz ND: Monitoring apoptosis in real time. Cancer J; 2002 Mar-Apr;8(2):82-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Monitoring apoptosis in real time.
  • Many therapeutically active anticancer treatments exert their effect by the induction of apoptosis and necrosis.
  • Serial biopsies in breast cancer patients have suggested that response to therapy correlates with early posttreatment increases in tumor apoptotic index.
  • Radiolabeled technetium Tc 99m-recombinant human (rh) annexin V provides a noninvasive technique for imaging treatment-induced cell death.
  • PS is normally found only on the inner leaflet of the cell membrane double layer, but it is actively transported to the outer layer as an early event in apoptosis and becomes available for annexin binding.
  • In vivo localization of intravenously administered Tc 99m-annexin V has been demonstrated in numerous preclinical models of apoptosis, including anti-Fas-mediated hepatic apoptosis, rejection of allogeneic heterotopic cardiac allografts, cyclophosphamide treatment of murine lymphoma, cyclophosphamide-induced apoptosis in bone marrow, and leukocyte apoptosis associated with abscess formation.
  • Scintigraphic studies in humans using Tc 99m-rh annexin V have demonstrated the feasibility of imaging cell death in acute myocardial infarction, in tumors with a high apoptotic index, and in response to anti-tumor chemotherapy of non-small cell lung cancer, small-cell lung cancer, breast cancer, lymphoma, and sarcoma.
  • Increased localization of Tc 99m-rh annexin V within 1 to 3 days of chemotherapy has been noted in some, but not all, subjects with these tumors.
  • To date, most subjects showing increased Tc 99m-rh annexin V uptake after the first course of chemotherapy have shown objective clinical responses.
  • A single site study in 15 subjects with 1-year follow-up has suggested that increased posttreatment Tc 99m-rh annexin uptake is associated with improved time to progression of disease and survival time.
  • In vivo imaging of cell death may have the potential to improve the treatment of cancer patients by allowing rapid, objective, patient-by-patient assessment of the efficacy of tumor cell killing.
  • [MeSH-minor] Animals. Humans. Myocardial Infarction / pathology. Myocardial Infarction / physiopathology. Myocardium / pathology. Necrosis. Neoplasms / pathology. Neoplasms / physiopathology. Neoplasms / therapy. Recombinant Proteins. Tomography, Emission-Computed, Single-Photon

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  • (PMID = 11999952.001).
  • [ISSN] 1528-9117
  • [Journal-full-title] Cancer journal (Sudbury, Mass.)
  • [ISO-abbreviation] Cancer J
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Radiopharmaceuticals; 0 / Recombinant Proteins; 7440-26-8 / Technetium
  • [Number-of-references] 37
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33. Singhal S, Mehta J: Thalidomide in cancer: potential uses and limitations. BioDrugs; 2001;15(3):163-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has been investigated in a number of cancers including multiple myeloma, myelodysplastic syndromes, gliomas, Kaposi's sarcoma, renal cell carcinoma, advanced breast cancer, and colon cancer.
  • It also acts synergistically with corticosteroids and chemotherapy in myeloma.
  • Responses have also been seen in one-third of patients with Kaposi's sarcoma, in a small proportion of patients with renal cell carcinoma and high grade glioma and, in combination with irinotecan, in some patients with colon cancer.
  • Despite the high frequency of adverse effects, those severe enough to necessitate cessation of therapy are seen in only 10 to 15% of patients.
  • A therapeutic trial of thalidomide should be considered in all patients with myeloma who are unresponsive to or relapse after standard therapy.
  • In other malignant diseases, the most appropriate way to use the drug is in the setting of well designed clinical trials.
  • In the absence of access to such studies, thalidomide could be considered singly or in combination with standard therapy in patients with no meaningful therapeutic options.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Immunosuppressive Agents / therapeutic use. Neoplasms / drug therapy. Thalidomide / therapeutic use

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  • (PMID = 11437682.001).
  • [ISSN] 1173-8804
  • [Journal-full-title] BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy
  • [ISO-abbreviation] BioDrugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 74
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34. O'Connell JB, Maggard MA, Ko CY: Cancer-directed surgery for localized disease: decreased use in the elderly. Ann Surg Oncol; 2004 Nov;11(11):962-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Previous studies report underuse of radiation and chemotherapy in the elderly, yet few have examined the rates of use (or underuse) of surgery.
  • METHODS: By using the Surveillance, Epidemiology, and End RESULTS database (1988-1997), patients (> or =40 years) were identified with localized adenocarcinoma of the breast, esophagus, stomach, pancreas, colon, or rectum; non-small-cell lung carcinoma; and sarcoma (n = 200,360).
  • However, CDS rates were >90% for breast and colon and >84% for rectal cancer in all age groups.
  • CONCLUSIONS: Although CDS for localized disease is being performed regularly in the elderly for some cancers (e.g. breast, colon, and rectum), this analysis shows that elderly patients are not receiving surgery for many potentially curable cancers.

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  • [CommentIn] Ann Surg Oncol. 2004 Nov;11(11):951-2 [15525821.001]
  • (PMID = 15525824.001).
  • [ISSN] 1068-9265
  • [Journal-full-title] Annals of surgical oncology
  • [ISO-abbreviation] Ann. Surg. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. Blackwell KL, Kirkpatrick JP, Snyder SA, Broadwater G, Farrell F, Jolliffe L, Brizel DM, Dewhirst MW: Human recombinant erythropoietin significantly improves tumor oxygenation independent of its effects on hemoglobin. Cancer Res; 2003 Oct 1;63(19):6162-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Tumor oxygenation is known to be an important predictive/prognostic marker in a variety of tumors, including cervix, head/neck, sarcoma, non-small cell of the lung, and breast.
  • This study randomized 30 nonanemic, female Fischer 344 rats into three treatment arms to examine the effects of recombinant human erythropoietin (EPO) on R3230 rodent mammary carcinoma oxygenation.
  • The three treatment arms were: (a) placebo;.
  • On day 22, median tumor volume was 399 mm(3) (range: 65-950 mm(3)), and no differences in tumor volume were seen between treatment arms.
  • Mean hematocrit was equal between arms at therapy initiation but were significantly higher for both arms receiving EPO at day 22 (placebo versus Arm B versus Arm C; Wilcoxon P = 0.052).
  • [MeSH-major] Adenocarcinoma / blood. Adenocarcinoma / drug therapy. Erythropoietin / pharmacology. Hemoglobins / metabolism. Mammary Neoplasms, Experimental / blood. Mammary Neoplasms, Experimental / drug therapy. Oxygen / blood

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  • (PMID = 14559797.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 40355
  • [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 / Hemoglobins; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; S88TT14065 / Oxygen
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36. Unger C, Häring B, Medinger M, Drevs J, Steinbild S, Kratz F, Mross K: Phase I and pharmacokinetic study of the (6-maleimidocaproyl)hydrazone derivative of doxorubicin. Clin Cancer Res; 2007 Aug 15;13(16):4858-66
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  • RESULTS: Treatment with DOXO-EMCH was well tolerated up to 200 mg/m2 without manifestation of drug-related side effects.
  • CONCLUSIONS: DOXO-EMCH showed a good safety profile and was able to induce tumor regressions in tumor types known to be anthracycline-sensitive tumors, such as breast cancer, small cell lung cancer, and sarcoma.
  • [MeSH-major] Antibiotics, Antineoplastic / adverse effects. Doxorubicin / analogs & derivatives. Hydrazones / adverse effects. Neoplasms / drug therapy. Prodrugs / adverse effects
  • [MeSH-minor] Adult. Aged. Female. Heart / drug effects. Humans. Male. Maximum Tolerated Dose. Middle Aged. Skin / drug effects

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  • (PMID = 17699865.001).
  • [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
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Hydrazones; 0 / Prodrugs; 151038-96-9 / doxorubicin(6-maleimidocaproyl)hydrazone; 80168379AG / Doxorubicin
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37. Peacock KH, Lesser GJ: Current therapeutic approaches in patients with brain metastases. Curr Treat Options Oncol; 2006 Nov;7(6):479-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current therapeutic approaches in patients with brain metastases.
  • The development of brain metastases is often viewed as the end stage of a disease course and engenders skepticism about the efficacy of treatment.
  • Single brain metastases should be treated with surgical resection or stereotactic radiosurgery, though it is unclear at this time if one modality is more effective than the other.
  • Surgical resection is preferred when a pathologic diagnosis is needed, for tumors larger than 3.5 cm, or when immediate tumor mass decompression is required.
  • Small tumors (ie, < 3.5 cm) that cause minimal edema and are surgically accessible may be treated with either surgery or SRS.
  • There is controversy over whether whole brain radiation therapy (WBRT) can be omitted following surgical resection or SRS.
  • Clinicians who choose to omit upfront WBRT are obligated to monitor the patient closely for intracranial recurrence, at which time further salvage therapy in the form of surgery, SRS, or WBRT may be considered.
  • Histology is of particular importance when considering WBRT for patients with radioresistant tumors such as melanoma, renal cell carcinoma, or sarcoma.
  • Chemotherapy has been demonstrated to improve response rates when used as an adjunct to radiation therapy.
  • Phase III trials to assess the benefit of motexafin in patients with metastatic lung cancer and efaproxiral in patients with metastatic breast cancer are ongoing.
  • Targeted therapies offer promise in achieving therapeutic efficacy while minimizing side effects.
  • [MeSH-major] Brain Neoplasms / therapy. Neoplasm Recurrence, Local / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Humans. Neoplasm Metastasis. Radiosurgery. Salvage Therapy. Stereotaxic Techniques

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  • [Cites] Cancer Treat Rev. 2005 Jun;31(4):256-73 [15951117.001]
  • [Cites] Cancer. 2005 Dec 15;104(12):2784-91 [16288488.001]
  • [Cites] J Neurooncol. 1998 Mar;37(1):1-8 [9525832.001]
  • [Cites] J Clin Oncol. 2003 Jul 1;21(13):2529-36 [12829672.001]
  • [Cites] Crit Rev Oncol Hematol. 2004 Dec;52(3):199-215 [15582786.001]
  • [Cites] J Neurosurg. 2005 Jan;102 Suppl:147-50 [15662799.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Feb 1;43(3):549-58 [10078636.001]
  • [Cites] Neurosurgery. 2005 Nov;57(5 Suppl):S54-65; discusssion S1-4 [16237290.001]
  • [Cites] Neurosurgery. 1991 Feb;28(2):201-5 [1997887.001]
  • [Cites] J Clin Oncol. 2002 Sep 1;20(17 ):3644-50 [12202665.001]
  • [Cites] Neurosurgery. 1997 Jul;41(1):44-8; discussion 48-9 [9218294.001]
  • [Cites] J Neurosurg. 1996 May;84(5):748-54 [8622147.001]
  • [Cites] Lancet Neurol. 2005 May;4(5):289-98 [15847842.001]
  • [Cites] J Neurooncol. 1999 Aug;44(1):53-7 [10582669.001]
  • [Cites] J Clin Oncol. 2006 Jan 1;24(1):106-14 [16314619.001]
  • [Cites] J Clin Oncol. 1999 Sep;17(9):2700-9 [10561344.001]
  • [Cites] Lancet. 2004 May 22;363(9422):1665-72 [15158627.001]
  • [Cites] Neurology. 2000 May 23;54(10):1886-93 [10822423.001]
  • [Cites] J Clin Oncol. 2004 Jun 1;22(11):2101-7 [15169796.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Jul 1;53(3):519-26 [12062592.001]
  • [Cites] Oncology (Williston Park). 1999 Jul;13(7):941-54, 957-61; discussion 961-2, 9 [10442342.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1979 Mar;5(3):419-25 [457486.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1996 Apr 1;35(1):27-35 [8641923.001]
  • [Cites] J Clin Oncol. 1999 Nov;17(11):3522-30 [10550150.001]
  • [Cites] Ann Oncol. 2004 Jul;15(7):1042-7 [15205197.001]
  • [Cites] Neurosurgery. 2003 Jun;52(6):1318-26; discussion 1326 [12762877.001]
  • [Cites] J Clin Oncol. 2005 Dec 1;23(34):8870-6 [16314647.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Oct 1;42(3):581-9 [9806518.001]
  • [Cites] J Clin Oncol. 2006 Mar 10;24(8):1295-304 [16525185.001]
  • [Cites] J Clin Oncol. 1998 Nov;16(11):3563-9 [9817276.001]
  • [Cites] J Natl Cancer Inst. 1995 Jan 4;87(1):34-40 [7666461.001]
  • [Cites] Neurosurgery. 2005 Nov;57(5 Suppl):S66-77; discusssion S1-4 [16237291.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2003 Apr 1;55(5):1169-76 [12654423.001]
  • [Cites] Expert Rev Neurother. 2004 Nov;4(6):1015-22 [15853528.001]
  • [Cites] Clin Cancer Res. 2003 Nov 15;9(15):5514-20 [14654531.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1997 Mar 1;37(4):745-51 [9128946.001]
  • [Cites] JAMA. 1998 Nov 4;280(17):1485-9 [9809728.001]
  • [Cites] J Neurosurg. 1993 Aug;79(2):210-6 [8331402.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1999 Sep 1;45(2):427-34 [10487566.001]
  • [Cites] Hematol Oncol Clin North Am. 2001 Dec;15(6):1085-107, vii [11770300.001]
  • [Cites] Cancer. 1996 Oct 1;78(7):1470-6 [8839553.001]
  • [Cites] Ann Neurol. 1993 Jun;33(6):583-90 [8498838.001]
  • [Cites] Neurosurgery. 2005 Nov;57(5 Suppl):S24-32; discusssion S1-4 [16237284.001]
  • [Cites] Lung Cancer. 2005 Jan;47(1):129-38 [15603863.001]
  • [Cites] J Cancer Res Clin Oncol. 2002 Aug;128(8):417-25 [12200598.001]
  • [Cites] Am J Clin Oncol. 2005 Apr;28(2):173-9 [15803013.001]
  • [Cites] J Clin Oncol. 2005 Feb 20;23(6):1209-17 [15718318.001]
  • [Cites] N Engl J Med. 1990 Feb 22;322(8):494-500 [2405271.001]
  • [Cites] Neurosurgery. 2006 Apr;58(4):701-9; discussion 701-9 [16575334.001]
  • [Cites] J Natl Cancer Inst. 1995 Feb 1;87(3):183-90 [7707405.001]
  • (PMID = 17032560.001).
  • [ISSN] 1527-2729
  • [Journal-full-title] Current treatment options in oncology
  • [ISO-abbreviation] Curr Treat Options Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 58
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38. Ridaforolimus. Drugs R D; 2010;10(3):165-78
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  • Ridaforolimus (AP23573; MK 8669) is an analog of sirolimus and a small molecule inhibitor of the mammalian target of rapamycin for the treatment of cancer.
  • Both intravenous and oral formulations of the compound are being tested in clinical trials for the treatment of soft-tissue and bone sarcomas.
  • It is in phase III development for sarcoma in the EU and US, and phase II for breast cancer, endometrial cancer, non-small cell lung cancer, and prostate cancer in the US and other markets in the world.
  • This review discusses the key development milestones and therapeutic trials of this drug.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Neoplasms / drug therapy. Sirolimus / analogs & derivatives. TOR Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Clinical Trials as Topic. Drug Screening Assays, Antitumor. Drugs, Investigational / pharmacology. Drugs, Investigational / therapeutic use. Humans

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  • (PMID = 20945947.001).
  • [ISSN] 1179-6901
  • [Journal-full-title] Drugs in R&D
  • [ISO-abbreviation] Drugs R D
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Investigational; 48Z35KB15K / ridaforolimus; EC 2.7.1.1 / TOR Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ PMC3586089
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39. Molteni A, Ward WF, Ts'ao CH, Taylor J, Small W Jr, Brizio-Molteni L, Veno PA: Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists. Curr Pharm Des; 2003;9(9):751-61
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  • [Title] Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists.
  • Angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AII) type 1 receptor antagonists have strong cytostatic properties on in vitro cultures of many normal and neoplastic cells.
  • They are effective, in particular, in reducing the growth of human lung fibroblasts, renal canine epithelial cells, bovine adrenal endothelial cells, simian T lymphocytes, and of neoplastic cell lines derived from human neuroblastomas, a ductal pancreatic carcinoma of the Syrian hamsters, human salivary glands adenocarcinomas, and two lines of human breast adenocarcinomas.
  • ACE inhibitors and AII type 1 receptor antagonists are also effective in reducing excessive vascular neoformation in a model of injury to the cornea of rats and rabbits, and in controlling the excessive angiogenesis observed in the Solt-Farber model of experimentally induced hepatoma, in methylcholantrene or radiation-induced fibrosarcomas, in radiation-induced squamous cell carcinomas and in the MA-16 viral-induced mammary carcinoma of the mouse.
  • Captopril was, in addition, effective in controlling tumor growth in a case of Kaposi's sarcoma in humans.
  • The mitogenic effect of AII is well established and a reduction of AII synthesis may well explain cell and neoplasm delayed growth.
  • Moreover, AII regulates and enhances the activity of several growth factors including transforming growth factor B (TGFB) and smooth muscle actin (SMA); and many of these factors are reduced in tissues of animals treated with ACE inhibitors and AII type 1 receptor antagonists.
  • The ACE inhibitors containing a sulphydril (SH) or thiol radical in their moiety (Captopril and CL242817) seemed to be more effective in controlling fibrosis and the growth of some neoplastic cells than those ACE inhibitors without this thiol radical in their structure, even if the second group of these drugs show in vitro a stronger inhibitory effect on converting enzyme activity.
  • However, although these additional properties are pharmacologically relevant, the blockade of AII synthesis plays an essential role in the cytostatic activity of these two categories of drugs.
  • These observations underline that in addition to the beneficial effect of these drugs on the cardiovascular system, new potential applications are opening for their wider deployment.
  • [MeSH-minor] Animals. Humans. Neoplasms / drug therapy. Neoplasms / metabolism. Receptors, Angiotensin / physiology

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  • (PMID = 12570792.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 24652; United States / NCI NIH HHS / CA / CA 52750; United States / NCI NIH HHS / CA / CA 64239; United States / NIDDK NIH HHS / DK / DK 15612; United States / NHLBI NIH HHS / HL / HL 25106
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiotensin Receptor Antagonists; 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Antineoplastic Agents; 0 / Receptors, Angiotensin
  • [Number-of-references] 70
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40. Kratz F: DOXO-EMCH (INNO-206): the first albumin-binding prodrug of doxorubicin to enter clinical trials. Expert Opin Investig Drugs; 2007 Jun;16(6):855-66
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  • DOXO-EMCH was able to induce tumor regressions in anthracycline-sensitive tumors (i.e., breast cancer, small cell lung cancer and sarcoma).
  • [MeSH-major] Albumins / metabolism. Antibiotics, Antineoplastic / therapeutic use. Doxorubicin / analogs & derivatives. Hydrazones / therapeutic use. Prodrugs / therapeutic use
  • [MeSH-minor] Animals. Clinical Trials as Topic. Humans. Neoplasms / drug therapy

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  • (PMID = 17501697.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Albumins; 0 / Antibiotics, Antineoplastic; 0 / DOXO-EMCH; 0 / Hydrazones; 0 / Prodrugs; 151038-96-9 / doxorubicin(6-maleimidocaproyl)hydrazone; 80168379AG / Doxorubicin
  • [Number-of-references] 46
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41. Tassinari D, Poggi B, Nicoletti S, Fantini M, Tamburini E, Possenti C, Sartori S: Zoledronic acid treatment at home: safety data from an observational prospective trial. J Palliat Med; 2007 Apr;10(2):352-8
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  • [Title] Zoledronic acid treatment at home: safety data from an observational prospective trial.
  • BACKGROUND: To prospectively assess feasibility, side effects, and safety of a home treatment with zoledronic acid in patients with bone metastases confined to home.
  • Primary end point of this observational trial was the safety assessment of the treatment at home; secondary end points were the clinical assessment of the time to treatment discontinuation and the definition of a pattern of patients who could benefit by a home treatment with intravenous bisphosphonates.
  • RESULTS: Nineteen patients had breast cancer; 7, multiple myeloma; 5, non-small-cell lung cancer; 4, renal cancer; 4, prostate cancer; 1, thyroid cancer; 1 non-Hodgkin's lymphoma; and 1 soft tissue sarcoma.
  • On the whole, 220 home treatments were administered in 3 years, with a median of 4 administrations per patient (range, 1-28).
  • Median time to treatment discontinuation was 130 days.
  • The treatment was interrupted for worsening of the performance status in 30 patients (71.4%), length of the treatment greater than 24 months in 2 patients (4.8%), hypocalcemia in 1 patient (2.4%), renal failure in 1 patient (2.4%).
  • No difference in median time to treatment discontinuation was observed among patients with breast cancer, multiple myeloma, or other tumors in univariate analysis.
  • Multivariate analysis showed no prognostic significance for kind of tumor, age at the time of entering the trial, gender, and number of extraosseous sites of disease.
  • No acute major side effects were observed during the treatment, and the treatment had to be interrupted for side effects in 2 patients (4.8%).
  • One patient had jaw osteonecrosis some months after the treatment was stopped.
  • CONCLUSIONS: The home treatment with zoledronic acid seems safe.
  • The appropriate use of biphosphonates in such a new setting needs a criterion to identify the subset of patients with bone metastases confined to home who can really benefit by this treatment.
  • [MeSH-major] Bone Density Conservation Agents / therapeutic use. Bone Neoplasms / drug therapy. Breast Neoplasms / pathology. Diphosphonates / therapeutic use. Home Care Services. Imidazoles / therapeutic use. Multiple Myeloma / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Creatinine / blood. Drug-Related Side Effects and Adverse Reactions. Feasibility Studies. Female. Humans. Karnofsky Performance Status. Male. Middle Aged. Observation. Prospective Studies. Survival Analysis. Time Factors

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  • (PMID = 17472506.001).
  • [ISSN] 1096-6218
  • [Journal-full-title] Journal of palliative medicine
  • [ISO-abbreviation] J Palliat Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid; AYI8EX34EU / Creatinine
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42. Kelloff GJ, Hoffman JM, Johnson B, Scher HI, Siegel BA, Cheng EY, Cheson BD, O'shaughnessy J, Guyton KZ, Mankoff DA, Shankar L, Larson SM, Sigman CC, Schilsky RL, Sullivan DC: Progress and promise of FDG-PET imaging for cancer patient management and oncologic drug development. Clin Cancer Res; 2005 Apr 15;11(8):2785-808
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  • [Title] Progress and promise of FDG-PET imaging for cancer patient management and oncologic drug development.
  • 2-[(18)F]Fluoro-2-deoxyglucose positron emission tomography (FDG-PET) assesses a fundamental property of neoplasia, the Warburg effect.
  • However, because it accurately detects recurrent or residual disease, FDG-PET also has significant potential for assessing therapy response.
  • In this regard, it can improve patient management by identifying responders early, before tumor size is reduced; nonresponders could discontinue futile therapy.
  • Moreover, a reduction in the FDG-PET signal within days or weeks of initiating therapy (e.g., in lymphoma, non-small cell lung, and esophageal cancer) significantly correlates with prolonged survival and other clinical end points now used in drug approvals.
  • These findings suggest that FDG-PET could facilitate drug development as an early surrogate of clinical benefit.
  • Its potential to facilitate drug development in seven oncologic settings (lung, lymphoma, breast, prostate, sarcoma, colorectal, and ovary) is addressed.
  • Recommendations include initial validation against approved therapies, retrospective analyses to define the magnitude of change indicative of response, further prospective validation as a surrogate of clinical benefit, and application as a phase II/III trial end point to accelerate evaluation and approval of novel regimens and therapies.
  • [MeSH-major] Fluorodeoxyglucose F18. Neoplasms / radionuclide imaging. Positron-Emission Tomography / methods

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  • (PMID = 15837727.001).
  • [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
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0Z5B2CJX4D / Fluorodeoxyglucose F18
  • [Number-of-references] 274
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