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1. Linehan WM, Bratslavsky G, Pinto PA, Schmidt LS, Neckers L, Bottaro DP, Srinivasan R: Molecular diagnosis and therapy of kidney cancer. Annu Rev Med; 2010;61:329-43
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  • Kidney cancer is not a single disease; it is made up of a number of cancers that occur in the kidney, each having a different histology, following a different clinical course, responding differently to therapy, and caused by a different gene.
  • Understanding the genetic basis of cancer of the kidney has significant implications for diagnosis and management of this disease.
  • Knowledge of this pathway provided the foundation for the development of novel therapeutic approaches now approved for treatment of this disease.
  • MET is the gene for the hereditary form of type 1 papillary renal carcinoma and is mutated in a subset of sporadic type 1 papillary kidney cancers.
  • Clinical trials are currently ongoing with agents targeting the tyrosine kinase domain of MET in sporadic and hereditary forms of papillary kidney cancer.
  • BHD is the gene for the hereditary type of chromophobe kidney cancer.
  • Hereditary leiomyomatosis renal cell carcinoma, a hereditary form of type 2 papillary renal carcinoma, is caused by inactivation of a Krebs cycle enzyme due to mutation.
  • Knowledge of these kidney cancer gene pathways has enabled new approaches in the management of this disease and has provided the foundation for the development of targeted therapeutics.

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  • [Cites] J Clin Oncol. 2009 Mar 20;27(9):1432-9 [19224847.001]
  • [Cites] Biochim Biophys Acta. 2009 Apr;1795(2):162-72 [19344680.001]
  • [Cites] Cancer. 2009 May 15;115(10 Suppl):2321-6 [19402067.001]
  • [Cites] Cancer. 2009 Jul 1;115(13):2844-52 [19402168.001]
  • [Cites] J Clin Oncol. 2009 Jul 10;27(20):3312-8 [19451442.001]
  • [Cites] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385.001]
  • [Cites] Mol Cell Biol. 2009 Aug;29(15):4080-90 [19470762.001]
  • [Cites] Fam Cancer. 2009;8(3):257-60 [19184535.001]
  • [Cites] J Urol. 2009 Oct;182(4):1280-6 [19683275.001]
  • [Cites] J Clin Oncol. 1997 Apr;15(4):1529-37 [9193349.001]
  • [Cites] Cancer Res. 1998 Apr 15;58(8):1719-22 [9563489.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12596-601 [9770531.001]
  • [Cites] Hum Mutat. 1998;12(6):417-23 [9829911.001]
  • [Cites] Science. 1999 Apr 16;284(5413):455-61 [10205047.001]
  • [Cites] J Urol. 1999 May;161(5):1475-9 [10210376.001]
  • [Cites] Science. 1999 Apr 23;284(5414):657-61 [10213691.001]
  • [Cites] JAMA. 1999 May 5;281(17):1628-31 [10235157.001]
  • [Cites] Oncogene. 1999 Apr 8;18(14):2343-50 [10327054.001]
  • [Cites] Nature. 1999 May 20;399(6733):271-5 [10353251.001]
  • [Cites] J Urol. 1999 Jul;162(1):43-5 [10379736.001]
  • [Cites] Am J Hum Genet. 2005 Jun;76(6):1023-33 [15852235.001]
  • [Cites] J Natl Cancer Inst. 2005 Jun 15;97(12):931-5 [15956655.001]
  • [Cites] Cancer Cell. 2005 Aug;8(2):143-53 [16098467.001]
  • [Cites] J Med Genet. 2006 Jan;43(1):18-27 [15937070.001]
  • [Cites] Nat Med. 2006 Jan;12(1):122-7 [16341243.001]
  • [Cites] N Engl J Med. 2006 Sep 28;355(13):1345-56 [17005952.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15552-7 [17028174.001]
  • [Cites] Br J Cancer. 1999 Oct;81(4):741-6 [10574265.001]
  • [Cites] J Clin Invest. 1999 Dec;104(11):1583-91 [10587522.001]
  • [Cites] J Urol. 2000 Feb;163(2):431-3 [10647647.001]
  • [Cites] Nat Cell Biol. 2000 Jul;2(7):423-7 [10878807.001]
  • [Cites] J Urol. 2001 Mar;165(3):777-81 [11176466.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3387-92 [11248088.001]
  • [Cites] Science. 2001 Apr 20;292(5516):468-72 [11292861.001]
  • [Cites] J Urol. 2001 May;165(5):1623-4 [11342935.001]
  • [Cites] N Engl J Med. 2001 Dec 6;345(23):1655-9 [11759643.001]
  • [Cites] Nat Genet. 2002 Apr;30(4):406-10 [11865300.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2002 Apr;11(4):393-400 [11927500.001]
  • [Cites] Cancer Cell. 2002 Aug;2(2):157-64 [12204536.001]
  • [Cites] Mol Cell Biol. 2002 Oct;22(20):7004-14 [12242281.001]
  • [Cites] Am J Surg Pathol. 2002 Dec;26(12):1542-52 [12459621.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):327-37 [12538485.001]
  • [Cites] Clin Cancer Res. 2003 Feb;9(2):802-11 [12576453.001]
  • [Cites] Am J Hum Genet. 2003 Jul;73(1):95-106 [12772087.001]
  • [Cites] N Engl J Med. 2003 Jul 31;349(5):427-34 [12890841.001]
  • [Cites] J Urol. 2003 Dec;170(6 Pt 1):2163-72 [14634372.001]
  • [Cites] Am J Hum Genet. 2004 Jan;74(1):153-9 [14685938.001]
  • [Cites] J Urol. 2004 Jun;171(6 Pt 1):2461-6 [15126876.001]
  • [Cites] J Urol. 2004 Jul;172(1):63-5 [15201738.001]
  • [Cites] JAMA. 2004 Aug 25;292(8):943-51 [15328326.001]
  • [Cites] Science. 1993 May 28;260(5112):1317-20 [8493574.001]
  • [Cites] Urology. 1993 Sep;42(3):250-7; discussion 257-8 [8379024.001]
  • [Cites] J Urol. 1994 Mar;151(3):561-6 [8308957.001]
  • [Cites] Nat Genet. 1994 May;7(1):85-90 [7915601.001]
  • [Cites] J Urol. 1995 Mar;153(3 Pt 2):913-6 [7853573.001]
  • [Cites] Science. 1995 Sep 8;269(5229):1402-6 [7660122.001]
  • [Cites] Science. 1995 Sep 8;269(5229):1444-6 [7660130.001]
  • [Cites] J Urol. 1995 Dec;154(6):2010-4; discussion 2014-5 [7500446.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Mar 18;94(6):2156-61 [9122164.001]
  • [Cites] Nat Genet. 1997 May;16(1):68-73 [9140397.001]
  • [Cites] N Engl J Med. 2007 Jan 11;356(2):115-24 [17215529.001]
  • [Cites] N Engl J Med. 2007 Jan 11;356(2):125-34 [17215530.001]
  • [Cites] Clin Cancer Res. 2007 Jan 15;13(2 Pt 2):671s-679s [17255292.001]
  • [Cites] Lancet Oncol. 2007 Apr;8(4):304-10 [17395103.001]
  • [Cites] Am J Respir Crit Care Med. 2007 May 15;175(10):1044-53 [17322109.001]
  • [Cites] J Urol. 2007 Jun;177(6):2074-9; discussion 2079-80 [17509289.001]
  • [Cites] N Engl J Med. 2007 May 31;356(22):2271-81 [17538086.001]
  • [Cites] J Urol. 2007 Jul;178(1):41-6 [17574056.001]
  • [Cites] Lancet Oncol. 2007 Nov;8(11):975-84 [17959415.001]
  • [Cites] Lancet Oncol. 2007 Nov;8(11):956-7 [17976606.001]
  • [Cites] N Engl J Med. 2008 Jan 10;358(2):140-51 [18184959.001]
  • [Cites] J Natl Cancer Inst. 2008 Jan 16;100(2):140-54 [18182616.001]
  • [Cites] Eur Urol. 2008 Mar;53(3):514-21 [17961910.001]
  • [Cites] Eur Urol. 2008 Apr;53(4):845-8 [18053636.001]
  • [Cites] Clin Cancer Res. 2008 Apr 15;14(8):2431-6 [18413834.001]
  • [Cites] Gene. 2008 May 31;415(1-2):60-7 [18403135.001]
  • [Cites] Expert Opin Biol Ther. 2008 Jun;8(6):779-90 [18476789.001]
  • [Cites] J Urol. 2008 Jul;180(1):94-8 [18485389.001]
  • [Cites] Clin Cancer Res. 2008 Aug 1;14(15):4726-34 [18676741.001]
  • [Cites] Lancet. 2008 Aug 9;372(9637):449-56 [18653228.001]
  • [Cites] Curr Oncol Rep. 2008 May;10(3):245-52 [18765155.001]
  • [Cites] J Natl Cancer Inst. 2008 Sep 3;100(17):1260-2 [18728283.001]
  • [Cites] Clin Endocrinol (Oxf). 2008 Oct;69(4):587-96 [18419787.001]
  • [Cites] BJU Int. 2008 Sep;102(6):692-6 [18410444.001]
  • [Cites] Mol Cancer Ther. 2008 Oct;7(10):3129-40 [18852116.001]
  • [Cites] Urology. 2008 Nov;72(5):1077-82 [18805573.001]
  • [Cites] Urol Clin North Am. 2008 Nov;35(4):627-34; vii [18992616.001]
  • [Cites] J Urol. 2008 Dec;180(6):2353-6; discussion 2356 [18930263.001]
  • [Cites] J Urol. 2009 Jan;181(1):55-61; discussion 61-2 [19012918.001]
  • [Cites] Clin Genitourin Cancer. 2009 Jan;7(1):24-7 [19213664.001]
  • [Cites] Clin Genitourin Cancer. 2009 Jan;7(1):28-33 [19213665.001]
  • (PMID = 20059341.001).
  • [ISSN] 1545-326X
  • [Journal-full-title] Annual review of medicine
  • [ISO-abbreviation] Annu. Rev. Med.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / BC / Z01 BC011089-01; United States / NCI NIH HHS / BC / Z01 BC011028-01; United States / Intramural NIH HHS / / ; United States / NCI NIH HHS / BC / Z01 BC011038-01; United States / PHS HHS / / HHSN261200800001E; United States / CCR NIH HHS / RC / HHSN261200800001C; United States / NCI NIH HHS / CA / HHSN261200800001E; United States / NCI NIH HHS / BC / Z01 BC011043-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / FLCN protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Growth Factor; 0 / Tumor Suppressor Proteins; 0 / tuberous sclerosis complex 1 protein; 4JG2LF96VF / tuberous sclerosis complex 2 protein; EC 2.7.10.1 / MET protein, human; EC 2.7.10.1 / Proto-Oncogene Proteins c-met; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Number-of-references] 94
  • [Other-IDs] NLM/ NIHMS223760; NLM/ PMC2921612
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2. Linehan WM, Pinto PA, Bratslavsky G, Pfaffenroth E, Merino M, Vocke CD, Toro JR, Bottaro D, Neckers L, Schmidt LS, Srinivasan R: Hereditary kidney cancer: unique opportunity for disease-based therapy. Cancer; 2009 May 15;115(10 Suppl):2252-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hereditary kidney cancer: unique opportunity for disease-based therapy.
  • Kidney cancer is not a single disease; it is comprised of several different types of cancer, each with a different histology, with a different clinical course, caused by a different gene, and responding differently to therapy.
  • Understanding the VHL-hypoxia inducible factor (HIF) pathway has provided the foundation for the development of several agents targeting this pathway, such as sunitinib, sorafenib, and temsirolimus.
  • Hereditary papillary renal carcinoma (HPRC) is a hereditary renal cancer syndrome in which affected individuals are at risk for the development of bilateral, multifocal, type 1 papillary renal cell carcinoma.
  • Mutations of MET also have been identified in a subset of tumors from patients with sporadic type 1 papillary renal cell carcinoma (RCC).
  • Preclinical studies are underway targeting the BHD gene pathway in preparation for clinical trials in Birt-Hogg-Dube and sporadic chromophobe RCC.
  • Patients with hereditary leiomyomatosis RCC (HLRCC) are at risk for developing cutaneous and uterine leiomyomas and a very aggressive type of RCC.
  • HLRCC is characterized by germline mutation of the Krebs cycle enzyme, fumarate hydratase (FH).


3. Krebs LJ: Calcimimetics and hyperparathyroidism. Curr Opin Investig Drugs; 2004 Oct;5(10):1080-5
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  • Results from clinical trials using calcimimetics to treat primary and secondary HPT, as well as primary HPT from parathyroid carcinoma, suggest that calcimimetic compounds could provide an effective alternative or additional therapeutic approach for various forms of HPT.
  • [MeSH-major] Calcium / metabolism. Hyperparathyroidism / drug therapy. Receptors, Calcium-Sensing / agonists
  • [MeSH-minor] Aniline Compounds / pharmacology. Aniline Compounds / therapeutic use. Humans. Hyperparathyroidism, Secondary / drug therapy. Hyperparathyroidism, Secondary / metabolism. Parathyroid Hormone / secretion

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  • (PMID = 15535429.001).
  • [ISSN] 1472-4472
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aniline Compounds; 0 / N-(2-chlorophenylpropyl)-1-(3-methoxyphenyl)ethylamine; 0 / Parathyroid Hormone; 0 / Receptors, Calcium-Sensing; SY7Q814VUP / Calcium
  • [Number-of-references] 47
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4. Perumal SS, Shanthi P, Sachdanandam P: Energy-modulating vitamins--a new combinatorial therapy prevents cancer cachexia in rat mammary carcinoma. Br J Nutr; 2005 Jun;93(6):901-9
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  • [Title] Energy-modulating vitamins--a new combinatorial therapy prevents cancer cachexia in rat mammary carcinoma.
  • Mammary carcinoma was induced by the oral administration of 7,12-dimethylbenz[a]anthracene (25 mg/kg body weight), and treatment was started by the oral administration of the energy-modulating vitamins riboflavin (45 mg/kg body weight per d), niacin (100 mg/kg body weight per d) and coenzyme Q10 (40 mg/kg body weight per d) for 28 d.
  • Mitochondria were isolated from the mammary gland and liver of all four groups, and the Krebs cycle and oxidative phosphorylation enzymes were assayed.
  • In mammary carcinoma-bearing animals, the activities of the Krebs cycle and oxidative phosphorylation enzymes were significantly decreased.
  • These activities were restored to a greater extent in animals treated with energy-modulating vitamins.
  • [MeSH-minor] Adenosine Triphosphate / metabolism. Administration, Oral. Animals. Antioxidants / administration & dosage. Citric Acid Cycle / physiology. Coenzymes. Drug Therapy, Combination. Energy Metabolism / physiology. Female. Liver / enzymology. Mammary Glands, Animal / enzymology. Mitochondria / enzymology. Niacin / administration & dosage. Oxidative Phosphorylation. Rats. Rats, Sprague-Dawley. Riboflavin / administration & dosage. Ubiquinone / administration & dosage. Ubiquinone / analogs & derivatives

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  • (PMID = 16022760.001).
  • [ISSN] 0007-1145
  • [Journal-full-title] The British journal of nutrition
  • [ISO-abbreviation] Br. J. Nutr.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Coenzymes; 12001-76-2 / Vitamin B Complex; 1339-63-5 / Ubiquinone; 2679MF687A / Niacin; 8L70Q75FXE / Adenosine Triphosphate; EJ27X76M46 / coenzyme Q10; TLM2976OFR / Riboflavin
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5. Toohey JI: Dehydroascorbic acid as an anti-cancer agent. Cancer Lett; 2008 May 18;263(2):164-9
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  • [Title] Dehydroascorbic acid as an anti-cancer agent.
  • In 1982, Poydock and colleagues found that dehydroascorbic acid has the remarkable ability to eliminate the aggressive mouse tumours, L1210, P388, Krebs sarcoma, and Ehrlich carcinoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Dehydroascorbic Acid / therapeutic use. Neoplasms / drug therapy
  • [MeSH-minor] Animals. Ascorbic Acid / therapeutic use. Homocysteine / analogs & derivatives. Homocysteine / metabolism. Humans. Methionine / metabolism. Mice

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  • (PMID = 18378072.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0LVT1QZ0BA / Homocysteine; AE28F7PNPL / Methionine; D5H88XF24X / homocysteine thiolactone; PQ6CK8PD0R / Ascorbic Acid; Y2Z3ZTP9UM / Dehydroascorbic Acid
  • [Number-of-references] 23
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6. Hogan AM, Collins D, Sheehan K, Zierau O, Baird AW, Winter DC: Rapid effects of phytoestrogens on human colonic smooth muscle are mediated by oestrogen receptor beta. Mol Cell Endocrinol; 2010 May 14;320(1-2):106-10
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  • Histologically normal colon was obtained from the proximal resection margin of colorectal carcinoma specimens.
  • Circular smooth muscle strips were microdissected and suspended under 1g of tension in organ baths containing oxygenated Krebs solution at 37 degrees C.
  • [MeSH-major] Colon / drug effects. Colon / metabolism. Estrogen Receptor beta / metabolism. Muscle, Smooth / drug effects. Muscle, Smooth / metabolism. Phytoestrogens / pharmacology
  • [MeSH-minor] Butadienes / pharmacology. Cycloheximide / pharmacology. Estradiol / analogs & derivatives. Estradiol / pharmacology. Humans. Imidazoles / pharmacology. In Vitro Techniques. Muscle Contraction / drug effects. NG-Nitroarginine Methyl Ester / pharmacology. Nitriles / pharmacology. Pyridines / pharmacology. Reproducibility of Results. Tissue Survival / drug effects

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  • [Copyright] (c) 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20109521.001).
  • [ISSN] 1872-8057
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Butadienes; 0 / Estrogen Receptor beta; 0 / Imidazoles; 0 / Nitriles; 0 / Phytoestrogens; 0 / Pyridines; 0 / SB 203580; 0 / U 0126; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol; 98600C0908 / Cycloheximide; V55S2QJN2X / NG-Nitroarginine Methyl Ester
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7. Schulte KM, Jonas C, Krebs R, Röher HD: Activin A and activin receptors in thyroid cancer. Thyroid; 2001 Jan;11(1):3-14
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  • Two subtypes of type I and type II activin receptors were demonstrated.
  • To our knowledge these are the first data to demonstrate reversal of activin and TGF-beta1 effects in thyroid malignancy and to demonstrate changes of the type Ib activin receptor expression in thyroid malignancy.
  • [MeSH-minor] Activin Receptors. Activins. Adenocarcinoma, Follicular / chemistry. Adenocarcinoma, Follicular / pathology. Aged. Alternative Splicing. Apoptosis. Carcinoma, Papillary / chemistry. Carcinoma, Papillary / pathology. Cell Division / drug effects. Child. Culture Media. Epithelial Cells / pathology. Female. Gene Expression. Humans. Lymphatic Metastasis. Male. Middle Aged. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor beta / pharmacology. Tumor Cells, Cultured

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  • (PMID = 11272093.001).
  • [ISSN] 1050-7256
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media; 0 / RNA, Messenger; 0 / Receptors, Growth Factor; 0 / Transforming Growth Factor beta; 104625-48-1 / Activins; 57285-09-3 / Inhibins; EC 2.7.11.30 / Activin Receptors
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8. [Very promising phytotherapeutic agent in cancer?]. Praxis (Bern 1994); 2005 Jan 12;94(1-2):48-9
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  • [Title] [Very promising phytotherapeutic agent in cancer?].
  • [Transliterated title] Vielversprechendes Phytotherapeutikum bei Krebs?
  • [MeSH-major] Antineoplastic Agents, Phytogenic / therapeutic use. Drugs, Chinese Herbal / therapeutic use. Isodon. Neoplasms / drug therapy. Phytotherapy
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Carcinoma / drug therapy. Cell Survival / drug effects. Drug Synergism. Female. Humans. Male. Mice. Neoplasm Transplantation. Prostatic Neoplasms / drug therapy. Transplantation, Heterologous. Tumor Cells, Cultured / drug effects

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  • (PMID = 15697150.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / herbal preparation PC-SPES
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9. Herbst RS, Giaccone G, Schiller JH, Natale RB, Miller V, Manegold C, Scagliotti G, Rosell R, Oliff I, Reeves JA, Wolf MK, Krebs AD, Averbuch SD, Ochs JS, Grous J, Fandi A, Johnson DH: Gefitinib in combination with paclitaxel and carboplatin in advanced non-small-cell lung cancer: a phase III trial--INTACT 2. J Clin Oncol; 2004 Mar 1;22(5):785-94
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  • PURPOSE: Preclinical studies indicate that gefitinib (Iressa, ZD1839; AstraZeneca, Wilmington, DE), an orally active epidermal growth factor receptor tyrosine kinase inhibitor, may enhance antitumor efficacy of cytotoxics, and combination with paclitaxel and carboplatin had acceptable tolerability in a phase I trial.
  • Gefitinib monotherapy demonstrated unparalleled antitumor activity for a biologic agent, with less toxicity than docetaxel, in phase II trials in refractory, advanced non-small-cell lung cancer (NSCLC).
  • After a maximum of six cycles, daily gefitinib or placebo continued until disease progression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Maximum Tolerated Dose. Paclitaxel / administration & dosage. Quinazolines / administration & dosage
  • [MeSH-minor] Adult. Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Infusions, Intravenous. Male. Middle Aged. Multivariate Analysis. Neoplasm Staging. Predictive Value of Tests. Prognosis. Reference Values. Risk Assessment. Survival Analysis. Treatment Outcome


10. Hou JM, Greystoke A, Lancashire L, Cummings J, Ward T, Board R, Amir E, Hughes S, Krebs M, Hughes A, Ranson M, Lorigan P, Dive C, Blackhall FH: Evaluation of circulating tumor cells and serological cell death biomarkers in small cell lung cancer patients undergoing chemotherapy. Am J Pathol; 2009 Aug;175(2):808-16
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  • Blood samples from 88 patients were assayed using enzyme-linked immunosorbent assays for various cytokeratin 18 products (eg, M65, cell death, M30, and apoptosis) as well as nucleosomal DNA.
  • Our results provide a rationale to include the use of serological biomarkers and CTCs in early clinical trials of new agents for small cell lung cancer.

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  • [Cites] Anticancer Res. 2006 May-Jun;26(3B):2387-92 [16821621.001]
  • [Cites] Br J Cancer. 2006 Jul 3;95(1):42-8 [16804528.001]
  • [Cites] Curr Opin Oncol. 2007 Mar;19(2):103-8 [17272981.001]
  • [Cites] J Thorac Oncol. 2006 Mar;1(3):270-8 [17409868.001]
  • [Cites] Clin Cancer Res. 2007 Jun 1;13(11):3198-206 [17545523.001]
  • [Cites] Mol Cancer Ther. 2008 Mar;7(3):455-63 [18347133.001]
  • [Cites] Ann Oncol. 2008 May;19(5):990-5 [18304966.001]
  • [Cites] J Clin Oncol. 2008 Jul 1;26(19):3213-21 [18591556.001]
  • [Cites] Neoplasia. 2008 Oct;10(10):1041-8 [18813353.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):6302-9 [18829513.001]
  • [Cites] Ann N Y Acad Sci. 2008 Aug;1137:98-107 [18837931.001]
  • [Cites] Ann N Y Acad Sci. 2008 Aug;1137:180-9 [18837945.001]
  • [Cites] Clin Cancer Res. 2008 Dec 1;14(23):7813-21 [19047109.001]
  • [Cites] J Thorac Oncol. 2009 Jan;4(1):30-6 [19096303.001]
  • [Cites] Lung Cancer. 2007 Jun;56(3):399-404 [17316892.001]
  • [Cites] Nat Biotechnol. 1999 Dec;17(12):1210-3 [10585720.001]
  • [Cites] Clin Cancer Res. 2000 Feb;6(2):597-601 [10690544.001]
  • [Cites] Clin Chem Lab Med. 2001 Jul;39(7):596-605 [11522104.001]
  • [Cites] Cytometry. 2002 Jun 15;50(3):160-7 [12116339.001]
  • [Cites] Lung Cancer. 2003 Mar;39(3):303-13 [12609569.001]
  • [Cites] Eur J Cancer. 2003 Apr;39(6):769-74 [12651202.001]
  • [Cites] Cancer. 2003 May 15;97(10):2404-11 [12733138.001]
  • [Cites] Blood. 2003 Sep 15;102(6):2243-50 [12775567.001]
  • [Cites] Cancer Res. 2004 Mar 1;64(5):1751-6 [14996736.001]
  • [Cites] Clin Biochem. 2004 Jul;37(7):605-17 [15234242.001]
  • [Cites] Shock. 2004 Sep;22(3):218-20 [15316390.001]
  • [Cites] Clin Cancer Res. 2004 Oct 15;10(20):6897-904 [15501967.001]
  • [Cites] J Clin Oncol. 1991 Jan;9(1):50-61 [1702146.001]
  • [Cites] Br J Cancer. 1996 Aug;74(3):463-7 [8695366.001]
  • [Cites] Br J Cancer. 2005 Feb 14;92(3):532-8 [15685240.001]
  • [Cites] J Viral Hepat. 2005 May;12(3):307-14 [15850472.001]
  • [Cites] Eur J Cancer. 2005 Aug;41(12):1690-6 [16043346.001]
  • [Cites] Lung Cancer. 2000 Oct;30(1):37-49 [11008008.001]
  • [Cites] Trends Mol Med. 2006 Mar;12(3):130-9 [16488189.001]
  • [Cites] J Natl Cancer Inst. 2006 May 3;98(9):580-98 [16670384.001]
  • [Cites] Expert Opin Investig Drugs. 2006 Jun;15(6):669-90 [16732718.001]
  • [Cites] Br J Cancer. 2006 Jun 5;94(11):1592-8 [16685278.001]
  • [Cites] Clin Cancer Res. 2006 Jul 15;12(14 Pt 1):4218-24 [16857794.001]
  • (PMID = 19628770.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
  • [Other-IDs] NLM/ PMC2716975
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11. Fan TW, Lane AN, Higashi RM, Farag MA, Gao H, Bousamra M, Miller DM: Altered regulation of metabolic pathways in human lung cancer discerned by (13)C stable isotope-resolved metabolomics (SIRM). Mol Cancer; 2009 Jun 26;8:41
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  • To this purpose, metabolic changes were investigated by infusing uniformly labeled 13C-glucose into human lung cancer patients, followed by resection and processing of paired non-cancerous lung and non small cell carcinoma tissues.
  • 13C-enrichment in lactate, Ala, succinate, Glu, Asp, and citrate was also higher in the tumors, suggesting more active glycolysis and Krebs cycle in the tumor tissues.
  • This is consistent with the transformations of glucose into Asp or Glu via glycolysis, anaplerotic pyruvate carboxylation (PC), and the Krebs cycle.
  • CONCLUSION: PC activation - revealed here for the first time in human subjects - may be important for replenishing the Krebs cycle intermediates which can be diverted to lipid, protein, and nucleic acid biosynthesis to fulfill the high anabolic demands for growth in lung tumor tissues.

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  • [Cites] Anal Chem. 2006 Jul 1;78(13):4334-41 [16808440.001]
  • [Cites] Rapid Commun Mass Spectrom. 2006;20(10):1577-84 [16628593.001]
  • [Cites] Metab Eng. 2006 Nov;8(6):639-52 [16904360.001]
  • [Cites] Am J Physiol Cell Physiol. 2006 Dec;291(6):C1114-20 [16760265.001]
  • [Cites] Drug Metab Rev. 2006;38(4):707-32 [17145697.001]
  • [Cites] J Cereb Blood Flow Metab. 2007 Feb;27(2):219-49 [16835632.001]
  • [Cites] Methods Cell Biol. 2008;84:541-88 [17964943.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19345-50 [18032601.001]
  • [Cites] Mol Cancer. 2008;7:79 [18939998.001]
  • [Cites] Biotechnol Bioeng. 1999;66(4):238-46 [10578094.001]
  • [Cites] Antioxid Redox Signal. 2001 Jun;3(3):361-73 [11491650.001]
  • [Cites] Adv Biochem Eng Biotechnol. 2001;73:9-29 [11816814.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):2708-13 [11880625.001]
  • [Cites] J Biol Chem. 2002 Jun 28;277(26):23111-5 [11943784.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5881-7 [12384552.001]
  • [Cites] Anticancer Res. 2003 Mar-Apr;23(2A):1149-54 [12820363.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13537-42 [14573703.001]
  • [Cites] Tumour Biol. 2003 Aug-Sep;24(4):199-202 [14654714.001]
  • [Cites] Biochem J. 2004 Feb 15;378(Pt 1):17-20 [14683524.001]
  • [Cites] Nucl Med Commun. 2004 Jan;25(1):11-7 [15061260.001]
  • [Cites] Biochem Biophys Res Commun. 1991 Aug 30;179(1):366-71 [1883366.001]
  • [Cites] Eur J Biochem. 1993 Oct 1;217(1):457-68 [7901007.001]
  • [Cites] Am J Physiol. 1998 May;274(5 Pt 1):E843-51 [9612242.001]
  • [Cites] Anal Biochem. 1998 Oct 15;263(2):139-49 [9799525.001]
  • [Cites] Hum Gene Ther. 1999 Jan 20;10(2):155-64 [10022541.001]
  • [Cites] Science. 1956 Feb 24;123(3191):309-14 [13298683.001]
  • [Cites] Genomics. 2004 Dec;84(6):1014-20 [15533718.001]
  • [Cites] Neoplasia. 2005 Jan;7(1):1-6 [15736311.001]
  • [Cites] Med Hypotheses. 2005;65(3):525-9 [15905043.001]
  • [Cites] J Chromatogr A. 2005 Aug 19;1084(1-2):145-51 [16114247.001]
  • [Cites] Biomarkers. 2005 Nov-Dec;10(6):401-16 [16308265.001]
  • [Cites] Oncogene. 2006 Aug 7;25(34):4675-82 [16892081.001]
  • (PMID = 19558692.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / 1R01CA118434-01A2; United States / NCI NIH HHS / CA / 1R01CA101199-01; United States / NCRR NIH HHS / RR / P20 RR018733; United States / NCRR NIH HHS / RR / RR018733; United States / NCI NIH HHS / CA / R01 CA118434; United States / NCI NIH HHS / CA / R01 CA101199
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carbon Isotopes; 33X04XA5AT / Lactic Acid; EC 6.4.1.1 / Pyruvate Carboxylase; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ PMC2717907
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12. Krebs LJ, Wang X, Nagy A, Schally AV, Prasad PN, Liebow C: A conjugate of doxorubicin and an analog of Luteinizing Hormone-Releasing Hormone shows increased efficacy against oral and laryngeal cancers. Oral Oncol; 2002 Oct;38(7):657-663
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  • Here, AN-152 was tested on oral (KB) and laryngeal (HEp-2) carcinoma cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Doxorubicin / administration & dosage. Doxorubicin / analogs & derivatives. Gonadotropin-Releasing Hormone / administration & dosage. Gonadotropin-Releasing Hormone / analogs & derivatives. Laryngeal Neoplasms / drug therapy. Mouth Neoplasms / drug therapy
  • [MeSH-minor] Cell Division / drug effects. Drug Screening Assays, Antitumor. Epidermal Growth Factor / pharmacology. Humans. Tumor Cells, Cultured

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  • (PMID = 12353491.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Grant] United States / NIDCR NIH HHS / DE / 5K16 DE 00158
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 27844X2J29 / LHRH, lysine(6)-doxorubicin; 33515-09-2 / Gonadotropin-Releasing Hormone; 62229-50-9 / Epidermal Growth Factor; 80168379AG / Doxorubicin
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13. Yang Y, Valera VA, Padilla-Nash HM, Sourbier C, Vocke CD, Vira MA, Abu-Asab MS, Bratslavsky G, Tsokos M, Merino MJ, Pinto PA, Srinivasan R, Ried T, Neckers L, Linehan WM: UOK 262 cell line, fumarate hydratase deficient (FH-/FH-) hereditary leiomyomatosis renal cell carcinoma: in vitro and in vivo model of an aberrant energy metabolic pathway in human cancer. Cancer Genet Cytogenet; 2010 Jan 1;196(1):45-55
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  • [Title] UOK 262 cell line, fumarate hydratase deficient (FH-/FH-) hereditary leiomyomatosis renal cell carcinoma: in vitro and in vivo model of an aberrant energy metabolic pathway in human cancer.
  • Hereditary leiomyomatosis renal cell carcinoma (HLRCC) is an aggressive form of RCC characterized by germline mutation of the Krebs cycle enzyme fumarate hydratase (FH), and one known to be highly metastatic and unusually lethal.


14. Middleton LP, Palacios DM, Bryant BR, Krebs P, Otis CN, Merino MJ: Pleomorphic lobular carcinoma: morphology, immunohistochemistry, and molecular analysis. Am J Surg Pathol; 2000 Dec;24(12):1650-6
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  • [Title] Pleomorphic lobular carcinoma: morphology, immunohistochemistry, and molecular analysis.
  • Infiltrating pleomorphic lobular carcinoma (PLC) is an aggressive variant of infiltrating lobular carcinoma.
  • Six patients were a pathologic stage I; 19, stage II; 12, stage III; and one, stage IV.
  • PLCIS was identified in 17 of 38 patients (45%), and lobular carcinoma in situ (LCIS) was noted in 8 patients (21%).
  • Seven patients had no evidence of disease at last examination (range, 1-15 years), three patients were alive with disease (range, 2-14 years), and nine patients were dead of disease (range, 2 months-9 years).
  • Analysis shows that PLC tends to appear in older postmenopausal women who present with locally advanced disease.
  • Overexpression of Her 2 in PLC may be therapeutically relevant, enabling the use of novel chemotherapeutic drugs like Herceptin.
  • [MeSH-major] Breast Neoplasms / genetics. Breast Neoplasms / pathology. Carcinoma, Lobular / genetics. Carcinoma, Lobular / pathology


15. Wells SA Jr, Gosnell JE, Gagel RF, Moley J, Pfister D, Sosa JA, Skinner M, Krebs A, Vasselli J, Schlumberger M: Vandetanib for the treatment of patients with locally advanced or metastatic hereditary medullary thyroid cancer. J Clin Oncol; 2010 Feb 10;28(5):767-72
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  • PURPOSE There is no effective therapy for patients with distant metastasis of medullary thyroid carcinoma (MTC).
  • The dose was adjusted additionally in some patients on the basis of observed toxicity until disease progression or any other withdrawal criterion was met.
  • An additional 53% of patients (ie, 16 of 30 patients) experienced stable disease at >/= 24 weeks, which yielded a disease control rate of 73% (ie, 22 of 30 patients).
  • CONCLUSION In this study, vandetanib demonstrated durable objective partial responses and disease control with a manageable adverse event profile.
  • These results demonstrate that vandetanib may provide an effective therapeutic option in patients with advanced hereditary MTC, a rare disease for which there has been no effective therapy.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Carcinoma, Medullary / drug therapy. Piperidines / administration & dosage. Protein Kinase Inhibitors / administration & dosage. Proto-Oncogene Proteins c-ret / antagonists & inhibitors. Quinazolines / administration & dosage. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Adult. Aged. Biomarkers, Tumor / blood. Calcitonin / blood. Carcinoembryonic Antigen / blood. Disease-Free Survival. Drug Administration Schedule. Female. France. Genetic Predisposition to Disease. Germ-Line Mutation. Humans. Kaplan-Meier Estimate. Male. Middle Aged. Pedigree. Risk Factors. Time Factors. Treatment Outcome. United States. Young Adult


16. Choi J, Credit K, Henderson K, Deverkadra R, He Z, Wiig H, Vanpelt H, Flessner MF: Intraperitoneal immunotherapy for metastatic ovarian carcinoma: Resistance of intratumoral collagen to antibody penetration. Clin Cancer Res; 2006 Mar 15;12(6):1906-12
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  • [Title] Intraperitoneal immunotherapy for metastatic ovarian carcinoma: Resistance of intratumoral collagen to antibody penetration.
  • After anesthesia, the tumor serosal surface was treated for 2 hours with Krebs solution (control), collagenase (37.5 unit/mL), or hyaluronidase (10 unit/mL) followed by 3 hours of convective delivery of radiolabeled IgG.
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / pharmacokinetics. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Biological Transport / drug effects. Cell Line, Tumor. Collagenases / administration & dosage. Extracellular Matrix / metabolism. Female. Humans. Hyaluronoglucosaminidase / administration & dosage. Injections, Intraperitoneal. Neoplasm Metastasis. Rats. Rats, Nude. Trastuzumab. Xenograft Model Antitumor Assays

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  • (PMID = 16551876.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA085984; United States / NIDDK NIH HHS / DK / DK048479
  • [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 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Immunoglobulin G; 9007-34-5 / Collagen; EC 3.2.1.35 / Hyaluronoglucosaminidase; EC 3.4.24.- / Collagenases; P188ANX8CK / Trastuzumab
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17. Svitkin YV, Sonenberg N: A highly efficient and robust in vitro translation system for expression of picornavirus and hepatitis C virus RNA genomes. Methods Enzymol; 2007;429:53-82
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  • A Krebs-2 cell-free extract that efficiently translates encephalomyocarditis virus (EMCV) RNA and extensively processes the viral polyprotein is also capable of supporting complete infectious EMCV replication.
  • The system displays high RNA synthesis activity and de novo synthesis of virus up to titers of 2 x 10(7) to 6 x 10(7) plaque-forming units (pfu)/ml.
  • The preparation of Krebs-2 cell extract and methods of analysis of EMCV-specific processes in vitro are described.
  • We also demonstrate that the Krebs-2 cell-free system translates the entire open reading frame of the hepatitis C virus (HCV) RNA and properly processes the viral polyprotein when supplemented with canine microsomal membranes.
  • In addition to processing, other posttranslational modifications of HCV proteins take place in vitro, such as the N-terminal glycosylation of the E1 and the E2 precursor (E2-p7) and phosphorylation of NS5A.
  • The HCV RNA-programmed Krebs-2 cell-free extract should prove very useful as a novel screen for drugs that inhibit NS3-mediated processing.
  • The use of this system should help fill the gap in understanding the regulation of synthesis and maturation of HCV proteins.
  • [MeSH-minor] Animals. Carcinoma, Krebs 2 / metabolism. Cell-Free System. Female. Glycosylation. Mice. Viral Envelope Proteins / metabolism

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  • (PMID = 17913619.001).
  • [ISSN] 0076-6879
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Viral; 0 / Viral Envelope Proteins
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18. Schmittel A, Schulze K, Hütter G, Krebs P, Thiel E, Keilholz U: Phase I dose escalation study of carboplatin to a fixed dose of irinotecan as first-line treatment of small cell lung cancer. Onkologie; 2004 Jun;27(3):280-4
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  • If no grade IV neutropenia lasting for > or =7 days or thrombopenia or non-hematologic toxicity > or = grade III occurred, treatment was continued in the next dose level.
  • DLT was reached in dose level 2 with 2 grade IV neutropenias and 1 grade IV thrombopenia and diarrhea.
  • Of 15 evaluable patients, 10 had a partial response, 3 had disease stabilization and 2 progressed.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Camptothecin / administration & dosage. Camptothecin / adverse effects. Camptothecin / analogs & derivatives. Carboplatin / administration & dosage. Carboplatin / adverse effects. Carcinoma, Small Cell / drug therapy
  • [MeSH-minor] Aged. Dose-Response Relationship, Drug. Female. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / radiography. Maximum Tolerated Dose. Middle Aged. Neutropenia / chemically induced. Thrombocytopenia / chemically induced. Treatment Outcome

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  • [Copyright] Copyright 2004 S. Karger GmbH, Freiburg
  • (PMID = 15249718.001).
  • [ISSN] 0378-584X
  • [Journal-full-title] Onkologie
  • [ISO-abbreviation] Onkologie
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Comparative Study; Controlled Clinical Trial; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 7673326042 / irinotecan; BG3F62OND5 / Carboplatin; XT3Z54Z28A / Camptothecin
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