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1. Borders EB, Bivona C, Medina PJ: Mammalian target of rapamycin: biological function and target for novel anticancer agents. Am J Health Syst Pharm; 2010 Dec 15;67(24):2095-106
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  • [Title] Mammalian target of rapamycin: biological function and target for novel anticancer agents.
  • PURPOSE: The biological function of the mammalian target of rapamycin (mTOR) and mechanisms of action of mTOR inhibitors currently available for clinical use are described.
  • SUMMARY: mTOR is a target for anticancer agents due to its role in cancer development, progression, and resistance to other antineoplastic agents.
  • Clinical trials comparing single-agent temsirolimus with interferon alfa-2a demonstrated an improvement in overall survival and progression-free survival (PFS) in patients with metastatic RCC.
  • Due to its role in the phosphatidylinositol 3-kinase (PI3K) signaling pathway, mTOR is a rational target for inhibition in combination with other agents, including traditional chemotherapy and agents that are affected by or target the PI3K pathway.
  • Data from these studies review the use of mTOR inhibitors in non-Hodgkin's lymphoma and endometrial, breast, and neuroendocrine tumors.
  • Although relatively safe, these drugs are associated with some unique adverse effects, such as hyperlipidemia, hyperglycemia, and pneumonitis, that require monitoring and may require clinical intervention.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Neoplasms / drug therapy. TOR Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Drug Delivery Systems. Drug Design. Drug Monitoring / methods. Drug Resistance, Neoplasm. Everolimus. Humans. Sirolimus / adverse effects. Sirolimus / analogs & derivatives. Sirolimus / pharmacology

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  • (PMID = 21116000.001).
  • [ISSN] 1535-2900
  • [Journal-full-title] American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists
  • [ISO-abbreviation] Am J Health Syst Pharm
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 624KN6GM2T / temsirolimus; 9HW64Q8G6G / Everolimus; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
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2. Krishnan AV, Swami S, Feldman D: Estradiol inhibits glucocorticoid receptor expression and induces glucocorticoid resistance in MCF-7 human breast cancer cells. J Steroid Biochem Mol Biol; 2001 Apr;77(1):29-37
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  • [Title] Estradiol inhibits glucocorticoid receptor expression and induces glucocorticoid resistance in MCF-7 human breast cancer cells.
  • Our study has shown that treatment of MCF-7 human breast cancer cells with 17-beta estradiol (E(2)) produced significant decreases in glucocorticoid receptor (GR) concentrations and GR mRNA levels.
  • The E(2) induced resistance to glucocorticoid action may be of potential clinical significance in a number of settings including breast cancer, neuroendocrine response to stress and osteoporosis and could possibly contribute to the differences in glucocorticoid responsiveness among patients.
  • [MeSH-major] Breast Neoplasms / metabolism. Dexamethasone / pharmacology. Drug Resistance, Neoplasm. Estradiol / pharmacology. Receptors, Glucocorticoid / metabolism

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  • (PMID = 11358672.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK42482
  • [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] 0 / RNA, Messenger; 0 / Receptors, Glucocorticoid; 4TI98Z838E / Estradiol; 7S5I7G3JQL / Dexamethasone
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3. Gilbert JA, Frederick LM, Ames MM: The aromatic-L-amino acid decarboxylase inhibitor carbidopa is selectively cytotoxic to human pulmonary carcinoid and small cell lung carcinoma cells. Clin Cancer Res; 2000 Nov;6(11):4365-72
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  • The carcinoid tumor is an uncommon neuroendocrine neoplasm the hallmark of which is excessive serotonin production.
  • Carbidopa (100 microM) decreased growth of (but did not kill) SK-N-SH neuroblastoma and A204 rhabdomyosarcoma cells and did not affect proliferation of DU 145 prostate, MCF7 breast, or NCI-H460 large cell lung carcinoma lines.
  • [MeSH-major] Aromatic Amino Acid Decarboxylase Inhibitors. Carbidopa / pharmacology. Carcinoid Tumor / drug therapy. Carcinoma, Small Cell / drug therapy. Enzyme Inhibitors / pharmacology. Lung Neoplasms / drug therapy
  • [MeSH-minor] Cell Division / drug effects. Humans. Ileum / enzymology. Liver / enzymology. Microscopy, Electron. Tumor Cells, Cultured

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  • (PMID = 11106255.001).
  • [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 / CA 58450
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Aromatic Amino Acid Decarboxylase Inhibitors; 0 / Enzyme Inhibitors; MNX7R8C5VO / Carbidopa
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4. Osamura RY: Roles of pathologists in molecular targeted cancer therapy. J Cell Mol Med; 2009 Nov-Dec;13(11-12):4286-90
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  • Somatostatin analogue (SA) is the unique situation for the therapy of neuroendocrine tumors (NETs) which possess somatostatin receptor (SSTR).
  • Good examples are (1) trastuzumab, hMAB against HER2 in breast cancers with HER2 over-expression and amplification, (2) imatinib, TKI, for gastrointestinal stromal tumors (GISTs) with c-kit mutation, (3) gefitinib, TKI, for lung adenocarcinoma with EGFR mutation.
  • The drug effects have been reported to be associated with these molecular and genetic changes.
  • [MeSH-minor] Genes, Neoplasm. Humans. Signal Transduction

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  • (PMID = 19891708.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 33
  • [Other-IDs] NLM/ PMC4515045
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5. Gulec SA, Mesoloras G, Dezarn WA, McNeillie P, Kennedy AS: Safety and efficacy of Y-90 microsphere treatment in patients with primary and metastatic liver cancer: the tumor selectivity of the treatment as a function of tumor to liver flow ratio. J Transl Med; 2007;5:15
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  • RESULTS: Of the 40 patients, 5 had hepatocellular cancer (HCC), and 35 had metastatic liver tumors (15 colorectal cancer, 10 neuroendocrine tumors, 4 breast cancer, 2 lung cancer, 1 ovarian cancer, 1 endometrial cancer, and 2 unknown primary adenocarcinoma).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Toll-Like Receptors / metabolism. Treatment Outcome. Yttrium Radioisotopes

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  • (PMID = 17359531.001).
  • [ISSN] 1479-5876
  • [Journal-full-title] Journal of translational medicine
  • [ISO-abbreviation] J Transl Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Toll-Like Receptors; 0 / Yttrium Radioisotopes; 58784XQC3Y / Yttrium
  • [Other-IDs] NLM/ PMC1845138
  • [General-notes] NLM/ Original DateCompleted: 20070802
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6. Marot D, Bieche I, Aumas C, Esselin S, Bouquet C, Vacher S, Lazennec G, Perricaudet M, Kuttenn F, Lidereau R, de Roux N: High tumoral levels of Kiss1 and G-protein-coupled receptor 54 expression are correlated with poor prognosis of estrogen receptor-positive breast tumors. Endocr Relat Cancer; 2007 Sep;14(3):691-702
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  • [Title] High tumoral levels of Kiss1 and G-protein-coupled receptor 54 expression are correlated with poor prognosis of estrogen receptor-positive breast tumors.
  • KiSS1 is a putative metastasis suppressor gene in melanoma and breast cancer-encoding kisspeptins, which are also described as neuroendocrine regulators of the gonadotropic axis.
  • Estrogen receptor alpha (ERalpha level is recognized as a marker of breast cancer, raising the question of whether expression of KiSS1 and its G-protein-coupled receptor (GPR54) is down- or upregulated by estrogens in breast cancer cells.
  • The clinical relevance of this negative regulation of KiSS1 and GPR54 by E(2) was then studied in postmenopausal breast cancers.
  • KiSS1 mRNA increased with the grade of the breast tumors.
  • Among ERalpha-positive breast tumors from postmenopausal women treated with TAM, high KiSS1 combined with high GPR54 mRNA tumoral levels was unexpectedly associated with shorter relapse-free survival (RFS) relative to tumors expressing low tumoral mRNA levels of both genes.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma, Ductal, Breast / diagnosis. Neoplasms, Hormone-Dependent / diagnosis. Receptors, Estrogen / metabolism. Receptors, G-Protein-Coupled / genetics. Tumor Suppressor Proteins / genetics
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Disease-Free Survival. Down-Regulation / drug effects. Estrogens / pharmacology. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic / drug effects. Humans. Kisspeptins. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Neoplasm Recurrence, Local / genetics. Prognosis. Tamoxifen / pharmacology. Tamoxifen / therapeutic use. Tumor Cells, Cultured

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  • (PMID = 17914099.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Estrogens; 0 / KISS1 protein, human; 0 / KISS1R protein, human; 0 / Kisspeptins; 0 / Receptors, Estrogen; 0 / Receptors, G-Protein-Coupled; 0 / Tumor Suppressor Proteins; 094ZI81Y45 / Tamoxifen
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7. Rasmussen N, Ditzel HJ: Scanning the cell surface proteome of cancer cells and identification of metastasis-associated proteins using a subtractive immunization strategy. J Proteome Res; 2009 Nov;8(11):5048-59
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  • [Title] Scanning the cell surface proteome of cancer cells and identification of metastasis-associated proteins using a subtractive immunization strategy.
  • Identification of the cell surface proteome and comparison of their expression between cells with different phenotypic characteristics is crucial to the discovery of novel cancer drug targets as well as elucidating the basic biologic processes of cancer.
  • Concurrently, this method gives rise to valuable reagents for further characterization of the identified proteins.
  • Importantly, analysis on an extended panel of breast cancer cell lines demonstrated that the four mAbs bound preferentially to cell lines known to be metastatic in vivo, suggesting that these markers have general applications.
  • Immunohistochemical analysis showed that mAb 11E6 reacted preferentially with neuroendocrine tumors while exhibiting no or very weak reactivity with normal tissues. mAb 15C7 stained a variety of cancers as well as some normal lymphoid organs and was subsequently identified to react with HLA-DR-beta.
  • The study demonstrates the advantage of using the exquisitely discriminating recognition system of the immune system itself to scan the cell surface proteome for differentially expressed proteins.
  • [MeSH-major] Immunization / methods. Neoplasm Invasiveness / physiopathology. Neoplasm Proteins / metabolism. Neoplasms. Proteome / analysis
  • [MeSH-minor] Animals. Antibodies, Monoclonal / immunology. Breast Neoplasms / immunology. Breast Neoplasms / pathology. Cell Line, Tumor. Female. HLA-DR Antigens / immunology. Male. Mice. Mice, Nude. Mice, SCID. Tissue Distribution

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  • (PMID = 19764822.001).
  • [ISSN] 1535-3907
  • [Journal-full-title] Journal of proteome research
  • [ISO-abbreviation] J. Proteome Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / HLA-DR Antigens; 0 / Neoplasm Proteins; 0 / Proteome
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8. Franchi S, Panerai AE, Sacerdote P: Buprenorphine ameliorates the effect of surgery on hypothalamus-pituitary-adrenal axis, natural killer cell activity and metastatic colonization in rats in comparison with morphine or fentanyl treatment. Brain Behav Immun; 2007 Aug;21(6):767-74
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  • In normal animals morphine and fentanyl stimulate the HPA axis, decrease NK activity and augment tumor metastasis, while buprenorphine is devoid of these effects.
  • Only buprenorphine was able to prevent the neuroendocrine and immune system alterations and ameliorate the increase of tumor metastasis induced by surgical stress.
  • These preclinical findings suggest that an adequate treatment of surgically induced stress immunosuppression with an opioid drug devoid of immunosuppressive effects may also play a protective role against the metastatic diffusion following cancer surgery.
  • [MeSH-major] Analgesics, Opioid / pharmacology. Breast Neoplasms / pathology. Buprenorphine / pharmacology. Immune Tolerance / drug effects. Lung Neoplasms / secondary. Stress, Physiological / immunology
  • [MeSH-minor] Analysis of Variance. Animals. Corticosterone / blood. Disease Models, Animal. Fentanyl / adverse effects. Fentanyl / immunology. Hypothalamo-Hypophyseal System / drug effects. Hypothalamo-Hypophyseal System / metabolism. Killer Cells, Natural / drug effects. Killer Cells, Natural / immunology. Laparotomy / adverse effects. Male. Morphine / adverse effects. Morphine / immunology. Neoplasm Metastasis. Neoplasms, Experimental / immunology. Pituitary-Adrenal System / drug effects. Pituitary-Adrenal System / metabolism. Rats. Rats, Inbred F344

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  • (PMID = 17291715.001).
  • [ISSN] 0889-1591
  • [Journal-full-title] Brain, behavior, and immunity
  • [ISO-abbreviation] Brain Behav. Immun.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 40D3SCR4GZ / Buprenorphine; 76I7G6D29C / Morphine; UF599785JZ / Fentanyl; W980KJ009P / Corticosterone
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9. Chen J, Emara N, Solomides C, Parekh H, Simpkins H: Resistance to platinum-based chemotherapy in lung cancer cell lines. Cancer Chemother Pharmacol; 2010 Nov;66(6):1103-11
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  • PURPOSE: A series of six lung cancer cell lines of different cell origin (including small cell and mesothelioma) were characterized immunohistochemically and the role of a series of protein candidates previously implicated in drug resistance were investigated.
  • The relationship appeared to hold true for those cell lines derived from lung epithelial primary tumors but not for the neuroendocrine/small-cell and mesothelioma cell lines. siRNA knockouts to DDH-1 and DDH-2 were prepared with the cell line exhibiting the greatest resistance to cisplatin (A549) resulting in marked decreases in the DDH isoforms as assessed by real-time PCR, western blot and enzymatic activity.

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  • (PMID = 20953859.001).
  • [ISSN] 1432-0843
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA098804-01A1; United States / NCI NIH HHS / CA / R01 CA098804; United States / NCI NIH HHS / CA / R01 CA098804-01A1; United States / NCI NIH HHS / CA / R01-CA098804
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Organoplatinum Compounds; 0 / Platinum Compounds; 04ZR38536J / oxaliplatin; EC 1.1.- / Hydroxysteroid Dehydrogenases; EC 1.1.1.- / AKR1C2 protein, human; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS184351; NLM/ PMC2957658
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10. Casini Raggi C, Pinzani P, Gelmini S, Tricarico C, Orlando C, CalabrĂ² A, Renzi D, Cianchi F, Valanzano R, Distante V, Cortesini C, Tonelli F, Cataliotti L, Cameron Smith M, Messerini L, Bianchi S, Pazzagli M, Serio M, Maggi M: [Somatostatin receptors in non-endocrine tumours]. Minerva Endocrinol; 2001 Sep;26(3):149-58
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Somatostatin receptors in non-endocrine tumours].
  • The study of the antiproliferative action of somatostatin (ss) is important not only to understand the regulation of neuroendocrine tumours that express receptors (sst), but also non-endocrine tumours which express these receptors.
  • Although the majority of neuroendocrine tumours expresses sst2, pancreas and prostate cancer express sst1 but not sst2, and are therefore insensitive to octreotide treatment which binds preferentially to sst2.
  • Tumours like colorectal carcinoma and breast cancer also express sst2 in their more favourable forms.
  • In breast cancer, it is possible that sensitivity to estrogens may have a positive influence on the expression of sst2.
  • This might justify clinical trials with ss in breast cancer.
  • [MeSH-major] Neoplasm Proteins / physiology. Neoplasms / metabolism. Receptors, Somatostatin / physiology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Antineoplastic Agents, Hormonal / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Colorectal Neoplasms / drug therapy. Colorectal Neoplasms / metabolism. Female. Humans. Male. Neuroblastoma / genetics. Neuroblastoma / metabolism. Octreotide / therapeutic use. Somatostatin / physiology. Somatostatin / therapeutic use

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  • (PMID = 11753238.001).
  • [ISSN] 0391-1977
  • [Journal-full-title] Minerva endocrinologica
  • [ISO-abbreviation] Minerva Endocrinol.
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Neoplasm Proteins; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
  • [Number-of-references] 77
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11. Polyzos A: Activity of SU11248, a multitargeted inhibitor of vascular endothelial growth factor receptor and platelet-derived growth factor receptor, in patients with metastatic renal cell carcinoma and various other solid tumors. J Steroid Biochem Mol Biol; 2008 Feb;108(3-5):261-6
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  • In fact, with a 37% response rate and an additional 48% stable disease sutent became the drug of choice for first line treatment in RCC.
  • Prolonged stable disease was also documented in neuroendocrine tumors.
  • In addition, a phase II study in multitreated women with breast cancer, sutent demonstrated a moderate activity with 16% clinical benefit.
  • Finally, in non-small cell lung cancer (NSCLC) in patients' progressing on chemotherapy sutent was able to achieve a 10% response rate, a level of activity similar to those documented by other agents approved for lung cancer.
  • The agent is being tested in other tumors with a modified schedule of dosage.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Renal Cell / drug therapy. Carcinoma, Renal Cell / pathology. Indoles / therapeutic use. Kidney Neoplasms / drug therapy. Pyrroles / therapeutic use
  • [MeSH-minor] Adult. Aged. Breast Neoplasms / drug therapy. Female. Gastrointestinal Stromal Tumors / drug therapy. Humans. Lung Neoplasms / drug therapy. Male. Middle Aged. Neoplasm Metastasis / drug therapy. Neuroendocrine Tumors / drug therapy. Receptors, Platelet-Derived Growth Factor / antagonists & inhibitors. Receptors, Vascular Endothelial Growth Factor / antagonists & inhibitors

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  • (PMID = 17945482.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyrroles; 0 / sunitinib; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Number-of-references] 29
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