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1. Yano A, Tsutsumi S, Soga S, Lee MJ, Trepel J, Osada H, Neckers L: Inhibition of Hsp90 activates osteoclast c-Src signaling and promotes growth of prostate carcinoma cells in bone. Proc Natl Acad Sci U S A; 2008 Oct 07;105(40):15541-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of Hsp90 activates osteoclast c-Src signaling and promotes growth of prostate carcinoma cells in bone.
  • However, the impact of Hsp90 inhibition on signaling pathways in normal tissues and the effect that this may have on the antitumor activity of these molecularly targeted drugs have not been rigorously examined.
  • Breast and prostate carcinomas are among those cancers that respond to Hsp90 inhibitors in animal xenograft models and in early studies in patients.
  • In the current study, we show that, in contrast to its activity against prostate cancer cells in vitro and its inhibition of s.c. prostate cancer xenografts, the Hsp90 inhibitor 17-AAG stimulates the intraosseous growth of PC-3M prostate carcinoma cells.
  • Hsp90 inhibition transiently activates osteoclast Src kinase and promotes Src-dependent Akt activation.
  • Both kinases are key drivers of osteoclast maturation, and three agents that block osteoclastogenesis, the Src inhibitor dasatinib, the bisphosphonate alendronate, and the osteoclast-specific apoptosis-inducer reveromycin A, markedly reduced 17-AAG-stimulated tumor growth in bone.
  • These data emphasize the importance of understanding the complex role played by Hsp90 in regulating signal transduction pathways in normal tissues as well as in cancer cells, and they demonstrate that drug-dependent modulation of the local tumor environment may profoundly affect the antitumor efficacy of Hsp90-directed therapy.
  • [MeSH-major] Bone Neoplasms / secondary. Carcinoma / secondary. HSP90 Heat-Shock Proteins / antagonists & inhibitors. Osteoclasts / enzymology. Prostatic Neoplasms / pathology. Proto-Oncogene Proteins pp60(c-src) / metabolism. Signal Transduction

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  • (PMID = 18840695.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzoquinones; 0 / HSP90 Heat-Shock Proteins; 0 / Integrin beta3; 0 / Lactams, Macrocyclic; 4GY0AVT3L4 / tanespimycin; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src); EC 2.7.11.1 / Oncogene Protein v-akt
  • [Other-IDs] NLM/ PMC2563126
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2. Hiscox S, Morgan L, Green T, Nicholson RI: Src as a therapeutic target in anti-hormone/anti-growth factor-resistant breast cancer. Endocr Relat Cancer; 2006 Dec;13 Suppl 1:S53-9
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  • [Title] Src as a therapeutic target in anti-hormone/anti-growth factor-resistant breast cancer.
  • Endocrine therapy is the treatment of choice in hormone receptor-positive breast cancer.
  • However, the effectiveness of anti-hormone drugs, such as tamoxifen, is limited because of the development of resistance, ultimately leading to disease progression and patient mortality.
  • Using in vitro cell models of anti-hormone resistance, we have previously demonstrated that altered growth factor signalling contributes to an endocrine insensitive phenotype.
  • Significantly, our recent studies have revealed that the acquisition of endocrine resistance in breast cancer is accompanied by a greatly enhanced migratory and invasive phenotype.
  • Furthermore, therapeutic intervention using anti-growth factor monotherapies, despite an initial growth suppressive phase, again results in the development of a resistant state and a further augmentation of their invasive phenotype.
  • Using the dual specific Src/Abl kinase inhibitor, AZD0530, we have highlighted a central role for Src kinase in promoting the invasive phenotype that accompanies both anti-hormone and anti-growth factor resistance.
  • Importantly, the use of Src inhibitors in combination with anti-growth factor therapies appears to be additive, producing a marked inhibitory effect on cell growth, migration and invasion and ultimately prevents the emergence of a resistant phenotype.
  • These observations suggest that the inhibition of Src activity may present a novel therapeutic intervention strategy, particularly when used as an adjuvant in endocrine-resistant breast disease, with the potential to delay or prevent the acquisition of subsequent resistance to anti-growth factor therapies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Carcinoma / drug therapy. Drug Resistance, Neoplasm. Epidermal Growth Factor / antagonists & inhibitors. Proto-Oncogene Proteins pp60(c-src) / physiology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / administration & dosage. Cadherins / physiology. Catenins / physiology. Cell Adhesion. Cell-Matrix Junctions / physiology. Humans. Neoplasm Invasiveness

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  • (PMID = 17259559.001).
  • [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; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Cadherins; 0 / Catenins; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
  • [Number-of-references] 63
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3. Diaz N, Minton S, Cox C, Bowman T, Gritsko T, Garcia R, Eweis I, Wloch M, Livingston S, Seijo E, Cantor A, Lee JH, Beam CA, Sullivan D, Jove R, Muro-Cacho CA: Activation of stat3 in primary tumors from high-risk breast cancer patients is associated with elevated levels of activated SRC and survivin expression. Clin Cancer Res; 2006 Jan 1;12(1):20-8
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  • [Title] Activation of stat3 in primary tumors from high-risk breast cancer patients is associated with elevated levels of activated SRC and survivin expression.
  • PURPOSE: Constitutive activation of signal transducer and activator of transcription 3 (Stat3) protein has been observed in a wide variety of tumors, including breast cancer, and contributes to oncogenesis at least in part by prevention of apoptosis.
  • In a study of 45 patients with high-risk breast cancer enrolled in a phase II neoadjuvant chemotherapy trial with docetaxel and doxorubicin, we evaluated the levels of Stat3 activation and potentially associated molecular biomarkers in invasive breast carcinoma compared with matched nonneoplastic tissues.
  • EXPERIMENTAL DESIGN: Using immunohistochemistry and image analysis, we quantified the levels of phospho-Stat3 (pY-Stat3), phospho-Src (pY-Src), epidermal growth factor receptor, HER2/neu, Ki-67, estrogen receptor, Bcl-2, Bcl-xL, Survivin, and apoptosis in formalin-fixed, paraffin-embedded sections from invasive carcinomas and their paired nonneoplastic parenchyma.
  • The levels of molecular biomarkers in nonneoplastic and tumor tissues were analyzed as continuous variables for statistically significant correlations.
  • RESULTS: Levels of activated pY-Stat3 and pY-Src measured by immunohistochemistry were significantly higher in invasive carcinoma than in nonneoplastic tissue (P < 0.001).
  • In tumors, elevated levels of pY-Stat3 correlated with those of pY-Src and Survivin.
  • CONCLUSIONS: Our findings suggest important roles for elevated activities of Stat3 and Src, as well as Survivin expression, in malignant progression of breast cancer.
  • These findings suggest that specific Stat3 or Src inhibitors could offer clinical benefits to patients with breast cancer.
  • [MeSH-major] Biomarkers, Tumor / analysis. Breast Neoplasms / metabolism. Microtubule-Associated Proteins / biosynthesis. Neoplasm Proteins / biosynthesis. STAT3 Transcription Factor / metabolism. src-Family Kinases / biosynthesis
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Apoptosis / physiology. Clinical Trials, Phase II as Topic. Doxorubicin / therapeutic use. Electrophoretic Mobility Shift Assay. Enzyme Activation / physiology. Female. Humans. Image Processing, Computer-Assisted. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins. Ki-67 Antigen / biosynthesis. Neoadjuvant Therapy. Proto-Oncogene Proteins c-bcl-2 / biosynthesis. Receptor, Epidermal Growth Factor / biosynthesis. Receptor, ErbB-2 / biosynthesis. Receptors, Estrogen / biosynthesis. Risk Factors. Taxoids / therapeutic use. bcl-X Protein / biosynthesis

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  • (PMID = 16397019.001).
  • [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 / CA55652; United States / NCI NIH HHS / CA / CA82533
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BCL2L1 protein, human; 0 / BIRC5 protein, human; 0 / Biomarkers, Tumor; 0 / Inhibitor of Apoptosis Proteins; 0 / Ki-67 Antigen; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Estrogen; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Taxoids; 0 / bcl-X Protein; 15H5577CQD / docetaxel; 80168379AG / Doxorubicin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.2 / src-Family Kinases
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4. Yang Z, Bagheri-Yarmand R, Wang RA, Adam L, Papadimitrakopoulou VV, Clayman GL, El-Naggar A, Lotan R, Barnes CJ, Hong WK, Kumar R: The epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 (Iressa) suppresses c-Src and Pak1 pathways and invasiveness of human cancer cells. Clin Cancer Res; 2004 Jan 15;10(2):658-67
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 (Iressa) suppresses c-Src and Pak1 pathways and invasiveness of human cancer cells.
  • PURPOSE: Abnormalities in the expression and signaling pathways downstream of the epidermal growth factor receptor (EGFR) contribute to the progression, invasion, and maintenance of the malignant phenotype in human cancers, including those of the head and neck and breast.
  • Accordingly, agents such as the EGFR tyrosine kinase inhibitor (EGFR-TKI) ZD1839 (Iressa) are promising, biologically based treatments that are in various stages of preclinical and clinical development.
  • The process of tumor progression requires, among other steps, increased transformation, directional migration, and enhanced cell survival; this study explored the effect of ZD1839 on the stimulation of c-Src and p21-activated kinase 1 (Pak1), which are vital for transformation, directional motility, and cell survival of cancer cells.
  • EXPERIMENTAL DESIGN: We examined the effect of ZD1839 on biochemical and functional assays indicative of directional motility and cell survival, using human head and neck squamous cancer cells and breast cancer cells.
  • RESULTS: ZD1839 effectively inhibited c-Src activation and Pak1 activity in exponentially growing cancer cells.
  • In addition, ZD1839 suppressed EGF-induced stimulation of EGFR autophosphorylation on Y1086 and Grb2-binding Y1068 sites, c-Src phosphorylation on Y215, and Pak1 activity.
  • CONCLUSIONS: These studies suggest that the EGFR-TKI ZD1839 may cause potent inhibition of the Pak1 and c-Src pathways and, therefore, have potential to affect the invasiveness of human cancer cells deregulated in these growth factor receptor pathways.
  • [MeSH-minor] Blotting, Western. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Cell Line, Tumor. Cell Movement. Cell Survival. Cytoskeleton / metabolism. Disease Progression. Dose-Response Relationship, Drug. Epidermal Growth Factor / metabolism. Head and Neck Neoplasms / metabolism. Head and Neck Neoplasms / pathology. Humans. Microscopy, Fluorescence. Neoplasm Invasiveness. Phenotype. Phosphorylation. Precipitin Tests. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction. Transfection. Vinculin / metabolism. p21-Activated Kinases. src-Family Kinases

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  • (PMID = 14760089.001).
  • [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 / CA97007; United States / NCI NIH HHS / CA / R01CA65746
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; 125361-02-6 / Vinculin; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / CSK tyrosine-protein kinase; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / PAK1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / p21-Activated Kinases; S65743JHBS / gefitinib
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5. Koppikar P, Choi SH, Egloff AM, Cai Q, Suzuki S, Freilino M, Nozawa H, Thomas SM, Gooding WE, Siegfried JM, Grandis JR: Combined inhibition of c-Src and epidermal growth factor receptor abrogates growth and invasion of head and neck squamous cell carcinoma. Clin Cancer Res; 2008 Jul 1;14(13):4284-91
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined inhibition of c-Src and epidermal growth factor receptor abrogates growth and invasion of head and neck squamous cell carcinoma.
  • PURPOSE: Increased expression and/or activation of epidermal growth factor receptor (EGFR) is associated with tumor progression and poor prognosis in many cancers, including head and neck squamous cell carcinoma (HNSCC).
  • Src family kinases, including c-Src, mediate a variety of intracellular or extracellular signals that contribute to tumor formation and progression.
  • This study was undertaken to elucidate the role of c-Src in the growth and invasion of HNSCC and to determine the effects of combined targeting of EGFR and Src kinases in HNSCC cell lines.
  • EXPERIMENTAL DESIGN: HNSCC cells were engineered to stably express a dominant-active form of c-Src and investigated in cell growth and invasion assays.
  • The biochemical effects of combined treatment with the Src inhibitor AZD0530, a potent, orally active Src inhibitor with Bcr/Abl activity, and the EGFR kinase inhibitor gefitinib were examined, as well as the consequences of dual Src/EGFR targeting on the growth and invasion of a panel of HNSCC cell lines.
  • RESULTS: HNSCC cells expressing dominant-active c-Src showed increased growth and invasion compared with vector-transfected controls.
  • Combined treatment with AZD0530 and gefitinib resulted in greater inhibition of HNSCC cell growth and invasion compared with either agent alone.
  • CONCLUSIONS: These results suggest that increased expression and activation of c-Src promotes HNSCC progression where combined targeting of EGFR and c-Src may be an efficacious treatment approach.

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  • (PMID = 18594011.001).
  • [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 / CA098372; United States / NCI NIH HHS / CA / CA77308; United States / NCI NIH HHS / CA / R01 CA077308; United States / NCI NIH HHS / CA / R01 CA098372; United States / NCI NIH HHS / CA / P50 CA097190; United States / NCI NIH HHS / CA / CA097190
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / src-Family Kinases
  • [Other-IDs] NLM/ NIHMS399598; NLM/ PMC3428119
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6. Yezhelyev MV, Koehl G, Guba M, Brabletz T, Jauch KW, Ryan A, Barge A, Green T, Fennell M, Bruns CJ: Inhibition of SRC tyrosine kinase as treatment for human pancreatic cancer growing orthotopically in nude mice. Clin Cancer Res; 2004 Dec 1;10(23):8028-36
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of SRC tyrosine kinase as treatment for human pancreatic cancer growing orthotopically in nude mice.
  • PURPOSE: The Src family comprises a family of nonreceptor intracellular tyrosine kinases that mediate a variety of cellular pathways.
  • Src kinases are overexpressed in a variety of human tumors, including cancer of the colon, breast, and pancreas, and they are an integral part of tumor cell signaling pathways associated with migration, proliferation, adhesion, and angiogenesis.
  • EXPERIMENTAL DESIGN: We investigated whether the blockade of Src kinase by daily oral administration of the novel Src tyrosine kinase inhibitor AZM475271 [kindly provided by AstraZeneca (Macclesfield, United Kingdom)], alone or in combination with intraperitoneal gemcitabine, can inhibit growth and metastasis of orthotopically implanted human pancreatic carcinoma cells in nude mice.
  • RESULTS: Treatment with AZM475271 alone reduced the primary pancreatic tumor volume by approximately 40%, whereas AZM475271 plus gemcitabine reduced tumor volume by 90%.
  • Furthermore, treatment with AZM475271 and gemcitabine significantly reduced metastasis: none of eight animals who received the combination treatment had lymph node or liver metastases, compared with five of five and three of five animals, respectively, in the control group (P = 0.001).
  • Src inhibition by AZM475271 (alone or with gemcitabine) was associated with significantly reduced tumor cell proliferation, decreased tumor microvessel density, and increased apoptosis in vivo.
  • CONCLUSIONS: Src inhibition by AZM475271, either alone or in combination with gemcitabine, demonstrated significant antitumor and antimetastatic activity in an orthotopic nude mouse model for human pancreatic cancer.
  • [MeSH-major] Apoptosis / drug effects. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Enzyme Inhibitors / therapeutic use. Pancreatic Neoplasms / drug therapy. src-Family Kinases / antagonists & inhibitors
  • [MeSH-minor] Administration, Oral. Animals. Cell Movement / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Drug Therapy, Combination. Flow Cytometry. Humans. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Male. Mice. Mice, Nude. NIH 3T3 Cells. Ribonucleotide Reductases / antagonists & inhibitors

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  • (PMID = 15585638.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; 0 / Mki67 protein, mouse; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / Ribonucleotide Reductases; EC 2.7.10.2 / src-Family Kinases
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7. Chu I, Sun J, Arnaout A, Kahn H, Hanna W, Narod S, Sun P, Tan CK, Hengst L, Slingerland J: p27 phosphorylation by Src regulates inhibition of cyclin E-Cdk2. Cell; 2007 Jan 26;128(2):281-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] p27 phosphorylation by Src regulates inhibition of cyclin E-Cdk2.
  • The kinase inhibitor p27Kip1 regulates the G1 cell cycle phase.
  • Here, we present data indicating that the oncogenic kinase Src regulates p27 stability through phosphorylation of p27 at tyrosine 74 and tyrosine 88.
  • Src inhibitors increase cellular p27 stability, and Src overexpression accelerates p27 proteolysis.
  • Src-phosphorylated p27 is shown to inhibit cyclin E-Cdk2 poorly in vitro, and Src transfection reduces p27-cyclin E-Cdk2 complexes.
  • Our data indicate that phosphorylation by Src impairs the Cdk2 inhibitory action of p27 and reduces its steady-state binding to cyclin E-Cdk2 to facilitate cyclin E-Cdk2-dependent p27 proteolysis.
  • Furthermore, we find that Src-activated breast cancer lines show reduced p27 and observe a correlation between Src activation and reduced nuclear p27 in 482 primary human breast cancers.
  • Importantly, we report that in tamoxifen-resistant breast cancer cell lines, Src inhibition can increase p27 levels and restore tamoxifen sensitivity.
  • These data provide a new rationale for Src inhibitors in cancer therapy.


8. Colak T, Akca T, Dirlik M, Caglikulekci M, Seyrek E, Cinel L, Bozdogan R, Aydin S: Signet ring cell carcinoma of the breast as a source of pelvic floor metastatic mass. A case report. Acta Chir Belg; 2005 Apr;105(2):224-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Signet ring cell carcinoma of the breast as a source of pelvic floor metastatic mass. A case report.
  • Primary signet ring cell carcinoma of the breast is a very rare tumour.
  • We present a case with pure signet ring cell carcinoma of the breast, which was recognized as metastasis on the pelvic floor, before developing breast symptoms and signs.
  • The histopathological examination revealed metastatic signet-ring cell carcinoma.
  • At the time of the first operation, the mammary glands were not suspicious.
  • No other sources of primary tumour were evidenced.
  • An inflammatory sign developed in right breast two months after biopsy of the pelvic metastasis.
  • The histopathology of the breast incisional biopsy revealed primary pure signet ring cell carcinoma of the breast.
  • Because the oestrogen and progesterone receptor were negative in the tumoral tissue, the patient underwent chemotherapy followed by modified radical mastectomy, chemotherapy, and palliative resection of the metastatic mass.
  • To our knowledge, in English literature, we believe that this case is the first report of signet ring cell carcinoma of the breast presenting with pelvic floor metastasis without breast sign.
  • [MeSH-major] Breast Neoplasms / pathology. Breast Neoplasms / therapy. Carcinoma, Signet Ring Cell / secondary. Carcinoma, Signet Ring Cell / therapy. Pelvic Neoplasms / secondary
  • [MeSH-minor] Adult. Biopsy, Needle. Chemotherapy, Adjuvant. Female. Follow-Up Studies. Humans. Immunohistochemistry. Mastectomy, Modified Radical / methods. Neoplasm Staging. Pelvic Floor. Rare Diseases. Risk Assessment. Treatment Outcome

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  • (PMID = 15906923.001).
  • [ISSN] 0001-5458
  • [Journal-full-title] Acta chirurgica Belgica
  • [ISO-abbreviation] Acta Chir. Belg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Belgium
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9. Golubovskaya VM, Virnig C, Cance WG: TAE226-induced apoptosis in breast cancer cells with overexpressed Src or EGFR. Mol Carcinog; 2008 Mar;47(3):222-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] TAE226-induced apoptosis in breast cancer cells with overexpressed Src or EGFR.
  • We have shown previously that the dominant-negative FAK, C-terminal FAK-CD, caused detachment and apoptosis in human breast cancer cells, and that overexpression of an activated form of Src tyrosine kinase or epidermal growth factor receptor, EGFR, suppressed FAK-CD induced apoptotic effects in breast cancer cells.
  • ), on the breast cancer cell lines.
  • We used stable breast cancer cell lines overexpressing Src (MCF-7-Src and BT474-Src) or overexpressing EGFR (BT474-EGFR), and control breast cancer cell lines for the treatment with different doses of TAE226 drug.
  • The TAE226 drug caused a dose-dependent increase of detachment and apoptosis in both BT474 and MCF-7-Vector and Src cells and in BT474-EGFR and BT474-pcDNA3 cells.
  • Both Src and EGFR-overexpressing cells were not resistant to the TAE226 treatment compared to FAK-CD treatment.
  • In addition, normal breast MCF-10A cell line was resistant to both TAE226 drug and to the Ad-FAK-CD inhibitor.
  • Thus, inhibition of autophosphorylation activity of FAK with the TAE226 inhibitor at 10-20 microM is effective in causing apoptosis in breast cancer cells, resistant to the Ad-FAK-CD inhibitor that can be used effectively in therapy.
  • [MeSH-major] Apoptosis / drug effects. Breast Neoplasms / pathology. Focal Adhesion Protein-Tyrosine Kinases / antagonists & inhibitors. Morpholines / pharmacology. Proto-Oncogene Proteins pp60(c-src) / metabolism. Receptor, Epidermal Growth Factor / metabolism
  • [MeSH-minor] Adenoviridae / genetics. Carcinoma, Ductal / pathology. Caspase 3 / metabolism. Cell Adhesion / drug effects. Cell Line. Cell Line, Tumor. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Enzyme Activation / drug effects. Female. Humans. Immunohistochemistry. Phosphorylation / drug effects. Transduction, Genetic

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17849451.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA65910
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Morpholines; 0 / TAE226; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src); EC 3.4.22.- / Caspase 3
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10. Johnson FM, Gallick GE: SRC family nonreceptor tyrosine kinases as molecular targets for cancer therapy. Anticancer Agents Med Chem; 2007 Nov;7(6):651-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] SRC family nonreceptor tyrosine kinases as molecular targets for cancer therapy.
  • The Src family of kinases has nine known members, all of which are nonreceptor tyrosine kinases involved in signal transduction in both normal and cancer cells.
  • Interest in these kinases has increased recently because of the development, initial clinical success, and low toxicity of pharmacologic inhibitors. c-Src is the best-studied member of the Src family and the one most often implicated in cancer progression. c-Src has multiple substrates that lead to diverse biologic effects, including changes in proliferation, motility, invasion, survival, and angiogenesis. c-Src has been most extensively studied in colon cancer where correlative and direct experimental evidence has shown that it mediates several aspects of cancer cell progression. c-Src has a similar role in multiple tumor types, including pancreatic cancer, breast cancer, lung cancer, head and neck squamous cell carcinoma, and prostate cancer.
  • Several inhibitors of the Src family kinases are in clinical development; three are currently being studied in clinical trials.
  • Future clinical development of these inhibitors will include trials in patients with solid tumors and of combination therapy.
  • [MeSH-major] Antineoplastic Agents / chemistry. Immunologic Factors / chemistry. Neoplasms / enzymology. src-Family Kinases
  • [MeSH-minor] Drug Design. Humans. Signal Transduction / drug effects

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  • (PMID = 18045060.001).
  • [ISSN] 1871-5206
  • [Journal-full-title] Anti-cancer agents in medicinal chemistry
  • [ISO-abbreviation] Anticancer Agents Med Chem
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1P20-CA101936-01-PP4; United States / NCI NIH HHS / CA / U54 CA 090810-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Immunologic Factors; EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 160
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11. Carey L, Winer E, Viale G, Cameron D, Gianni L: Triple-negative breast cancer: disease entity or title of convenience? Nat Rev Clin Oncol; 2010 Dec;7(12):683-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Triple-negative breast cancer: disease entity or title of convenience?
  • This Review outlines the understanding and management of triple-negative breast cancer (TNBC).
  • TNBC shares morphological and genetic abnormalities with basal-like breast cancer (BLBC), a subgroup of breast cancer defined by gene-expression profiling.
  • Breast cancers found in BRCA1 mutation carriers are also frequently triple negative and basal like.
  • These tumors respond to conventional chemotherapy but relapse more frequently than hormone receptor-positive, luminal subtypes and have a worse prognosis.
  • New systemic therapies are urgently needed as most patients with TNBC and/or BLBC relapse with distant metastases, and hormonal therapies and HER2-targeted agents are ineffective in this group of tumors.
  • Poly (ADP-ribose) polymerase inhibitors, angiogenesis inhibitors, EGFR-targeted agents, and src kinase and mTOR inhibitors are among the therapeutic agents being actively investigated in clinical trials in patients with TNBC and/or BRCA1-associated tumors.
  • Increased understanding of the genetic abnormalities involved in the pathogenesis of TNBC, BLBC and BRCA1-associated tumors is opening up new therapeutic possibilities for these hard-to-treat breast cancers.
  • [MeSH-major] Breast Neoplasms / classification. Carcinoma, Ductal, Breast / classification. Neoplasm Proteins / analysis. Receptor, ErbB-2 / analysis. Receptors, Estrogen / analysis. Receptors, Progesterone / analysis
  • [MeSH-minor] Antineoplastic Agents / classification. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. BRCA1 Protein / deficiency. BRCA1 Protein / physiology. Case Management. Combined Modality Therapy. Drug Resistance, Neoplasm. Female. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genes, BRCA1. Genes, erbB-2. Humans. Mitotic Index. Neoplasm Invasiveness. Neoplasm Metastasis. Neoplasm Recurrence, Local. Prognosis


12. Giaccone G, Zucali PA: Src as a potential therapeutic target in non-small-cell lung cancer. Ann Oncol; 2008 Jul;19(7):1219-23
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Src as a potential therapeutic target in non-small-cell lung cancer.
  • Lung cancer is the most common cause of cancer-related death, with non-small-cell lung cancer (NSCLC) accounting for 80%-85% of all cases.
  • For these patients, palliation and improvements in quality of life are the primary goals of therapy.
  • Although chemotherapeutic agents remain the cornerstone of first-line therapy, these agents have limited use in patients who have relapsed and have metastatic disease.
  • One such target is Src, a tyrosine kinase that is involved in multiple aspects of tumorigenesis including proliferation, migration and angiogenesis.
  • Increased levels of Src expression have been found in a range of cancers, especially breast, colorectal, prostate and lung.
  • Preliminary preclinical data and pharmacodynamic data suggest that Src inhibition is a viable therapeutic option in the treatment of advanced NSCLC.

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  • (PMID = 18388349.001).
  • [ISSN] 1569-8041
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 50
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13. Wheeler DL, Iida M, Kruser TJ, Nechrebecki MM, Dunn EF, Armstrong EA, Huang S, Harari PM: Epidermal growth factor receptor cooperates with Src family kinases in acquired resistance to cetuximab. Cancer Biol Ther; 2009 Apr;8(8):696-703
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epidermal growth factor receptor cooperates with Src family kinases in acquired resistance to cetuximab.
  • Cetuximab is an EGFR-blocking antibody that is FDA approved for use in patients with metastatic colorectal cancer (mCRC) and head and neck squamous cell carcinoma (HNSCC).
  • Although cetuximab has shown strong clinical benefit for a subset of cancer patients, most become refractory to cetuximab therapy.
  • We now present data that Src family kinases (SFKs) are highly activated in cetuximab-resistant cells and enhance EGFR activation of HER3 and PI(3)K/Akt.
  • Studies using the Src kinase inhibitor dasatinib decreased HER3 and PI(3)K/Akt activity.
  • These results indicate that SFKs and EGFR cooperate in acquired resistance to cetuximab and suggest a rationale for clinical strategies that investigate combinatorial therapy directed at both the EGFR and SFKs in patients with acquired resistance to cetuximab.

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  • (PMID = 19276677.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA014520; United States / NCI NIH HHS / CA / R01 CA113448; None / None / / P30 CA014520-30; United States / NCI NIH HHS / CA / R01 CA 113448-01; United States / NCI NIH HHS / CA / P30 CA014520-30
  • [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 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / EGFR protein, human; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; PQX0D8J21J / Cetuximab; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS211787; NLM/ PMC2895567
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14. Egloff AM, Grandis JR: Targeting epidermal growth factor receptor and SRC pathways in head and neck cancer. Semin Oncol; 2008 Jun;35(3):286-97
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting epidermal growth factor receptor and SRC pathways in head and neck cancer.
  • Epidermal growth factor receptor (EGFR), a member of the ErbB family of receptor tyrosine kinases (RTKs), is highly expressed in head and neck squamous cell carcinoma (HNSCC) where increased EGFR expression levels in tumors are associated with decreased survival.
  • Tumor signaling pathway components that work in cooperation with EGFR or provide compensation for the loss of EGFR-initiated signaling will be ideal targets for therapies to be used in combination with EGFR-targeted agents.
  • Based on the current understanding of molecular signaling pathways and available agents, ErbB family-targeted and Src family-targeted agents represent strategies for further exploration.
  • Here, we discuss agents targeting ErbB and Src family kinases in clinical development, provide an overview of completed and ongoing clinical trials, and outline a molecular rationale for combining ErbB- and Src-targeted therapeutics.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Drug Delivery Systems / methods. Head and Neck Neoplasms / drug therapy. Proto-Oncogene Proteins pp60(c-src) / antagonists & inhibitors. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Clinical Trials as Topic. Humans. Models, Biological. Signal Transduction

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  • (PMID = 18544443.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P50 CA097190; United States / NCI NIH HHS / CA / P50 CA097190-01A1; United States / NCI NIH HHS / CA / R01 CA077308; United States / NCI NIH HHS / CA / R01 CA077308-10
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
  • [Number-of-references] 109
  • [Other-IDs] NLM/ NIHMS56291; NLM/ PMC2587085
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15. Wang F, Anderson PW, Salem N, Kuang Y, Tennant BC, Lee Z: Gene expression studies of hepatitis virus-induced woodchuck hepatocellular carcinoma in correlation with human results. Int J Oncol; 2007 Jan;30(1):33-44
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  • [Title] Gene expression studies of hepatitis virus-induced woodchuck hepatocellular carcinoma in correlation with human results.
  • The lack of good molecular markers for diagnosis as well as treatment assessment has rendered the hepatocellular carcinoma (HCC) a major challenge in health care.
  • An analysis approach combing supervised significant analysis of microarray (SAM), prediction analysis of microarray (PAM), and unsupervised hierarchical cluster methodologies statistically determined 211 upregulated and 78 downregulated genes between liver cancer and non-cancer liver tissues, and demonstrated > or = 93% accuracy in classifying the tissue samples.
  • Our study showed that differentially expressed genes were involved in transcription, RNA splicing, translation, cell cycle, metabolism, protein folding and degradation, apoptosis, immune response, metal binding, etc.
  • Interestingly, some genes were involved with signaling pathways such as Ras/MAPK (MAPKAP1), Src-dependent pathways (CSK), hedgehog signaling pathway (HHIP), while Wnt signaling pathway may not be dominant in woodchuck HCC as shown by the downregulation of beta-catenin (TNNB1) and the upregulation of CXXC4 and CSNK2B.
  • Numerous genes found in this study were also differentially expressed in human HCC and many other human cancers including breast, prostate and lung cancers, etc., serving as tumor suppressors, promoters, prognostic markers or chemotherapy targets.

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  • (PMID = 17143510.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / T32 EB007509; United States / NCI NIH HHS / CA / CA095307; United States / NCI NIH HHS / CA / P30 CA43703
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 63231-63-0 / RNA
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16. Moulder S, Yan K, Huang F, Hess KR, Liedtke C, Lin F, Hatzis C, Hortobagyi GN, Symmans WF, Pusztai L: Development of candidate genomic markers to select breast cancer patients for dasatinib therapy. Mol Cancer Ther; 2010 May;9(5):1120-7
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  • [Title] Development of candidate genomic markers to select breast cancer patients for dasatinib therapy.
  • Patient selection is important for targeted therapies, yet phase I/II trials are often underpowered for developing predictors of drug response.
  • Gene expression profiles of dasatinib-sensitive and dasatinib-resistant cell lines (n = 23) were compared to develop a dasatinib-sensitivity index (modified DS index).
  • A Src pathway activity index (revised Src index) was defined using genes induced by the Src transfection of mammary epithelial cells and was optimized to be reproducible across cell lines and human specimens.
  • The performance of these prediction models was assessed in independent cell lines with known dasatinib sensitivity.
  • The feasibility of applying these genomic tests to human samples was evaluated on 133 biopsies of primary breast cancers.
  • The modified DS index showed 90% accuracy in independent breast cancer cell lines (n = 12) and the target index, but not the revised Src index signature, also distinguished dasatinib-sensitive and dasatinib-resistant cells (P = 0.0024).
  • The genomic predictors showed acceptable reproducibility in replicate cell line and human gene expression data.
  • We defined three conceptually different potential predictors of dasatinib response that were reproducible across cell lines and human data.
  • [MeSH-major] Biomarkers, Pharmacological / analysis. Biomarkers, Tumor / genetics. Breast Neoplasms / drug therapy. Carcinoma / drug therapy. Pyrimidines / therapeutic use. Thiazoles / therapeutic use
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Dasatinib. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Female. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genetic Association Studies. Genome, Human. Humans. Matched-Pair Analysis. Oligonucleotide Array Sequence Analysis. Patient Selection. Prognosis

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  • (PMID = 20423993.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Pharmacological; 0 / Biomarkers, Tumor; 0 / Pyrimidines; 0 / Thiazoles; RBZ1571X5H / Dasatinib
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17. Song H, Wang R, Wang S, Lin J: A low-molecular-weight compound discovered through virtual database screening inhibits Stat3 function in breast cancer cells. Proc Natl Acad Sci U S A; 2005 Mar 29;102(13):4700-5
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  • [Title] A low-molecular-weight compound discovered through virtual database screening inhibits Stat3 function in breast cancer cells.
  • This study focused on the screening of small-molecule inhibitors that target signal transducers and activators of transcription 3 (Stat3) in human breast carcinoma.
  • The constitutive activation of Stat3 is frequently detected in human breast cancer cell lines as well as clinical breast cancer specimens and may play an important role in the oncogenesis of breast carcinoma.
  • Activated Stat3 may participate in oncogenesis by stimulating cell proliferation, promoting tumor angiogenesis, and resisting apoptosis.
  • Because a variety of human cancers are associated with constitutively active Stat3, Stat3 represents an attractive target for cancer therapy.
  • In this study, of the nearly 429,000 compounds screened by virtual database screening, chemical samples of top 100 compounds identified as candidate small-molecule inhibitors of Stat3 were evaluated by using Stat3-dependent luciferase reporter as well as other cell-based assays.
  • Through serial functional evaluation based on our established cell-based assays, one compound, termed STA-21, was identified as the best match for our selection criteria.
  • Moreover, STA-21 reduces the survival of breast carcinoma cells with constitutive Stat3 signaling but has minimal effect on the cells in which constitutive Stat3 signaling is absent.
  • Together, these results demonstrate that STA-21 inhibits breast cancer cells that express constitutively active Stat3.

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  • (PMID = 15781862.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / P30 CA46592
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Polycyclic Compounds; 0 / STA-21; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Trans-Activators; EC 1.13.12.- / Luciferases
  • [Other-IDs] NLM/ PMC555708
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18. Haugan Moi LL, Hauglid Flågeng M, Gandini S, Guerrieri-Gonzaga A, Bonanni B, Lazzeroni M, Gjerde J, Lien EA, DeCensi A, Mellgren G: Effect of low-dose tamoxifen on steroid receptor coactivator 3/amplified in breast cancer 1 in normal and malignant human breast tissue. Clin Cancer Res; 2010 Apr 1;16(7):2176-86
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  • [Title] Effect of low-dose tamoxifen on steroid receptor coactivator 3/amplified in breast cancer 1 in normal and malignant human breast tissue.
  • In a preoperative trial, dose reduction from 20 to 1 mg tamoxifen was associated with retained antiproliferative effect on breast cancer.
  • Here, we assessed the gene expression of the steroid receptor coactivators SRC-1, SRC-2/transcription intermediary factor 2, and SRC-3/amplified in breast cancer 1 (AIB1) and the growth factor receptor HER-2/neu under three tamoxifen dose regimens.
  • EXPERIMENTAL DESIGN: Surgical specimens from estrogen receptor-positive breast cancer and adjacent normal breast tissue from 64 patients treated 4 weeks preoperatively with 20, 5, or 1 mg/d tamoxifen and 28 nontreated breast cancer controls were analyzed for coactivator and HER-2/neu mRNA expression using real-time reverse transcription-PCR.
  • RESULTS: The coactivators and HER-2/neu mRNA levels were higher in malignant compared with normal tissue (P < 0.001).
  • Tamoxifen significantly increased the expression of coactivators in normal and malignant tissue irrespective of dose, especially for SRC-3/AIB1 (P < 0.001 tamoxifen-treated versus nontreated subjects).
  • SRC-3/AIB1 and HER-2/neu mRNA levels were positively correlated (P = 0.016), but the coactivators could not explain the variability of Ki67, insulin-like growth factor I, and sex hormone binding.
  • Although not significant, SRC-3/AIB1 tended to be higher in subjects with poor clinical outcome and unfavorable prognostic factors.
  • [MeSH-major] Breast / drug effects. Breast Neoplasms / drug therapy. Carcinoma / drug therapy. Nuclear Receptor Coactivator 3 / genetics. Tamoxifen / administration & dosage
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / administration & dosage. Antineoplastic Agents / pharmacology. Dose-Response Relationship, Drug. Double-Blind Method. Drug Resistance, Neoplasm / genetics. Female. Follow-Up Studies. Gene Expression Regulation, Neoplastic / drug effects. Humans. Middle Aged. Randomized Controlled Trials as Topic

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  • [Copyright] Copyright 2010 AACR.
  • [ErratumIn] Clin Cancer Res. 2010 Oct 15;16(20):5087. De Censi, Andrea [corrected to DeCensi, Andrea]
  • (PMID = 20332317.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 094ZI81Y45 / Tamoxifen; EC 2.3.1.48 / NCOA3 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 3
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19. Fan S, Meng Q, Laterra JJ, Rosen EM: Scatter factor protects tumor cells against apoptosis caused by TRAIL. Anticancer Drugs; 2010 Jan;21(1):10-24
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  • Scatter factor (SF) and its receptor c-Met are overexpressed in various tumor types, and their expression often correlates with a poor prognosis.
  • The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), is a proposed tumor-specific chemotherapy agent, but its clinical usage is limited by acquisition of TRAIL resistance by tumors.
  • We used MTT assays, trypan blue dye exclusion assays, apoptosis assays, RNA interference, luciferase reporter assays, immunoprecipitation/western blotting, and other cell biological techniques to study SF protection of cultured human tumor cells against TRAIL.
  • SF conferred resistance to TRAIL in various human prostate carcinoma and breast carcinoma cell lines.
  • SF inhibited TRAIL-induced caspase-3 activation, poly (ADP-ribose) polymerase cleavage, and cell death.
  • SF protection against TRAIL required c-Akt; but unlike protection against adriamycin, it did not require Src signaling or the classical pathway of nuclear factor-kappaB activation.

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  • (PMID = 19823077.001).
  • [ISSN] 1473-5741
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] ENG
  • [Grant] United States / NINDS NIH HHS / NS / R01 NS043987; United States / NIEHS NIH HHS / ES / R01-ES09169; United States / NINDS NIH HHS / NS / R01-NS43987
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 5-((2,6-dichlorobenzyl)sulfonyl)-3-((3,5-dimethyl-4-((2-(pyrrolidin-1-ylmethyl)pyrrolidin-1-yl)carbonyl)-1H-pyrrol-2-yl)methylene)-1,3-dihydro-2H-indol-2-one; 0 / Cyclooxygenase 2 Inhibitors; 0 / Indoles; 0 / NF-kappa B; 0 / RNA, Small Interfering; 0 / Recombinant Proteins; 0 / Sulfones; 0 / TNF-Related Apoptosis-Inducing Ligand; 67256-21-7 / Hepatocyte Growth Factor; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Proto-Oncogene Proteins c-met
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20. Schmidmaier R, Baumann P: ANTI-ADHESION evolves to a promising therapeutic concept in oncology. Curr Med Chem; 2008;15(10):978-90
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  • [Title] ANTI-ADHESION evolves to a promising therapeutic concept in oncology.
  • All five classes of cell adhesion molecules (CAM) - integrins, cadherins, immunoglobulin-like CAMs, selectins and CD44s - are characteristically dysregulated in human cancer.
  • Furthermore, cell adhesion mediates drug resistance (CAM-DR) in multiple myeloma, malignant lymphoma, acute and chronic leukaemias, as well as in pancreatic cancer, neuroblastoma, small cell and non-small cell lung cancer, mesothelioma, colorectal carcinoma, and breast cancer.
  • Cell adhesion protects from death by radiation, genotoxic chemotherapy, or targeted pathway inhibitors.
  • Adhesion molecules are overexpressed on drug resistant cells (e.g. multiple myeloma or prostate cancer).
  • Very recently, several cell adhesion mediated survival pathways have been elucidated, with key mediators being LFA-1, VLA-4, FAK, ILK, Src, PI3K, Akt, Ras, MEK, Erk, HMG-CoA reductase, Rho, Rho kinase, PKC, and NFkB.
  • Because the surface and the intracellular targets are now known and because specific compounds are becoming increasingly available, first clinical trials regarding ANTI-ADHESION therapies are ongoing.
  • However, in comparison to the comprehensive preclinical and clinical knowledge about CAMs, the number of drugs developed thusfar is quite low.
  • ANTI-ADHESION strategies include targeting of surface antigens, inhibition of cell adhesion associated pathways, inhibition of CAM-DR, and targeted drug delivery.
  • As ANTI-ADHESION is based on general characteristics of cancer cells independent of specific disease entities or treatment modalities, it may become a successful, low-toxic and broadly applicable concept in cancer treatment.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cell Adhesion / drug effects. Cell Adhesion Molecules / antagonists & inhibitors. Neoplasms / drug therapy. Signal Transduction / drug effects


21. Ku TK, Crowe DL: Coactivator-mediated estrogen response in human squamous cell carcinoma lines. J Endocrinol; 2007 Apr;193(1):147-55
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  • [Title] Coactivator-mediated estrogen response in human squamous cell carcinoma lines.
  • A number of cofactors such as nuclear receptor corepressor (NCoR), CREB-binding protein (CBP), and steroid receptor coactivator 1 (SRC-1) interact with estrogen receptors (ERs) to regulate transcriptional repression or activation of target genes.
  • Estrogen signaling in non-reproductive tract tissues such as skin is less well characterized and the effectiveness of anti-estrogen therapy for cancer arising from these tissues is unknown.
  • We show that tamoxifen (TAM) treatment inhibited cell cycle progression and proliferation of human cancer lines derived from stratified squamous epithelium squamous cell carcinoma (SCC).
  • The E2 treatment promoted displacement of the NCoR from ERalpha and recruitment of CBP to the receptor.
  • SRC-1 expression was not detected in these SCC lines; however, transient transfection of SRC-1, CBP, or both coactivators enhanced transactivation of an estrogen responsive promoter in cancer cells treated with E2 or TAM.
  • In stable clones expressing SRC-1, the coactivator was recruited to ERalpha along with CBP in E2 but not in TAM-treated cells.
  • SRC-1 expression restored the E2-mediated proliferative response to human SCC lines.
  • SRC-1 and CBP were recruited to the proximal ERK1 promoter region in E2 but not in TAM-treated cells.
  • We concluded that SRC-1 was a key molecular determinant of estrogen-mediated proliferation in human SCC lines.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Estrogen Antagonists / pharmacology. Estrogen Receptor alpha / metabolism. Estrogens / pharmacology. Histone Acetyltransferases / metabolism. Tamoxifen / pharmacology. Transcription Factors / metabolism
  • [MeSH-minor] Blotting, Western / methods. Breast Neoplasms. CREB-Binding Protein / genetics. CREB-Binding Protein / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Chromatin Immunoprecipitation. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Lipids / administration & dosage. Lipids / genetics. Nuclear Receptor Coactivator 1. Reverse Transcriptase Polymerase Chain Reaction. Transfection / methods

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  • (PMID = 17400812.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CREBBP protein, human; 0 / Estrogen Antagonists; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Lipids; 0 / Lipofectamine; 0 / Transcription Factors; 094ZI81Y45 / Tamoxifen; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / NCOA1 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 1; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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22. Kobayashi O, Murakami H, Yoshida T, Cho H, Yoshikawa T, Tsuburaya A, Sairenji M, Motohashi H, Sugiyama Y, Kameda Y: Clinical diagnosis of metastatic gastric tumors: clinicopathologic findings and prognosis of nine patients in a single cancer center. World J Surg; 2004 Jun;28(6):548-51
MedlinePlus Health Information. consumer health - Stomach Cancer.

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  • [Title] Clinical diagnosis of metastatic gastric tumors: clinicopathologic findings and prognosis of nine patients in a single cancer center.
  • MGTs were detected simultaneously with the primary tumors in three and afterward in six patients at 14 to 74 months.
  • The primary tumors included one each of squamous cell carcinoma of the esophagus, signet-ring cell carcinoma of the breast, large-cell or small-cell carcinoma of the lung, renal cell carcinoma, hepatocellular carcinoma, squamous cell or epidermoid carcinoma of the uterus, and melanoma.
  • Five patients were treated by chemotherapy with no apparent survival benefit.
  • A median survival after MGT diagnosis was 170 days (range 16-892 days) for all cases, 384 days for those who underwent gastrectomy (n = 6), and 27 days for those without active treatment (n = 3) (p = 0.002).
  • [MeSH-major] Stomach Neoplasms / diagnosis. Stomach Neoplasms / mortality

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  • (PMID = 15366743.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Li C, Iida M, Dunn EF, Wheeler DL: Dasatinib blocks cetuximab- and radiation-induced nuclear translocation of the epidermal growth factor receptor in head and neck squamous cell carcinoma. Radiother Oncol; 2010 Nov;97(2):330-7
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  • [Title] Dasatinib blocks cetuximab- and radiation-induced nuclear translocation of the epidermal growth factor receptor in head and neck squamous cell carcinoma.
  • BACKGROUND AND PURPOSE: The aberrant expression of epidermal growth factor receptor (EGFR) has been linked to the etiology of head and neck squamous cell carcinoma (HNSCC).
  • In this report we sought to determine how to block cetuximab- and radiation-induced translocation of EGFR to the nucleus in HNSCC cell lines.
  • MATERIAL AND METHODS: We utilized three established HNSCC cell lines, SCC1, SCC6 and SCC1483 and measured nuclear translocation of EGFR after treatment with cetuximab or radiation.
  • We then utilized dasatinib (BMS-354825), a potent, orally bioavailable inhibitor of several tyrosine kinases, including the Src family kinases, to determine if SFKs blockade could abrogate cetuximab- and radiation-induced nuclear EGFR translocation.
  • RESULTS: Cetuximab and radiation treatment of all three HNSCC lines lead to translocation of the EGFR to the nucleus.

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  • [Copyright] Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
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  • (PMID = 20667610.001).
  • [ISSN] 1879-0887
  • [Journal-full-title] Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
  • [ISO-abbreviation] Radiother Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA014520; United States / NCI NIH HHS / CA / CA009614-17; United States / NCRR NIH HHS / RR / UL1 RR025011; United States / NCI NIH HHS / CA / P30CA014520; United States / NCRR NIH HHS / RR / 1UL1RR025011; United States / NCI NIH HHS / CA / T32 CA009614
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab; RBZ1571X5H / Dasatinib
  • [Other-IDs] NLM/ NIHMS223644; NLM/ PMC2974772
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24. Sasaki CY, Lin Hc, Passaniti A: Expression of E-cadherin reduces bcl-2 expression and increases sensitivity to etoposide-induced apoptosis. Int J Cancer; 2000 Jun 1;86(5):660-6
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  • Expression of Bcl-2 is important in determining cancer cell resistance to chemotherapy.
  • However, it is not clear whether cell-cell interactions regulate Bcl-2 expression.
  • Using rat breast carcinoma cells selected for loss of hormone responsiveness, we found that parental E-cadherin-expressing cells (E cells) were more sensitive to etoposide-induced apoptosis than hormone-non-responsive cells (F cells), which failed to express E-cadherin.
  • Expression of beta-catenin and pp120 src substrate proteins, which associate with E-cadherin, was unaffected.
  • Cad) showed increased sensitivity to etoposide treatment compared with control clones (F.Neo).
  • Unlike F cells, F.Cad transfectants were not able to express Bcl-2, but transient transfection of bcl-2 resulted in re-expression and resistance to etoposide treatment.
  • Loss of E-cadherin in invasive tumor cells may lead to increased Bcl-2 expression and resistance to chemotherapeutic drugs.

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  • (PMID = 10797287.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cadherins; 0 / Proto-Oncogene Proteins c-bcl-2; 6PLQ3CP4P3 / Etoposide
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25. Agatsuma T, Ogawa H, Akasaka K, Asai A, Yamashita Y, Mizukami T, Akinaga S, Saitoh Y: Halohydrin and oxime derivatives of radicicol: synthesis and antitumor activities. Bioorg Med Chem; 2002 Nov;10(11):3445-54
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  • Novel halohydrin and oxime derivatives of radicicol (1) were prepared and evaluated for their v-src tyrosine kinase inhibitory, antiproliferative, and antitumor activities.
  • Some of the resulting derivatives showed significantly improved antitumor activities than those of 1 in vitro as tested in a cell proliferation assay and in vivo using sc-inoculated human breast carcinoma and epidermoid tumor models.
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / pathology. Chromatography, High Pressure Liquid. Drug Screening Assays, Antitumor. Enzyme Inhibitors / chemical synthesis. Enzyme Inhibitors / pharmacology. Female. Humans. Indicators and Reagents. Macrolides. Structure-Activity Relationship. Tumor Cells, Cultured. src-Family Kinases / antagonists & inhibitors

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  • (PMID = 12213458.001).
  • [ISSN] 0968-0896
  • [Journal-full-title] Bioorganic & medicinal chemistry
  • [ISO-abbreviation] Bioorg. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Indicators and Reagents; 0 / Lactones; 0 / Macrolides; 0 / Oximes; 12772-57-5 / monorden; EC 2.7.10.2 / src-Family Kinases
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26. Marcu MG, Schulte TW, Neckers L: Novobiocin and related coumarins and depletion of heat shock protein 90-dependent signaling proteins. J Natl Cancer Inst; 2000 Feb 2;92(3):242-8
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  • BACKGROUND: Heat shock protein 90 (Hsp90) interacts with and stabilizes several oncogenic protein kinases (e.g., p185(erbB2), p60(v-src), and Raf-1) and is required for the stability and dominant-negative function of mutated p53 protein.
  • Since the nucleotide-binding site of gyrase B is targeted by coumarin antibiotics (e.g., novobiocin), we investigated whether these drugs can also interact with Hsp90 and affect its activity.
  • METHODS: We used immobilized novobiocin, geldanamycin, or radicicol to isolate either endogenous Hsp90 from cell lysates or Hsp90 deletion fragments translated in vitro.
  • All three coumarins markedly reduced cellular levels of p185(erbB2), p60(v-src), Raf-1, and mutated p53.
  • Furthermore, novobiocin reduced Raf-1 levels in the spleens of mice treated with the drug.
  • CONCLUSIONS: These coumarin antibiotics, particularly novobiocin, represent a first-generation alternative to other Hsp90-targeting drugs that are not as well tolerated.
  • Novobiocin's unique interaction with Hsp90 identifies an additional site on this protein amenable to pharmacologic interference with small molecules.
  • [MeSH-minor] Aminocoumarins. Animals. Blotting, Western. Breast Neoplasms / drug therapy. Carcinoma / drug therapy. Carrier Proteins / drug effects. Carrier Proteins / metabolism. DNA Topoisomerases, Type II / metabolism. Enzyme Inhibitors / pharmacology. Female. Fibroblasts. Humans. Mice. Oncogene Protein pp60(v-src) / drug effects. Oncogene Protein pp60(v-src) / metabolism. Protein Binding / drug effects. Proto-Oncogene Proteins c-raf / drug effects. Proto-Oncogene Proteins c-raf / metabolism. Spleen / cytology. Spleen / metabolism. Topoisomerase II Inhibitors. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / drug effects. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 10655441.001).
  • [ISSN] 0027-8874
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Aminocoumarins; 0 / Antibiotics, Antineoplastic; 0 / Carrier Proteins; 0 / Coumarins; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Intracellular Signaling Peptides and Proteins; 0 / TOB1 protein, human; 0 / Tob1 protein, mouse; 0 / Topoisomerase II Inhibitors; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 17EC19951N / Novobiocin; 39868-96-7 / clorobiocin; EC 2.7.10.2 / Oncogene Protein pp60(v-src); EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 5.99.1.3 / DNA Topoisomerases, Type II; PCH9QZ1IIH / coumermycin
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27. Rabbani SA, Valentino ML, Arakelian A, Ali S, Boschelli F: SKI-606 (Bosutinib) blocks prostate cancer invasion, growth, and metastasis in vitro and in vivo through regulation of genes involved in cancer growth and skeletal metastasis. Mol Cancer Ther; 2010 May;9(5):1147-57
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  • In the current study, we have examined the efficacy of a Src/Abl kinase inhibitor SKI-606 (Bosutinib) for its effect on prostate cancer growth and skeletal metastasis.
  • Treatment of highly invasive human prostate cancer cells PC-3 and DU-145 with different doses of SKI-606 decreased Src activation, cell proliferation, migration, and invasion as determined by Matrigel Boyden chamber invasion assay.
  • Experimental animals treated with SKI-606 developed tumors of a significantly smaller volume and a significant decrease (50%) in experimental skeletal lesion area.
  • A marked increase (32%) in bone volume to tumor volume ratio was also seen by micro-computed tomography analysis of tibias from control and experimental groups of animals.
  • SKI-606 is currently in clinical trials for breast cancer and chronic myelogenous leukemia.
  • [MeSH-major] Aniline Compounds / therapeutic use. Bone Neoplasms / secondary. Carcinoma / drug therapy. Cell Proliferation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Nitriles / therapeutic use. Prostatic Neoplasms / drug therapy. Quinolines / therapeutic use
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Mice, SCID. Neoplasm Invasiveness. Neoplasm Metastasis. Tumor Burden / drug effects. Tumor Burden / genetics. Xenograft Model Antitumor Assays


28. Turkson J, Kim JS, Zhang S, Yuan J, Huang M, Glenn M, Haura E, Sebti S, Hamilton AD, Jove R: Novel peptidomimetic inhibitors of signal transducer and activator of transcription 3 dimerization and biological activity. Mol Cancer Ther; 2004 Mar;3(3):261-9
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  • The critical role of signal transducer and activator of transcription 3 (Stat3) in the growth and survival of human tumor cells identifies it as a promising target for cancer drug discovery.
  • In this context, the representative peptidomimetic ISS 610 with 4-cyanobenzoate substitution inhibits constitutive Stat3 activity in Src-transformed mouse fibroblasts and human breast and lung carcinoma cells.
  • Moreover, ISS 610 induces cell growth inhibition and apoptosis of Src-transformed fibroblasts that contain persistently active Stat3.
  • We present the first report of a peptidomimetic approach to design of small-molecule inhibitors of Stat3 that are also among the first examples of disruptors of transcription factor dimerization with the potential for novel cancer therapy.
  • [MeSH-minor] Agar / chemistry. Animals. Apoptosis. Baculoviridae / genetics. Benzoates / pharmacology. Bromodeoxyuridine / pharmacology. Cell Division. Cell Line. Cell Line, Tumor. Cell Nucleus / metabolism. Coloring Agents / pharmacology. Cytosol / metabolism. Dimerization. Dose-Response Relationship, Drug. Fibroblasts / metabolism. Flow Cytometry. Humans. Hydrogen Bonding. Inhibitory Concentration 50. Insects. Luciferases / metabolism. Mice. Models, Chemical. Models, Molecular. NIH 3T3 Cells. Peptides / chemistry. Phosphorylation. Plasmids / metabolism. Protein Binding. Protein Conformation. STAT3 Transcription Factor. Time Factors

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  • (PMID = 15026546.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA55652; United States / NCI NIH HHS / CA / CA78038
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzoates; 0 / Coloring Agents; 0 / DNA-Binding Proteins; 0 / Peptides; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Stat3 protein, mouse; 0 / Trans-Activators; 619-65-8 / 4-cyanobenzoic acid; 9002-18-0 / Agar; EC 1.13.12.- / Luciferases; G34N38R2N1 / Bromodeoxyuridine
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29. Li C, Iida M, Dunn EF, Ghia AJ, Wheeler DL: Nuclear EGFR contributes to acquired resistance to cetuximab. Oncogene; 2009 Oct 29;28(43):3801-13
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  • Cetuximab is an EGFR-blocking antibody that has been approved for the treatment of patients with head and neck squamous cell carcinoma and metastatic colorectal cancer.
  • Previous reports have shown that EGFR translocation to the nucleus is associated with cell proliferation.
  • Here we investigated mechanisms of acquired resistance to cetuximab using a model derived from the non-small cell lung cancer line H226.
  • Overexpression of these ligands is associated with the nuclear translocation of the EGFR and this process was mediated by the Src family kinases (SFK).
  • Treatment of cetuximab-resistant cells with the SFK inhibitor, dasatinib, resulted in loss of nuclear EGFR, increased membrane expression of the EGFR and resensitization to cetuximab.
  • Collectively, these data suggest that nuclear expression of EGFR may be an important molecular determinant of resistance to cetuximab therapy and provides a rationale for investigating nuclear EGFR as a biomarker for cetuximab response.

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  • (PMID = 19684613.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA014520; None / None / / P30 CA014520-30; United States / NCI NIH HHS / CA / P30 CA014520-30
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Nuclear Localization Signals; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / src-Family Kinases; PQX0D8J21J / Cetuximab
  • [Other-IDs] NLM/ NIHMS212184; NLM/ PMC2900381
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30. Blaskovich MA, Sun J, Cantor A, Turkson J, Jove R, Sebti SM: Discovery of JSI-124 (cucurbitacin I), a selective Janus kinase/signal transducer and activator of transcription 3 signaling pathway inhibitor with potent antitumor activity against human and murine cancer cells in mice. Cancer Res; 2003 Mar 15;63(6):1270-9
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  • To discover disrupters of aberrant STAT3 signaling pathways as novel anticancer drugs, we developed a phosphotyrosine STAT3 cytoblot.
  • JSI-124 suppressed the levels of phosphotyrosine STAT3 in v-Src-transformed NIH 3T3 cells and human cancer cells potently (IC(50) value of 500 nM in the human lung adenocarcinoma A549) and rapidly (complete inhibition within 1-2 h).
  • JSI-124 also decreased the levels of tyrosine-phosphorylated Janus kinase (JAK) but not those of Src.
  • Finally, JSI-124 (1 mg/kg/day) potently inhibited the growth in nude mice of A549 tumors, v-Src-transformed NIH 3T3 tumors, and the human breast carcinoma MDA-MB-468, all of which express high levels of constitutively activated STAT3, but it did not affect the growth of oncogenic Ras-transformed NIH 3T3 tumors that are STAT3 independent or of the human lung adenocarcinoma Calu-1, which has barely detectable levels of phosphotyrosine STAT3.
  • These results give strong support for pharmacologically targeting the JAK/STAT3 signaling pathway for anticancer drug discovery.
  • [MeSH-minor] 3T3 Cells. Animals. Apoptosis / drug effects. Cell Division / drug effects. Humans. Janus Kinase 2. MAP Kinase Signaling System / drug effects. Melanoma, Experimental / drug therapy. Mice. Mice, Inbred C57BL. Mice, Nude. Phosphorylation. Phosphotyrosine / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. STAT3 Transcription Factor. Signal Transduction / drug effects. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12649187.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA78038
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Stat3 protein, mouse; 0 / Trans-Activators; 0 / Triterpenes; 21820-51-9 / Phosphotyrosine; 2222-07-3 / cucurbitacin I; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Jak2 protein, mouse; EC 2.7.10.2 / Janus Kinase 2; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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31. Fehrenbacher N, Bastholm L, Kirkegaard-Sørensen T, Rafn B, Bøttzauw T, Nielsen C, Weber E, Shirasawa S, Kallunki T, Jäättelä M: Sensitization to the lysosomal cell death pathway by oncogene-induced down-regulation of lysosome-associated membrane proteins 1 and 2. Cancer Res; 2008 Aug 15;68(16):6623-33
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  • [Title] Sensitization to the lysosomal cell death pathway by oncogene-induced down-regulation of lysosome-associated membrane proteins 1 and 2.
  • Here, we show that transformation of murine embryonic fibroblasts with v-H-ras or c-src(Y527F) changes the distribution, density, and ultrastructure of the lysosomes, decreases the levels of lysosome-associated membrane proteins (LAMP-1 and LAMP-2) in an extracellular signal-regulated kinase (ERK)- and cathepsin-dependent manner, and sensitizes the cells to lysosomal cell death pathways induced by various anticancer drugs (i.e., cisplatin, etoposide, doxorubicin, and siramesine).
  • Importantly, K-ras and erbb2 elicit a similar ERK-mediated activation of cysteine cathepsins, cathepsin-dependent down-regulation of LAMPs, and increased drug sensitivity in human colon and breast carcinoma cells, respectively.
  • Notably, reconstitution of LAMP levels by ectopic expression or by cathepsin inhibitors protects transformed cells against the lysosomal cell death pathway.
  • Furthermore, knockdown of either lamp1 or lamp2 is sufficient to sensitize the cells to siramesine-induced cell death and photo-oxidation-induced lysosomal destabilization.
  • Thus, the transformation-associated ERK-mediated up-regulation of cysteine cathepsin expression and activity leads to a decrease in the levels of LAMPs, which in turn contributes to the enhanced sensitivity of transformed cells to drugs that trigger lysosomal membrane permeabilization.
  • These data indicate that aggressive cancers with high cysteine cathepsin levels are especially sensitive to lysosomal cell death pathways and encourage the further development of lysosome-targeting compounds for cancer therapy.
  • [MeSH-major] Apoptosis / physiology. Cell Transformation, Neoplastic. Colonic Neoplasms / metabolism. Embryo, Mammalian / metabolism. Fibroblasts / metabolism. Lysosomal-Associated Membrane Protein 1 / metabolism. Lysosomal-Associated Membrane Protein 2 / metabolism. Lysosomes / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Cathepsins / metabolism. Cell Communication. Cell Membrane Permeability. Cells, Cultured. Down-Regulation. Extracellular Signal-Regulated MAP Kinases / metabolism. Genes, ras / physiology. Humans. Mice. NIH 3T3 Cells. Proto-Oncogene Proteins c-raf / metabolism. Proto-Oncogene Proteins p21(ras) / physiology. RNA Interference

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  • (PMID = 18701486.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Lysosomal-Associated Membrane Protein 1; 0 / Lysosomal-Associated Membrane Protein 2; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.- / Cathepsins; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
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32. Glaeser M, Niederacher D, Djahansouzi S, Hanstein B, Dittrich R, Beckmann MW, Fasching PA, Ackermann S: Effects of the antiestrogens tamoxifen and raloxifene on the estrogen receptor transactivation machinery. Anticancer Res; 2006 Jan-Feb;26(1B):735-44
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  • The influence of 17beta-estradiol (E2), tamoxifen (TAM) and raloxifen (RLX) on the proliferation of breast (BC) and endometrial carcinoma cell lines (EC) and the expression of different compounds of the estrogen receptor (ER)-transactivation machinery were studied.
  • TAM showed a biphasic effect on ER-positive cell lines.
  • The steroid receptor coactivator (SRC) AIB1 expression was slightly decreased by E2 but not by antiestrogens (antiE).
  • TIF2 expression was increased by E2, TAM and RLX, but SRC-1 expression was not.
  • [MeSH-major] Estrogen Receptor Modulators / pharmacology. Raloxifene Hydrochloride / pharmacology. Receptors, Estrogen / biosynthesis. Tamoxifen / pharmacology. Transcriptional Activation / drug effects
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Growth Processes / drug effects. Cell Line, Tumor. Endometrial Neoplasms / drug therapy. Endometrial Neoplasms / genetics. Endometrial Neoplasms / metabolism. Endometrial Neoplasms / pathology. Estradiol / pharmacology. Female. Humans. Receptors, Progesterone / biosynthesis. Receptors, Progesterone / genetics

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  • (PMID = 16739346.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Estrogen Receptor Modulators; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 094ZI81Y45 / Tamoxifen; 4F86W47BR6 / Raloxifene Hydrochloride; 4TI98Z838E / Estradiol
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33. Labrie F, Labrie C, Bélanger A, Simard J, Giguère V, Tremblay A, Tremblay G: EM-652 (SCH57068), a pure SERM having complete antiestrogenic activity in the mammary gland and endometrium. J Steroid Biochem Mol Biol; 2001 Dec;79(1-5):213-25
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  • [Title] EM-652 (SCH57068), a pure SERM having complete antiestrogenic activity in the mammary gland and endometrium.
  • In order to minimize the risks of endometrial cancer and the development of resistance to antiestrogen therapy, we have synthesized the orally active antiestrogen EM-652 which is the most potent of the known antiestrogens and exerts pure antiestrogenic activity in the mammary gland and endometrium.
  • EM-652, thus, inhibits Ras-induced transcriptional activity and blocks SRC-1-stimulated activity of the two receptors.
  • The absence of blockade of AF-1 by OH-TAM could explain why resistance develops to Tamoxifen treatment.
  • Not only the development, but also the growth of established DMBA-induced mammary carcinoma is inhibited by treatment with EM-800, the prodrug of EM-652.
  • EM-652 is the most potent antiestrogen to inhibit the growth of human breast cancer ZR-75-1, MCF-7 and T-47D cells in vitro.
  • When incubated with human Ishikawa endometrial carcinoma cells, EM-800 has no stimulatory effect on the estrogen-sensitive parameter alkaline phosphatase activity.
  • EM-800 has shown benefits in women with breast cancer who had failed Tamoxifen.
  • The above-summarized preclinical and clinical data clearly suggest the interest of studying this compounds in the neoadjuvant and adjuvant settings and, most importantly, for the prevention of breast and uterine cancer.
  • [MeSH-major] Breast / drug effects. Endometrium / drug effects. Estrogen Receptor Modulators / pharmacology. Piperidines / pharmacology. Selective Estrogen Receptor Modulators / pharmacology
  • [MeSH-minor] Animals. Benzopyrans / pharmacology. Breast Neoplasms / drug therapy. Breast Neoplasms / prevention & control. Cholesterol / blood. Endometrial Neoplasms / drug therapy. Endometrial Neoplasms / prevention & control. Estrogen Receptor alpha. Estrogen Receptor beta. Female. Humans. Mammary Neoplasms, Experimental / prevention & control. Mice. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / prevention & control. Osteoporosis / prevention & control. Propionates / pharmacology. Rats. Receptors, Estrogen / antagonists & inhibitors. Receptors, Estrogen / genetics. Tamoxifen / pharmacology. Transcription, Genetic / drug effects. Triglycerides / blood. Tumor Cells, Cultured

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  • (PMID = 11850228.001).
  • [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] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Benzopyrans; 0 / EM 800; 0 / Estrogen Receptor Modulators; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / Piperidines; 0 / Propionates; 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; 0 / Triglycerides; 094ZI81Y45 / Tamoxifen; 37607-02-6 / ritetronium; 97C5T2UQ7J / Cholesterol
  • [Number-of-references] 112
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34. Visram H, Greer PA: 17beta-estradiol and tamoxifen stimulate rapid and transient ERK activationin MCF-7 cells via distinct signaling mechanisms. Cancer Biol Ther; 2006 Dec;5(12):1677-82
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  • While the precise mechanism of this action is still under investigation, it is known that activation of the epidermal growth factor receptor, the Src tyrosine kinase, and metalloproteinases are involved in this process.
  • More recently, tamoxifen, an anti-hormonal agent used to treat breast cancer, has been shown to also activate ERK.
  • Using the MCF-7 human breast carcinoma cell line as a model system, we show that ERK is rapidly and transiently activated in cells challenged with epidermal growth factor (EGF), 17beta-estradiol (E2) or tamoxifen.
  • In contrast, inhibition of Src or metalloproteinases caused distinct effects on ERK activation by E2 and tamoxifen.
  • Thus, while both E2 and tamoxifen induced activation of ERK, the differences in the effects of inhibitors of Src or metalloproteinases on ERK activation indicated that E2 and tamoxifen do so via distinct molecular mechanisms.
  • [MeSH-minor] Breast Neoplasms. Cell Line, Tumor. Enzyme Activation / drug effects. Estrogen Receptor alpha / genetics. Female. Humans. Receptor, Epidermal Growth Factor / genetics

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  • [CommentIn] Cancer Biol Ther. 2007 Jan;6(1):119-20 [17264668.001]
  • (PMID = 17106250.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 094ZI81Y45 / Tamoxifen; 4TI98Z838E / Estradiol; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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35. Liao YC, Lo SH: Deleted in liver cancer-1 (DLC-1): a tumor suppressor not just for liver. Int J Biochem Cell Biol; 2008;40(5):843-7
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  • Deleted in liver cancer 1 (DLC-1), as its name implied, was originally isolated as a potential tumor suppressor gene often deleted in hepatocellular carcinoma.
  • Further studies have indicated that down-expression of DLC-1 either by genomic deletion or DNA methylation is associated with a variety of cancer types including lung, breast, prostate, kidney, colon, uterus, ovary, and stomach.
  • Re-expression of DLC-1 in cancer cells regulates the structure of actin cytoskeleton and focal adhesions and significantly inhibits cell growth, supporting its role as a tumor suppressor.
  • This tumor suppressive function relies on DLC-1's RhoGTPase activating protein (RhoGAP) activity and steroidogenic acute regulatory (StAR)-related lipid transfer (START) domain, as well as its focal adhesion localization, which is recruited by the Src Homology 2 (SH2) domains of tensins in a phosphotyrosine-independent fashion.
  • Therefore, the expression and subcellular localization of DLC-1 could be a useful molecular marker for cancer prognosis, whereas DLC-1 and its downstream signaling molecules might be therapeutic targets for the treatment of cancer.

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  • (PMID = 17521951.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R56 CA102537; United States / NCI NIH HHS / CA / R01 CA102537-04; United States / NCI NIH HHS / CA / CA102537; United States / NCI NIH HHS / CA / R01 CA102537; United States / NCI NIH HHS / CA / CA102537-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DLC1 protein, human; 0 / GTPase-Activating Proteins; 0 / Tumor Suppressor Proteins
  • [Number-of-references] 32
  • [Other-IDs] NLM/ NIHMS45166; NLM/ PMC2323245
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36. Shirasaka T, Tsukuda M, Inuyama Y, Taguchi T: [New oral anticancer drug, TS-1 (S-1)--from bench to clinic]. Gan To Kagaku Ryoho; 2001 Jun;28(6):855-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [New oral anticancer drug, TS-1 (S-1)--from bench to clinic].
  • We describe in this paper a therapeutic modality which is based on a self-rescuing concept (SRC) featuring dual activity, i.e., effect-enhancing activity and adverse reaction-reducing activity.
  • We devised a novel oral anticancer agent, S-1, as a combination drug with a molar ratio of 1:0.4:1 for FT, CDHP, and Oxo, respectively.
  • To compare S-1, FT, and UFT in terms of their anticancer activity and adverse reactions, a colon cancer implantation model in rats was used for 4-week consecutive oral administration from the time when the postimplantation tumor weight become about 2 g.
  • Antitumor activity was more marked with S-1 than FT and UFT.
  • Adverse reaction, i.e., stomatitis, depilation, and weight loss, were less frequent in the S-1 group than in the other groups.
  • Median survival time (MST) was 224 days.
  • Grade 4 hemoglobin decrease was observed in one case; however, this returned to normal after the termination of drug administration and blood transfusion.
  • A late phase II clinical trial of S-1 was conducted to evaluate the efficacy and toxicities in patients with metastatic colorectal carcinoma.
  • Sixty-three patients with measurable metastatic colorectal carcinoma were enrolled in this clinical trial.
  • Late phase II clinical trials of S-1 are in progress for colorectal cancer, breast cancer and non-small cell lung cancer.
  • To establish the standard therapeutic modality for cancers, including gastrointestinal cancers, in Japan, the conduction of clinical trials combining S-1 and other anticancer drugs holds promise for the future.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use
  • [MeSH-minor] Administration, Oral. Animals. Clinical Trials as Topic. Colorectal Neoplasms / drug therapy. Drug Combinations. Drug Synergism. Head and Neck Neoplasms / drug therapy. Humans. Oxonic Acid / administration & dosage. Pyridines / administration & dosage. Rats. Stomach Neoplasms / drug therapy. Tegafur / administration & dosage

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  • (PMID = 11432358.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0 / Pyridines; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid
  • [Number-of-references] 19
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37. Tanjoni I, Walsh C, Uryu S, Tomar A, Nam JO, Mielgo A, Lim ST, Liang C, Koenig M, Sun C, Patel N, Kwok C, McMahon G, Stupack DG, Schlaepfer DD: PND-1186 FAK inhibitor selectively promotes tumor cell apoptosis in three-dimensional environments. Cancer Biol Ther; 2010 May 15;9(10):764-77
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] PND-1186 FAK inhibitor selectively promotes tumor cell apoptosis in three-dimensional environments.
  • This is mediated in part through survival signals that bypass normal growth restraints controlled by integrin cell surface receptors.
  • PND-1186 has an IC50 of ~100 nM in breast carcinoma cells as determined by anti-phospho-specific immunoblotting to FAK Tyr-397.
  • PND-1186 did not alter c‑Src or p130Cas tyrosine phosphorylation in adherent cells, yet functioned to restrain cell movement.
  • Notably, 1.0 µM PND-1186 (>5-fold above IC50) had limited effects on cell proliferation.
  • However, under non-adherent conditions as spheroids and as colonies in soft agar, 0.1 µM PND-1186 blocked FAK and p130Cas tyrosine phosphorylation, promoted caspase-3 activation, and triggered cell apoptosis.
  • PND-1186 inhibited 4T1 breast carcinoma subcutaneous tumor growth correlated with elevated tumor cell apoptosis and caspase 3 activation.
  • Addition of PND-1186 to the drinking water of mice was well tolerated and inhibited ascites- and peritoneal membrane-associated ovarian carcinoma tumor growth associated with the inhibition of FAK Tyr-397 phosphorylation.
  • Our results with low-level PND-1186 treatment support the conclusion that FAK activity selectively promotes tumor cell survival in three-dimensional environments.

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  • (PMID = 20234191.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102310-08; United States / NCI NIH HHS / CA / R01 CA102310; United States / NCI NIH HHS / CA / CA102310; United States / NCI NIH HHS / CA / CA107263; United States / NCI NIH HHS / CA / R01 CA107263; United States / NCI NIH HHS / CA / CA102310-08
  • [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] United States
  • [Chemical-registry-number] 0 / Aminopyridines; 0 / Antineoplastic Agents; 0 / Crk-Associated Substrate Protein; 0 / PND 1186; 42HK56048U / Tyrosine; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2 / src-Family Kinases; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS205870; NLM/ PMC2933317
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38. Lurje G, Lenz HJ: EGFR signaling and drug discovery. Oncology; 2009;77(6):400-10
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] EGFR signaling and drug discovery.
  • Conversely, inhibition of ErbB pathways with targeted agents, such as monoclonal antibodies (MoAbs) or tyrosine kinase inhibitors (TKIs), blocks cell cycle progression, inhibits the production of pro-angiogenic factors and induces apoptosis in numerous in vitro and xenograft models.
  • Accordingly, the ErbB receptor family with their most prominent members EGFR and HER-2 represents validated targets for anti-cancer therapy, and anti-ErbB MoAbs (cetuximab, panitumumab, and trastuzumab) and TKIs (gefitinib, erlotinib, and lapatinib) have now been approved for the treatment of advanced colorectal cancer, squamous cell carcinoma of the head and neck, advanced non-small-cell lung cancer, as well as pancreatic and breast cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Drug Discovery. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / physiology. Signal Transduction / drug effects
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Drug Resistance, Neoplasm. Genes, ras. Humans. Neoplasms / drug therapy. Phosphatidylinositol 3-Kinases / physiology. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-akt / physiology. src-Family Kinases / physiology

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  • [Copyright] Copyright (c) 2010 S. Karger AG, Basel.
  • (PMID = 20130423.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Protein Kinase Inhibitors; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.2 / src-Family Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Number-of-references] 111
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