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1. Passardi A, Massa I, Zoli W, Gianni L, Milandri C, Zumaglini F, Nanni O, Maltoni R, Frassineti GL, Amadori D: Phase II study of gemcitabine, doxorubicin and paclitaxel (GAT) as first-line chemotherapy for metastatic breast cancer: a translational research experience. BMC Cancer; 2006;6:76
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  • [Title] Phase II study of gemcitabine, doxorubicin and paclitaxel (GAT) as first-line chemotherapy for metastatic breast cancer: a translational research experience.
  • BACKGROUND: Patients with metastatic breast cancer are frequently treated with anthracyclines and taxanes, which are among the most active agents in this disease.
  • Gemcitabine is an interesting candidate for a three-drug combination because of its different mechanism of action and non-overlapping toxicity with respect to the other two drugs.
  • We aimed to evaluate the activity and toxicity of the GAT (gemcitabine, doxorubicin and paclitaxel) regimen, derived from experimental preclinical studies, as first-line chemotherapy in patients with stage IIIB-IV breast cancer.
  • METHODS: Patients with locally advanced or metastatic breast cancer and at least one bidimensionally measurable lesion were included in the present study.
  • Only prior adjuvant non anthracycline-based chemotherapy was permitted.
  • Treatment consisted of doxorubicin 50 mg/m2 on day 1, paclitaxel 160 mg/m2 on day 2 and gemcitabine 800 mg/m2 on day 6, repeated every 21-28 days.
  • RESULTS: Thirty-three consecutive breast cancer patients were enrolled onto the trial (7 stage IIIB and 26 stage IV).
  • Median time to progression and overall survival were 10.2 and 36.4 months, respectively.
  • One patient died from sepsis during the first treatment cycle before the administration of gemcitabine.
  • CONCLUSION: The strong synergism among the three drugs found in the preclinical setting was confirmed in terms of both clinical activity and hematological toxicity.
  • Our results seem to indicate that the GAT regimen is effective in anthracycline-naïve metastatic breast cancer and provides a feasible chemotherapeutic option in this clinical setting.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Disease Progression. Doxorubicin / administration & dosage. Female. Humans. Infusions, Intravenous. Middle Aged. Neoplasm Metastasis. Paclitaxel / administration & dosage. Survival Analysis. Treatment Outcome

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  • [Cites] J Clin Oncol. 2001 Mar 15;19(6):1707-15 [11251000.001]
  • [Cites] Breast Cancer Res Treat. 2001 Jul;68(2):171-9 [11688520.001]
  • [Cites] J Clin Oncol. 2002 Jul 15;20(14):3114-21 [12118025.001]
  • [Cites] J Clin Oncol. 2003 Mar 15;21(6):968-75 [12637459.001]
  • [Cites] J Chemother. 2003 Oct;15(5):488-94 [14598942.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):7081-8 [16192591.001]
  • [Cites] Semin Oncol. 1997 Oct;24(5 Suppl 17):S17-19-S17-25 [9374087.001]
  • [Cites] Int J Cancer. 1999 Jan 29;80(3):413-6 [9935183.001]
  • [Cites] Cancer. 2005 Feb 15;103(4):672-9 [15637696.001]
  • [Cites] J Clin Oncol. 2005 Mar 1;23(7):1401-8 [15735116.001]
  • [Cites] Br J Cancer. 2005 Aug 8;93(3):293-301 [16052223.001]
  • [Cites] Oncology (Williston Park). 2003 Dec;17(12 Suppl 14):36-40 [14768404.001]
  • (PMID = 16551351.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 80168379AG / Doxorubicin; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC1434761
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2. Seidman AD: Gemcitabine as single-agent therapy in the management of advanced breast cancer. Oncology (Williston Park); 2001 Feb;15(2 Suppl 3):11-4
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  • [Title] Gemcitabine as single-agent therapy in the management of advanced breast cancer.
  • Many active cytotoxic agents exist for breast cancer therapy, and numerous combination chemotherapy regimens are derived from them.
  • Creating these combinations is sometimes empirically motivated by non-overlapping toxicities or the expectation of non-cross resistance.
  • Yet, there is usually no absolute division of these aspects among cytotoxic agents, and the median survival for patients with metastatic breast cancer has not been dramatically prolonged by this approach.
  • When the outcome of treatment is palliation rather than cure, it becomes paramount to optimize the dynamic equilibrium between chemotherapy-induced side effects and the benefits attributable to relief of cancer-related symptoms.
  • To this end, several recent clinical trials have evaluated the novel nucleoside analog gemcitabine (Gemzar) as single-agent therapy for advanced breast cancer.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Breast Neoplasms / drug therapy. Deoxycytidine / therapeutic use
  • [MeSH-minor] Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Female. Humans. Neoplasm Metastasis. Palliative Care

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  • (PMID = 11252882.001).
  • [ISSN] 0890-9091
  • [Journal-full-title] Oncology (Williston Park, N.Y.)
  • [ISO-abbreviation] Oncology (Williston Park, N.Y.)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Number-of-references] 44
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3. Thiery JP, Sastre-Garau X, Vincent-Salomon B, Sigal-Zafrani X, Pierga JY, Decraene C, Meyniel JP, Gravier E, Asselain B, De Rycke Y, Hupe P, Barillot E, Ajaz S, Faraldo M, Deugnier MA, Glukhova M, Medina D, Breast Cancer Group: Challenges in the stratification of breast tumors for tailored therapies. Bull Cancer; 2006 Aug;93(8):E81-9
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  • [Title] Challenges in the stratification of breast tumors for tailored therapies.
  • Studying the molecular stratification of breast carcinoma is a real challenge considering the extreme heterogeneity of these tumors.
  • However a significant fraction of these breast cancer patients do not need adjuvant chemotherapies while other patients receive inefficacious therapies.
  • High density gene expression arrays have been designed to attempt to establish expression profiles that could be used as prognostic indicators or as predictive markers for response to treatment.
  • The combined analysis of transcriptomic and genomic alteration data from relatively large numbers of well annotated tumor specimens may offer an opportunity to overcome the current difficulties in validating recently published non overlapping gene lists as prognostic or therapeutic indicators.
  • There is also hope for identifying and deciphering signal transduction pathways driving tumor progression with newly developed algorithms and semi quantitative parameters obtained in simplified in vitro or in vivo models for specific transduction pathways.
  • [MeSH-major] Breast Neoplasms / classification. Breast Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / therapeutic use. Carcinoma, Ductal, Breast / classification. Carcinoma, Ductal, Breast / pathology. Carcinoma, Intraductal, Noninfiltrating / classification. Carcinoma, Intraductal, Noninfiltrating / pathology. Female. Gene Expression Profiling. Humans. Mice. Mice, Transgenic. Models, Animal. Mutation / genetics. Neoplasm Metastasis. Neoplasm Staging. Neoplastic Stem Cells / pathology

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  • (PMID = 16935776.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 84
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4. Ocaña A, Hortobagyi GN, Esteva FJ: Concomitant versus sequential chemotherapy in the treatment of early-stage and metastatic breast cancer. Clin Breast Cancer; 2006 Feb;6(6):495-504
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  • [Title] Concomitant versus sequential chemotherapy in the treatment of early-stage and metastatic breast cancer.
  • Breast cancer is one of the most common malignancies in the Western world.
  • Chemotherapy improves disease-free survival (DFS) and overall survival (OS) rates in women with early-stage breast cancer.
  • In metastatic breast cancer, cytotoxic chemotherapy is the treatment of choice for patients with hormone receptor-negative tumors or rapidly progressive disease, regardless of hormone receptor status.
  • The combination of chemotherapy and trastuzumab improves DFS and OS rates in patients with HER2-overexpressing metastatic breast cancer.
  • In patients with HER2-negative tumors, the choice of single-agent sequential versus combination chemotherapy should be individualized.
  • Sequential chemotherapy can produce OS rates similar to those of combination regimens and avoids the overlapping toxic effects of combination chemotherapy.
  • However, response rates are generally higher and time to progression is longer with combination chemotherapy.
  • At present, no predictive markers of response to chemotherapy are clinically useful in making treatment decisions for individual patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology
  • [MeSH-minor] Disease-Free Survival. Drug Administration Schedule. Female. Humans. Neoadjuvant Therapy. Neoplasm Staging. Patient Care Planning. Receptor, ErbB-2 / biosynthesis


5. Ohno S, Mitsuyama S, Tamura K, Nishimura R, Tanaka M, Hamada Y, Kuroki S, Kyushu Breast Cancer Study Group: Dosage of capecitabine and cyclophosphamide combination therapy in patients with metastatic breast cancer. Anticancer Res; 2007 Mar-Apr;27(2):1009-13
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  • [Title] Dosage of capecitabine and cyclophosphamide combination therapy in patients with metastatic breast cancer.
  • BACKGROUND: Capecitabine is a highly effective and well-tolerated treatment for metastatic breast cancer (MBC) and extends survival when combined with docetaxel.
  • Capecitabine and cyclophosphamide are orally administered and have preclinical synergy and non-overlapping toxicities.
  • RESULTS: Among the ten patients receiving capecitabine/cyclophosphamide 829/33 mg/m2 bid on days 1 to 14, two experienced dose-limiting toxicities (DLT, treatment delay > 1 week due to grade 2 leukopenia).
  • Because neither patient developed further grade > 1 toxicity and none of the patients experienced grade 3/4 toxicities or further DLTs, this dose level is the recommended regimen, producing partial responses in two of five evaluable patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Breast Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Adult. Aged. Capecitabine. Cyclophosphamide / administration & dosage. Cyclophosphamide / adverse effects. Deoxycytidine / administration & dosage. Deoxycytidine / adverse effects. Deoxycytidine / analogs & derivatives. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Synergism. Fluorouracil / administration & dosage. Fluorouracil / adverse effects. Fluorouracil / analogs & derivatives. Humans. Middle Aged. Neoplasm Metastasis

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  • (PMID = 17465235.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; 8N3DW7272P / Cyclophosphamide; U3P01618RT / Fluorouracil
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6. Kim SH, Castro F, Gonzalez D, Maciag PC, Paterson Y, Gravekamp C: Mage-b vaccine delivered by recombinant Listeria monocytogenes is highly effective against breast cancer metastases. Br J Cancer; 2008 Sep 2;99(5):741-9
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  • [Title] Mage-b vaccine delivered by recombinant Listeria monocytogenes is highly effective against breast cancer metastases.
  • New therapies are needed that target breast cancer metastases.
  • In previous studies, we have shown that vaccination with pcDNA3.1-Mage-b DNA vaccine is effective against breast cancer metastases.
  • Three overlapping fragments of Mage-b as well as the complete protein-encoding region of Mage-b have been expressed as a fusion protein with a truncated non-cytolytic form of listeriolysin O (LLO) in recombinant LM.
  • These different Mage-b vaccine strains were preventively tested for their efficacy against breast cancer metastases in a syngeneic mouse tumour model 4T1.
  • The LM-LLO-Mage-b/2nd, expressing position 311-660 of the cDNA of Mage-b, was the most effective vaccine strain against metastases in the 4T1 mouse breast tumour model.

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  • [Cites] Genomics. 1999 Jan 15;55(2):176-84 [9933564.001]
  • [Cites] Clin Exp Metastasis. 1999 Mar;17(2):163-70 [10411109.001]
  • [Cites] Cancer Immun. 2004 Nov 3;4:12 [15521719.001]
  • [Cites] J Exp Med. 2005 Jan 17;201(2):249-57 [15657294.001]
  • [Cites] Mol Cell Proteomics. 2005 Apr;4(4):492-522 [15695426.001]
  • [Cites] Int J Epidemiol. 2005 Apr;34(2):405-12 [15737977.001]
  • [Cites] Breast Cancer Res Treat. 2005 May;91(1):19-28 [15868428.001]
  • [Cites] J Immunol. 2005 Sep 15;175(6):3663-73 [16148111.001]
  • [Cites] Int J Cancer. 2005 Nov 20;117(4):596-604 [15945101.001]
  • [Cites] Curr Opin Mol Ther. 2005 Oct;7(5):454-60 [16248280.001]
  • [Cites] J Clin Oncol. 2005 Dec 10;23(35):9008-21 [16061912.001]
  • [Cites] J Immunother. 2006 May-Jun;29(3):233-40 [16699366.001]
  • [Cites] J Immunol. 2007 Apr 1;178(7):4411-6 [17371998.001]
  • [Cites] Exp Gerontol. 2007 May;42(5):441-50 [17197144.001]
  • [Cites] J Immunol. 2007 Aug 15;179(4):2457-66 [17675507.001]
  • [Cites] J Immunol. 2007 Oct 1;179(7):4685-93 [17878367.001]
  • [Cites] J Immunol. 2007 Oct 15;179(8):4969-78 [17911581.001]
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9954-62 [17942928.001]
  • [Cites] Cancer Immunol Immunother. 2008 Jul;57(7):1067-77 [18094967.001]
  • [Cites] Oral Oncol. 2008 Sep;44(9):870-7 [18221909.001]
  • [Cites] Cancer Res. 1999 Oct 15;59(20):5264-9 [10537307.001]
  • [Cites] J Exp Med. 1999 Dec 6;190(11):1669-78 [10587357.001]
  • [Cites] Zhonghua Zhong Liu Za Zhi. 1998 Jul;20(4):305-7 [10920992.001]
  • [Cites] Cancer Lett. 2001 Aug 10;169(1):87-95 [11410329.001]
  • [Cites] Clin Microbiol Rev. 2001 Jul;14(3):584-640 [11432815.001]
  • [Cites] J Immunol. 2001 Dec 1;167(11):6471-9 [11714814.001]
  • [Cites] Drugs Aging. 2001;18(10):761-72 [11735623.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8851-8 [11751408.001]
  • [Cites] J Immunol Methods. 2002 Aug 1;266(1-2):79-86 [12133624.001]
  • [Cites] CMAJ. 2002 Jul 23;167(2):154-5 [12160123.001]
  • [Cites] Blood. 2002 Sep 1;100(5):1728-33 [12176894.001]
  • [Cites] J Immunol. 2002 Sep 1;169(5):2756-61 [12193750.001]
  • [Cites] Drugs Aging. 2002;19(8):605-22 [12207554.001]
  • [Cites] Eur J Cancer. 2003 Jan;39(1):70-7 [12504661.001]
  • [Cites] Nat Biotechnol. 2003 Sep;21(9):1088-92 [12910245.001]
  • [Cites] J Immunol. 2003 Nov 1;171(9):4792-800 [14568957.001]
  • [Cites] Nat Rev Cancer. 2003 Dec;3(12):895-902 [14737120.001]
  • [Cites] Exp Biol Med (Maywood). 2004 Jul;229(7):665-75 [15229361.001]
  • [Cites] J Immunol. 2004 Sep 15;173(6):3844-54 [15356132.001]
  • [Cites] Cancer Res. 1992 Mar 15;52(6):1399-405 [1540948.001]
  • [Cites] Br J Cancer. 1992 May;65(5):641-8 [1586590.001]
  • [Cites] Science. 1993 Apr 23;260(5107):547-9 [8097338.001]
  • [Cites] Genomics. 1995 Jul 1;28(1):74-83 [7590750.001]
  • (PMID = 18728665.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NIA NIH HHS / AG / R01 AG023096; United States / NIA NIH HHS / AG / 1R01 AG023096-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / DNA Primers; 0 / Mageb1 protein, mouse; 0 / Mageb2 protein, mouse; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2528142
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7. Maisano R, Caristi N, Mare M, Mafodda A, Carboni R, Montalto E, Iorfida M, Nardi M: Mitomycin C and capecitabine combination (MiXe) in heavily pretreated metastatic breast cancer patients. A dose-finding study. Anticancer Res; 2005 Nov-Dec;25(6C):4513-7
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  • [Title] Mitomycin C and capecitabine combination (MiXe) in heavily pretreated metastatic breast cancer patients. A dose-finding study.
  • BACKGROUND: No standard chemotherapy has been defined for metastatic breast cancer patients pretreated with anthracyclines and taxanes.
  • In preclinical studies, mitomycin C (MMC) and capecitabine showed a synergistic effect by up-regulation of thymidine phosphorylase, and both drugs were active against breast cancer with a lack of overlapping toxicity, making their combination a well-tolerated regimen.
  • RESULTS: Twenty-one patients were enrolled, with metastatic breast cancer pretreated at least with anthracyclines and taxanes (3 at dose level I, 15 at dose level II, 3 at dose level III).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Breast Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Capecitabine. Deoxycytidine / administration & dosage. Deoxycytidine / adverse effects. Deoxycytidine / analogs & derivatives. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Fluorouracil / analogs & derivatives. Humans. Middle Aged. Mitomycin / administration & dosage. Mitomycin / adverse effects. Neoplasm Metastasis

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  • (PMID = 16334135.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 50SG953SK6 / Mitomycin; 6804DJ8Z9U / Capecitabine; U3P01618RT / Fluorouracil
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8. Addeo R, Faiola V, Guarrasi R, Montella L, Vincenzi B, Capasso E, Cennamo G, Rotundo MS, Tagliaferri P, Caraglia M, Del Prete S: Liposomal pegylated doxorubicin plus vinorelbine combination as first-line chemotherapy for metastatic breast cancer in elderly women > or = 65 years of age. Cancer Chemother Pharmacol; 2008 Jul;62(2):285-92
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  • [Title] Liposomal pegylated doxorubicin plus vinorelbine combination as first-line chemotherapy for metastatic breast cancer in elderly women > or = 65 years of age.
  • PURPOSE: No standard chemotherapy has been so far definitely settled for elderly patients with metastatic breast cancer (MBC).
  • In order to identify a regimen with acceptable efficacy and low burden of non-overlapping toxic effects, a combination consisting of liposomal pegilated doxorubicin (PLD) with alternating oral and intravenous vinorelbine (NVB) has been investigated in a phase II study.
  • Median overall survival time was 13 months and the median time to progression 8 months.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Disease-Free Survival. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Doxorubicin / analogs & derivatives. Doxorubicin / therapeutic use. Drug Administration Schedule. Female. Humans. Injections, Intravenous. Kaplan-Meier Estimate. Liposomes. Neoplasm Metastasis. Polyethylene Glycols / administration & dosage. Polyethylene Glycols / adverse effects. Polyethylene Glycols / therapeutic use. Prospective Studies. Quality of Life. Vinblastine / administration & dosage. Vinblastine / adverse effects. Vinblastine / analogs & derivatives. Vinblastine / therapeutic use

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  • (PMID = 17922275.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Liposomes; 0 / liposomal doxorubicin; 30IQX730WE / Polyethylene Glycols; 5V9KLZ54CY / Vinblastine; 80168379AG / Doxorubicin; Q6C979R91Y / vinorelbine
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9. Specht K, Harbeck N, Smida J, Annecke K, Reich U, Naehrig J, Langer R, Mages J, Busch R, Kruse E, Klein-Hitpass L, Schmitt M, Kiechle M, Hoefler H: Expression profiling identifies genes that predict recurrence of breast cancer after adjuvant CMF-based chemotherapy. Breast Cancer Res Treat; 2009 Nov;118(1):45-56
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  • [Title] Expression profiling identifies genes that predict recurrence of breast cancer after adjuvant CMF-based chemotherapy.
  • Cyclophosphamide, methotrexate and 5-fluorouracile (CMF)-based chemotherapy for adjuvant treatment of breast cancer reduces the risk of relapse.
  • Using Affymetrix U133A GeneChips, RNA samples from 19 patients with primary breast cancer who had been uniformly treated with adjuvant CMF chemotherapy were analyzed.
  • Applying different algorithms to evaluate our microarray data, we identified two gene expression signatures of 21 and 12 genes containing eight overlapping genes, that predict recurrence in 19 cases with high accuracy (94%).
  • Quantitative RT-PCR demonstrated that six genes from the combined signatures (CXCL9, ITSN2, GNAI2, H2AFX, INDO, and MGC10986) were significantly differentially expressed in the recurrence versus the non-recurrence group of the 19 cases and the independent breast cancer patient cohort (n = 51) treated with CMF.
  • Our data highlight the feasibility of a prognostic assay that is applicable to therapeutic decision-making for breast cancer.
  • Whether the biomarker profile is chemotherapy-specific or whether it is a more general indicator of bad prognosis of breast cancer patients remains to be explored.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / genetics. Carcinoma / genetics. Chemotherapy, Adjuvant. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / genetics
  • [MeSH-minor] Adaptor Proteins, Vesicular Transport / biosynthesis. Adaptor Proteins, Vesicular Transport / genetics. Adult. Aged. Algorithms. Chemokine CXCL9 / biosynthesis. Chemokine CXCL9 / genetics. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Disease-Free Survival. Feasibility Studies. Female. Fluorouracil / administration & dosage. Follow-Up Studies. GTP-Binding Protein alpha Subunit, Gi2 / biosynthesis. GTP-Binding Protein alpha Subunit, Gi2 / genetics. Histones / biosynthesis. Histones / genetics. Humans. Indoleamine-Pyrrole 2,3,-Dioxygenase / biosynthesis. Indoleamine-Pyrrole 2,3,-Dioxygenase / genetics. Mastectomy. Methotrexate / administration & dosage. Middle Aged. Oligonucleotide Array Sequence Analysis. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Recurrence

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  • (PMID = 18925433.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Adaptor Proteins, Vesicular Transport; 0 / CXCL9 protein, human; 0 / Chemokine CXCL9; 0 / H2AFX protein, human; 0 / Histones; 0 / ITSN2 protein, human; 0 / Indoleamine-Pyrrole 2,3,-Dioxygenase; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 8N3DW7272P / Cyclophosphamide; EC 3.6.5.1 / GNAI2 protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunit, Gi2; U3P01618RT / Fluorouracil; YL5FZ2Y5U1 / Methotrexate; CMF regimen
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10. Yardley DA: Gemcitabine plus paclitaxel in breast cancer. Semin Oncol; 2005 Aug;32(4 Suppl 6):S14-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gemcitabine plus paclitaxel in breast cancer.
  • The combining of gemcitabine and paclitaxel in chemotherapy for metastatic breast cancer is supported by sound evidence of single-agent activity, beneficial pharmacologic interaction, and largely non-overlapping toxicities.
  • In phase II studies in both heavily pretreated patients and chemotherapy-naive patients, the combination has produced remarkably high rates of response and has been exceptionally well tolerated.
  • A recent phase III trial of the combination as first-line treatment for metastatic breast cancer showed significant improvements in objective response, time to disease progression, and overall survival compared with paclitaxel alone, leading to the approval of gemcitabine in combination with paclitaxel for this indication.
  • Continued investigation of the role of gemcitabine/taxane combinations in early and advanced breast cancer is ongoing, including additional investigation of biweekly schedules and use of the combination as part of triplet therapy with trastuzumab.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Disease-Free Survival. Drug Administration Schedule. Female. Humans. Neoplasm Metastasis. Paclitaxel / administration & dosage. Survival Rate

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  • (PMID = 16143163.001).
  • [ISSN] 0093-7754
  • [Journal-full-title] Seminars in oncology
  • [ISO-abbreviation] Semin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel
  • [Number-of-references] 40
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11. Huang L, Johnson KA, Mariotto AB, Dignam JJ, Feuer EJ: Population-based survival-cure analysis of ER-negative breast cancer. Breast Cancer Res Treat; 2010 Aug;123(1):257-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Population-based survival-cure analysis of ER-negative breast cancer.
  • This study investigated the trends over time in age and stage specific population-based survival of estrogen receptor negative (ER-) breast cancer patients by examining the fraction of cured patients and the median survival time for uncured patients.
  • Survival trends were compared with adjuvant chemotherapy data available from an overlapping patterns-of-care study.
  • Increases in cure fraction correspond with increases in the use of adjuvant chemotherapy, particularly for the oldest age group.
  • In this article, for the first time, we estimate the cure fraction for ER- patients.
  • We notice that at age >o5r=70, the accelerated increase in cure fraction from 1992 to 1998 for women with stage II N+ compared with stage III suggests a selective benefit for chemotherapy in the lower stage group.
  • [MeSH-major] Breast Neoplasms / mortality
  • [MeSH-minor] Age Factors. Aged. Antineoplastic Agents / therapeutic use. Chemotherapy, Adjuvant. Female. Humans. Kaplan-Meier Estimate. Middle Aged. Neoplasm Staging. Receptors, Estrogen / biosynthesis. Receptors, Estrogen / genetics. SEER Program. Treatment Outcome

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  • (PMID = 20130982.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / NCI-U10-CA-69651; United States / PHS HHS / / NCI-U10-NCIU10-
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Receptors, Estrogen
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12. Ferrazzi E, Stievano L: Gemcitabine: monochemotherapy of breast cancer. Ann Oncol; 2006 May;17 Suppl 5:v169-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gemcitabine: monochemotherapy of breast cancer.
  • BACKGROUND: Gemcitabine is a nucleoside analogue with proven activity in advanced and metastatic breast cancer.
  • Its unique mechanism of action along with not overlapping toxicity is particularly useful both in combination treatment with other active drugs and a sequential therapy in the palliative setting.
  • RESULTS AND CONCLUSIONS: Despite some conflicting results in some trials, gemcitabine confirmed to be a useful drug to treat this condition.

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  • (PMID = 16807449.001).
  • [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] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antimetabolites, Antineoplastic; 0 / Taxoids; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Number-of-references] 16
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13. Zielinski CC: Gemcitabine/anthracycline combinations in metastatic breast cancer. Clin Breast Cancer; 2002 May;3 Suppl 1:30-3
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  • [Title] Gemcitabine/anthracycline combinations in metastatic breast cancer.
  • Gemcitabine has demonstrated single-agent efficacy in the treatment of advanced breast cancer, with response rates of up to 42%.
  • The agent is well tolerated, with relatively mild side effects, and has limited overlapping toxicities with other drugs used in combination chemotherapy for breast cancer.
  • It is, therefore, a good candidate for inclusion in multidrug regimens for the treatment of this disease.
  • This article reviews results of gemcitabine/anthracycline-containing double- and triple-drug combinations used to treat patients with early-stage and advanced breast cancer.
  • Results from phase I and II trials were promising, with good tolerability and overall response rates ranging from 33%-89% in advanced disease and up to 95% in the neoadjuvant treatment of early-stage disease.
  • A phase III trial is currently comparing gemcitabine/epirubicin/paclitaxel and 5-fluorouracil/epirubicin/cyclophosphamide in patients with advanced breast cancer.
  • Preliminary toxicity data on 78 patients show that both regimens were well tolerated, with similar incidences of treatment-related effects.
  • Additional comparative studies of gemcitabine-containing drug regimens in breast cancer are warranted.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Deoxycytidine / analogs & derivatives
  • [MeSH-minor] Anthracyclines / administration & dosage. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Cyclophosphamide / administration & dosage. Epirubicin / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Neoplasm Metastasis. Paclitaxel / administration & dosage. Taxoids. Treatment Outcome

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  • (PMID = 12057043.001).
  • [ISSN] 1526-8209
  • [Journal-full-title] Clinical breast cancer
  • [ISO-abbreviation] Clin. Breast Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Taxoids; 0W860991D6 / Deoxycytidine; 3Z8479ZZ5X / Epirubicin; 8N3DW7272P / Cyclophosphamide; B76N6SBZ8R / gemcitabine; P88XT4IS4D / Paclitaxel; U3P01618RT / Fluorouracil; FEC protocol; GET protocol
  • [Number-of-references] 20
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14. Waterhouse DN, Gelmon KA, Klasa R, Chi K, Huntsman D, Ramsay E, Wasan E, Edwards L, Tucker C, Zastre J, Wang YZ, Yapp D, Dragowska W, Dunn S, Dedhar S, Bally MB: Development and assessment of conventional and targeted drug combinations for use in the treatment of aggressive breast cancers. Curr Cancer Drug Targets; 2006 Sep;6(6):455-89
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Development and assessment of conventional and targeted drug combinations for use in the treatment of aggressive breast cancers.
  • Combination chemotherapy has been at the forefront of cancer treatment for over 40 years.
  • However, the rationale for selecting drug combinations and the process used to demonstrate clinical effectiveness has primarily followed trial and error methodology.
  • Typically, the selection and assessment of combined drug therapies has been based on the effectiveness of each agent as monotherapy in treating the neoplasm and avoiding overlapping toxicities, followed by clinical trials to establish dose scheduling, toxicity, and efficacy.
  • Unfortunately, this scheme is inefficient in terms of the time required to complete and revise these clinical trials based on the outcome to optimize the drug combination.
  • A more rational approach for the development of combination oncology products should consider (i) in vitro assays for assessing therapeutic effects of drug combinations (antagonistic, additive or synergistic interactions) when added simultaneously;.
  • (iii) the importance of understanding pharmacokinetic and biodistribution parameters when using drug combinations;.
  • Therefore, the goal of this article is to provide a road map for the preclinical development of drug combination products that will have improved therapeutic activity and a high likelihood of providing beneficial therapeutic outcomes in patients with aggressive cancers with a specific focus on patients with breast cancer.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Drug Delivery Systems / methods
  • [MeSH-minor] Animals. Drug Therapy, Combination. Humans. Neoplasm Invasiveness

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  • [ErratumIn] Curr Cancer Drug Targets. 2006 Dec;6(8):753. Zhang, YZ [corrected to Wang, YZ]
  • (PMID = 17017873.001).
  • [ISSN] 1873-5576
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 296
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15. Hess D, Thürlimann B, Pagani O, Aebi S, Rauch D, Ballabeni P, Rufener B, Castiglione-Gertsch M, Goldhirsch A, Swiss Group of Clinical Cancer Research (SAKK): Capecitabine and vinorelbine in elderly patients (> or =65 years) with metastatic breast cancer: a phase I trial (SAKK 25/99). Ann Oncol; 2004 Dec;15(12):1760-5
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  • [Title] Capecitabine and vinorelbine in elderly patients (> or =65 years) with metastatic breast cancer: a phase I trial (SAKK 25/99).
  • BACKGROUND: Few chemotherapy regimens are suitable for the treatment of elderly patients with advanced breast cancer.
  • With the aim of finding a regimen with a low burden of subjective non-overlapping toxic effects, vinorelbine and capecitabine were chosen to be investigated in a phase I dose-finding study.
  • PATIENTS AND METHODS: Thirty-six patients with advanced breast cancer were stratified for the presence of bone and non-bone involvement and treated at four dose levels from capecitabine 800 mg/m2 orally days 1-14 and vinorelbine 20 mg/m2 intravenously days 1 and 8, to capecitabine 1250 mg/m2 orally days 1-14 and vinorelbine 25 mg/m2 intravenously days 1 and 8, for a maximum of six cycles.
  • None of the patients had received prior chemotherapy for metastatic/advanced disease.
  • For patients without bone involvement the overall response rate was 48% and the time to progression (TTP) was 4.5 months [95% confidence interval (CI) 3.3-6.9].
  • CONCLUSIONS: This regimen of capecitabine and vinorelbine is well tolerated and effective in elderly patients with metastatic breast cancer.

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  • (PMID = 15550580.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 5V9KLZ54CY / Vinblastine; 6804DJ8Z9U / Capecitabine; Q6C979R91Y / vinorelbine; U3P01618RT / Fluorouracil
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16. Nabholtz JM: Docetaxel-anthracycline combinations in metastatic breast cancer. Breast Cancer Res Treat; 2003;79 Suppl 1:S3-9
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  • [Title] Docetaxel-anthracycline combinations in metastatic breast cancer.
  • The taxanes and anthracyclines have emerged as the most active agents for treating women with advanced breast cancer.
  • As such, investigation of the two drug classes in combination regimens has been eagerly pursued.
  • The rationale for combining docetaxel with an anthracycline includes high clinical activity of each individual agent, lack of complete clinical cross resistance, and non-overlapping toxicity profiles.
  • Phase II trials of the docetaxel combinations with either doxorubicin or epirubicin showed high activity, with acceptable tolerability in patients with metastatic breast cancer.
  • Consequently, three randomized trials have compared docetaxel-anthracycline-based regimens with standard anthracycline-based polychemotherapies as first-line therapy for women with advanced breast cancer.
  • Therefore, docetaxel-anthracycline combinations represent a validated option in first-line treatment for women with advanced breast cancer, and are further evaluated as adjuvant treatment for early stage breast cancer, with already promising prospects and the potential to change the natural history of breast cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Paclitaxel / analogs & derivatives. Taxoids
  • [MeSH-minor] Antibiotics, Antineoplastic / administration & dosage. Clinical Trials, Phase II as Topic. Disease-Free Survival. Doxorubicin / administration & dosage. Epirubicin / administration & dosage. Female. Humans. Neoplasm Metastasis. Randomized Controlled Trials as Topic

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  • (PMID = 12868800.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Taxoids; 15H5577CQD / docetaxel; 3Z8479ZZ5X / Epirubicin; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel
  • [Number-of-references] 27
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17. Yang DC, Jiang X, Elliott RL, Head JF: Antisense ferritin oligonucleotides inhibit growth and induce apoptosis in human breast carcinoma cells. Anticancer Res; 2002 May-Jun;22(3):1513-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antisense ferritin oligonucleotides inhibit growth and induce apoptosis in human breast carcinoma cells.
  • MATERIALS AND METHODS: In this study four pairs of antisense oligodeoxynucleotides (ODNs) were synthesized: FerH-A1 and FerL-A1 were complementary to the 24-base pair sequence overlapping the starting codons of the FerH and FerL genes, respectively, but the sequences of FerH-A2 and FerL-A2 only covered the coding sequences of the ferritin genes.
  • RESULTS: Treatment with FerH-S1, FerH-A1, FerH-S2, FerH-A2, FerL-S1, FerL-A1, FerL-S2 and FerL-A2 at 40 microM, 25 microM, 30 microM, 17 microM, 45 microM, 18 microM, 40 microM and 26 microM, respectively, for 72 hours resulted in 50% inhibition of DNA synthesis (IC50) in MCF-7 breast carcinoma cells, as measured by [3H]-thymidine incorporation.
  • Further, the antisense ferritin ODNs promote programmed cell death with low ratios of Bcl-2 to Bax mRNA and protein expression providing evidence that antisense ferritin ODNs specifically inhibit MCF-7 breast carcinoma cell growth through increased apoptosis.
  • Finally, since the IC50 concentrations of FerH-A1 and FerH-A2, and FerL-A1 and FerL-A2 are very similar for inhibition of DNA synthesis and gene expression in human breast carcinoma MCF-7 cells, it does not seem necessary for the antisense ODNs to overlap the starting codons of ferritin gene to maximize inhibition.
  • [MeSH-major] Breast Neoplasms / drug therapy. Ferritins / genetics. Oligodeoxyribonucleotides, Antisense / pharmacology
  • [MeSH-minor] Apoptosis / drug effects. Cell Division / drug effects. DNA, Neoplasm / biosynthesis. Growth Inhibitors / chemical synthesis. Growth Inhibitors / genetics. Growth Inhibitors / pharmacology. Humans. Iron / metabolism. RNA, Messenger / antagonists & inhibitors. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Tumor Cells, Cultured

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  • (PMID = 12168831.001).
  • [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 / DNA, Neoplasm; 0 / Growth Inhibitors; 0 / Oligodeoxyribonucleotides, Antisense; 0 / RNA, Messenger; 9007-73-2 / Ferritins; E1UOL152H7 / Iron
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18. Shuhendler AJ, Cheung RY, Manias J, Connor A, Rauth AM, Wu XY: A novel doxorubicin-mitomycin C co-encapsulated nanoparticle formulation exhibits anti-cancer synergy in multidrug resistant human breast cancer cells. Breast Cancer Res Treat; 2010 Jan;119(2):255-69
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel doxorubicin-mitomycin C co-encapsulated nanoparticle formulation exhibits anti-cancer synergy in multidrug resistant human breast cancer cells.
  • Anthracycline-containing treatment regimens are currently the most widely employed regimens for the management of breast cancer.
  • These drug combinations are often designed based on non-cross resistance and minimal overlapping toxicity rather than drug synergism.
  • Moreover, aggressive doses are normally used in chemotherapy to achieve a greater therapeutic benefit at the cost of more acute and long-term toxic effects.
  • To increase chemotherapeutic efficacy while decreasing toxic effects, rational design of drug synergy-based regimens is needed.
  • Our previous work showed a synergistic effect of doxorubicin (DOX) and mitomycin C (MMC) on murine breast cancer cells in vitro and improved efficacy and reduced systemic toxicity of DOX-loaded solid polymer-lipid hybrid nanoparticles (PLN) in animal models of breast cancer.
  • Herein we have demonstrated true anticancer synergy of concurrently applied DOX and MMC, and have rationally designed PLN to effectively deliver this combination to multidrug resistant (MDR) MDA435/LCC6 human breast cancer cells.
  • DOX-MMC co-loaded PLN were effective in killing MDR cells at 20-30-fold lower doses than the free drugs.
  • Importantly, co-encapsulation of dual agents into a nanoparticle formulation was much more effective than concurrent application of single agent-containing PLN, demonstrating the requirement of simultaneous uptake of both drugs by the same cells to enhance the drug synergy.
  • The rationally designed combination chemotherapeutic PLN can overcome multidrug resistance at a significantly lower dose than free drugs, exhibiting the potential to enhance chemotherapy and reduce the therapeutic limitations imposed by systemic toxicity.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Breast Neoplasms / pathology. Drug Resistance, Multiple / drug effects. Drug Resistance, Neoplasm / drug effects. Nanoparticles
  • [MeSH-minor] Apoptosis / drug effects. Biological Transport. Cell Line, Tumor. Cell Survival / drug effects. Chemistry, Pharmaceutical. DNA Damage. Dose-Response Relationship, Drug. Doxorubicin / pharmacology. Drug Compounding. Drug Synergism. Female. Humans. Kinetics. Mitomycin / pharmacology. Solubility. Time Factors

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  • (PMID = 19221875.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Grant] Canada / Canadian Institutes of Health Research / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 80168379AG / Doxorubicin
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19. Bentz EK, Pils D, Bilban M, Kaufmann U, Hefler LA, Reinthaller A, Singer CF, Huber JC, Horvat R, Tempfer CB: Gene expression signatures of breast tissue before and after cross-sex hormone therapy in female-to-male transsexuals. Fertil Steril; 2010 Dec;94(7):2688-96
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  • [Title] Gene expression signatures of breast tissue before and after cross-sex hormone therapy in female-to-male transsexuals.
  • OBJECTIVE: To evaluate gene expression signatures of breast tissue in female-to-male (FtM) transsexuals under cross-sex hormone therapy (HT).
  • INTERVENTION(S): Breast tissue biopsy before and after 2 years of intramuscular testosterone undecanoate (1,000 mg every 12 wk) and oral lynestrenole (5 mg daily), and gene signature analysis by global gene expression array covering 28,869 genes.
  • We identified eight breast cancer-associated gene expression signatures significantly overlapping with differentially regulated probe sets after cross-sex HT.
  • CONCLUSION(S): Cross-sex HT in FtM transsexuals leads to the up-regulation and down-regulation of 243 and 2,007 distinct genes, respectively, and is associated with breast cancer-related gene expression signatures.
  • [MeSH-major] Breast / metabolism. Gene Expression Profiling. Gonadal Steroid Hormones / therapeutic use. Transsexualism / drug therapy. Transsexualism / genetics
  • [MeSH-minor] Administration, Oral. Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Breast Neoplasms / genetics. Carcinoma / genetics. Carcinoma / metabolism. Chemotaxis, Leukocyte / physiology. Female. Gene Expression / drug effects. Genes, Neoplasm. Humans. Injections, Intramuscular. Lynestrenol / administration & dosage. Lynestrenol / pharmacology. Male. Microarray Analysis. Sex Reassignment Procedures. Testosterone / administration & dosage. Testosterone / analogs & derivatives. Testosterone / pharmacology. Validation Studies as Topic

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  • [Copyright] Copyright © 2010 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20537635.001).
  • [ISSN] 1556-5653
  • [Journal-full-title] Fertility and sterility
  • [ISO-abbreviation] Fertil. Steril.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Gonadal Steroid Hormones; 3XMK78S47O / Testosterone; H16A5VCT9C / testosterone undecanoate; N2Z8ALG4U5 / Lynestrenol
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20. Perez EA: Gemcitabine and platinum combinations in patients with breast cancer previously treated with anthracyclines and/or taxanes. Clin Breast Cancer; 2004 Jan;4 Suppl 3:S113-6
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  • [Title] Gemcitabine and platinum combinations in patients with breast cancer previously treated with anthracyclines and/or taxanes.
  • As anthracycline-based regimens have become a standard treatment and are frequently used in the adjuvant therapy of breast cancer, the number of anthracycline-resistant cancers has begun to increase.
  • Taxanes have also become more commonly used in the first-line metastatic and adjuvant setting, producing a need for new treatment options that are not cross-resistant with anthracyclines or taxanes and that have a relative non-overlapping toxicity profile with these agents.
  • The combination of gemcitabine/cisplatin has been shown to have synergistic cytotoxic activity in vitro in breast cancer cell lines.
  • In addition, several phase II trials have suggested that this combination is feasible and active in patients who have received prior anthracycline and/or taxane therapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Deoxycytidine / analogs & derivatives
  • [MeSH-minor] Anthracyclines / therapeutic use. Bridged-Ring Compounds / therapeutic use. Carboplatin / administration & dosage. Cisplatin / administration & dosage. Clinical Trials as Topic. Female. Humans. Neoplasm Metastasis. Taxoids / therapeutic use

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  • (PMID = 14754468.001).
  • [ISSN] 1526-8209
  • [Journal-full-title] Clinical breast cancer
  • [ISO-abbreviation] Clin. Breast Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Bridged-Ring Compounds; 0 / Taxoids; 0W860991D6 / Deoxycytidine; 1605-68-1 / taxane; B76N6SBZ8R / gemcitabine; BG3F62OND5 / Carboplatin; Q20Q21Q62J / Cisplatin
  • [Number-of-references] 21
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21. Umar A, Kang H, Timmermans AM, Look MP, Meijer-van Gelder ME, den Bakker MA, Jaitly N, Martens JW, Luider TM, Foekens JA, Pasa-Tolić L: Identification of a putative protein profile associated with tamoxifen therapy resistance in breast cancer. Mol Cell Proteomics; 2009 Jun;8(6):1278-94
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  • [Title] Identification of a putative protein profile associated with tamoxifen therapy resistance in breast cancer.
  • Tamoxifen resistance is a major cause of death in patients with recurrent breast cancer.
  • Current clinical factors can correctly predict therapy response in only half of the treated patients.
  • Identification of proteins that are associated with tamoxifen resistance is a first step toward better response prediction and tailored treatment of patients.
  • In the present study we intended to identify putative protein biomarkers indicative of tamoxifen therapy resistance in breast cancer using nano-LC coupled with FTICR MS.
  • Comparative proteome analysis was performed on approximately 5,500 pooled tumor cells (corresponding to approximately 550 ng of protein lysate/analysis) obtained through laser capture microdissection (LCM) from two independently processed data sets (n = 24 and n = 27) containing both tamoxifen therapy-sensitive and therapy-resistant tumors.
  • Peptides and proteins were identified by matching mass and elution time of newly acquired LC-MS features to information in previously generated accurate mass and time tag reference databases.
  • 1,713 overlapping proteins between the two data sets were used for further analysis.
  • The presence and relative abundance for 47 differentially abundant proteins were verified by targeted nano-LC-MS/MS in a selection of unpooled, non-microdissected discovery set tumor tissue extracts.
  • ENPP1, EIF3E, and GNB4 were significantly associated with progression-free survival upon tamoxifen treatment for recurrent disease.
  • Differential abundance of our top discriminating protein, extracellular matrix metalloproteinase inducer, was validated by tissue microarray in an independent patient cohort (n = 156).
  • Extracellular matrix metalloproteinase inducer levels were higher in therapy-resistant tumors and significantly associated with an earlier tumor progression following first line tamoxifen treatment (hazard ratio, 1.87; 95% confidence interval, 1.25-2.80; p = 0.002).
  • In summary, comparative proteomics performed on laser capture microdissection-derived breast tumor cells using nano-LC-FTICR MS technology revealed a set of putative biomarkers associated with tamoxifen therapy resistance in recurrent breast cancer.

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  • [Cites] J Proteome Res. 2005 Nov-Dec;4(6):2397-403 [16335993.001]
  • [Cites] Histopathology. 1991 Nov;19(5):403-10 [1757079.001]
  • [Cites] Oncogene. 2006 Mar 2;25(9):1413-9 [16261164.001]
  • [Cites] Proteomics. 2006 Mar;6(6):1989-2002 [16470630.001]
  • [Cites] J Clin Oncol. 2006 Apr 10;24(11):1665-71 [16505412.001]
  • [Cites] Electrophoresis. 2006 May;27(9):1840-52 [16645950.001]
  • [Cites] Proteomics. 2006 May;6(9):2903-15 [16596714.001]
  • [Cites] J Clin Oncol. 2006 May 20;24(15):2261-7 [16636340.001]
  • [Cites] Int J Cancer. 2006 Oct 15;119(8):1800-10 [16721788.001]
  • [Cites] J Proteome Res. 2006 Sep;5(9):2194-206 [16944931.001]
  • [Cites] Rapid Commun Mass Spectrom. 2006;20(20):3039-55 [16986208.001]
  • [Cites] Anal Chem. 2006 Nov 1;78(21):7397-409 [17073405.001]
  • [Cites] Anal Chem. 2006 Nov 15;78(22):7796-801 [17105173.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17384-9 [17090686.001]
  • [Cites] Proteomics. 2006 Nov;6(22):5973-82 [17051647.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):9-15 [17210677.001]
  • [Cites] Proteomics. 2007 Jan;7(2):323-9 [17163580.001]
  • [Cites] Endocr Relat Cancer. 2006 Dec;13 Suppl 1:S15-24 [17259554.001]
  • [Cites] J Biol Chem. 2007 Apr 27;282(17):12707-16 [17324924.001]
  • [Cites] Int J Oncol. 2007 Jun;30(6):1545-51 [17487377.001]
  • [Cites] J Biomed Sci. 2007 May;14(3):395-405 [17385060.001]
  • [Cites] Cancer Sci. 2007 Jul;98(7):1027-34 [17459053.001]
  • [Cites] Curr Opin Clin Nutr Metab Care. 2007 Jul;10(4):403-9 [17563456.001]
  • [Cites] J Am Soc Mass Spectrom. 2007 Jul;18(7):1332-43 [17531500.001]
  • [Cites] Mol Cell Proteomics. 2007 Jul;6(7):1147-57 [17360931.001]
  • [Cites] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4407-14 [17671123.001]
  • [Cites] Bioinformatics. 2007 Aug 1;23(15):2021-3 [17545182.001]
  • [Cites] Breast Cancer Res. 2007;9(4):R42 [17626637.001]
  • [Cites] Oncol Res. 2007;16(11):497-506 [18306929.001]
  • [Cites] Eur J Surg Oncol. 2008 Apr;34(4):357-64 [17566693.001]
  • [Cites] Bioinformatics. 2008 Apr 1;24(7):1021-3 [18304935.001]
  • [Cites] J Proteome Res. 2008 Apr;7(4):1500-7 [18386930.001]
  • [Cites] Breast Cancer Res. 2008;10(2):106 [18430260.001]
  • [Cites] Curr Cancer Drug Targets. 2008 Jun;8(4):243-52 [18537548.001]
  • [Cites] Obesity (Silver Spring). 2008 Jul;16(7):1708-13 [18464750.001]
  • [Cites] Int J Cancer. 2008 Nov 1;123(9):2188-94 [18711698.001]
  • [Cites] J Natl Cancer Inst. 2005 Aug 17;97(16):1180-4 [16106022.001]
  • [Cites] Science. 1996 Nov 8;274(5289):998-1001 [8875945.001]
  • [Cites] Anal Chem. 1999 Aug 1;71(15):2957-64 [10450147.001]
  • [Cites] Biotechniques. 2004 Oct;37(4):621-4, 626-33, 636 passim [15517975.001]
  • [Cites] J Clin Oncol. 2005 Feb 1;23(4):732-40 [15681518.001]
  • [Cites] Lancet. 2005 Feb 19-25;365(9460):671-9 [15721472.001]
  • [Cites] Mol Cancer Res. 2005 May;3(5):287-96 [15886300.001]
  • [Cites] Lancet. 2005 May 14-20;365(9472):1687-717 [15894097.001]
  • [Cites] J Proteome Res. 2005 May-Jun;4(3):674-89 [15952714.001]
  • [Cites] Proteomics. 2005 Jul;5(10):2680-8 [15892168.001]
  • [Cites] Electrophoresis. 2000 Jun;21(11):2235-42 [10892734.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):747-52 [10963602.001]
  • [Cites] Cell Biol Toxicol. 2000;16(4):207-19 [11101003.001]
  • [Cites] Int J Oncol. 2001 Jan;18(1):175-9 [11115556.001]
  • [Cites] Am J Pathol. 2001 Jun;158(6):1921-8 [11395366.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815.001]
  • [Cites] Lancet. 2002 Oct 12;360(9340):1155-62 [12387968.001]
  • [Cites] Anal Chem. 2003 Mar 1;75(5):1039-48 [12641221.001]
  • [Cites] Proteomics. 2003 Jun;3(6):1037-46 [12833528.001]
  • [Cites] Oncogene. 2003 Oct 20;22(47):7316-39 [14576841.001]
  • [Cites] Anal Chem. 2004 Jan 1;76(1):144-54 [14697044.001]
  • [Cites] J Proteome Res. 2004 Jan-Feb;3(1):68-75 [14998165.001]
  • [Cites] Clin Cancer Res. 2004 May 15;10(10):3422-8 [15161697.001]
  • [Cites] J Proteome Res. 2004 May-Jun;3(3):604-12 [15253443.001]
  • [Cites] J Proteome Res. 2004 Sep-Oct;3(5):1063-8 [15473696.001]
  • [Cites] Cancer. 1977 Mar;39(3):1289-94 [912660.001]
  • [Cites] J Investig Dermatol Symp Proc. 2005 Nov;10(2):105-9 [16358817.001]
  • (PMID = 19329653.001).
  • [ISSN] 1535-9484
  • [Journal-full-title] Molecular & cellular proteomics : MCP
  • [ISO-abbreviation] Mol. Cell Proteomics
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / P41 RR018522; United States / NCRR NIH HHS / RR / RR18522
  • [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 / Neoplasm Proteins; 094ZI81Y45 / Tamoxifen; EC 3.4.21.4 / Trypsin
  • [Other-IDs] NLM/ PMC2690491
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22. Chu I, Arnaout A, Loiseau S, Sun J, Seth A, McMahon C, Chun K, Hennessy B, Mills GB, Nawaz Z, Slingerland JM: Src promotes estrogen-dependent estrogen receptor alpha proteolysis in human breast cancer. J Clin Invest; 2007 Aug;117(8):2205-15
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  • [Title] Src promotes estrogen-dependent estrogen receptor alpha proteolysis in human breast cancer.
  • Here we observed variable and overlapping ESR1 mRNA levels in 200 ER alpha-negative and 50 ER alpha-positive primary breast cancers examined, which suggests important posttranscriptional ER alpha regulation.
  • Src and ER alpha levels were inversely correlated in primary breast cancers.
  • ER alpha-negative primary breast cancers and cell lines showed increased Src levels and/or activity compared with ER alpha-positive cancers and cells.
  • Oncogenic Src activation may promote not only proliferation, but also estrogen-activated ER alpha loss in a subset of ER alpha-negative breast cancers, altering prognosis and response to therapy.
  • [MeSH-major] Breast Neoplasms / metabolism. Estrogen Receptor alpha / biosynthesis. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / biosynthesis. Protein Processing, Post-Translational. src-Family Kinases / metabolism
  • [MeSH-minor] Cell Line, Tumor. Enzyme Activation / drug effects. Estrogens / metabolism. Estrogens / pharmacology. Female. Humans. Prognosis. Proteasome Endopeptidase Complex / metabolism. Protein Kinase Inhibitors / pharmacology. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. RNA, Small Interfering / pharmacology. Transcription, Genetic / drug effects. Ubiquitin / metabolism

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  • [Cites] Nature. 2002 Jan 31;415(6871):530-6 [11823860.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Nov 12;99(23):14783-8 [12415108.001]
  • [Cites] Mol Cell. 2003 Mar;11(3):695-707 [12667452.001]
  • [Cites] Endocrinology. 2003 Aug;144(8):3469-76 [12865327.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):2076-81 [14764897.001]
  • [Cites] Mol Endocrinol. 2004 Mar;18(3):493-9 [14673136.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 10;101(32):11599-604 [15289619.001]
  • [Cites] Mol Endocrinol. 2004 Nov;18(11):2603-15 [15284335.001]
  • [Cites] Mol Endocrinol. 2001 Aug;15(8):1344-59 [11463858.001]
  • [Cites] Cancer Res. 2001 Aug 15;61(16):5979-84 [11507038.001]
  • [Cites] Science. 2001 Aug 31;293(5535):1651-3 [11463878.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815.001]
  • [Cites] J Biol Chem. 2001 Sep 21;276(38):35684-92 [11473106.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11462-7 [11562467.001]
  • [Cites] Front Biosci. 2001 Oct 1;6:D1379-91 [11578956.001]
  • [Cites] J Biol Chem. 2001 Oct 5;276(40):36869-72 [11459850.001]
  • [Cites] Biochemistry. 1999 Oct 26;38(43):14146-56 [10571988.001]
  • [Cites] Steroids. 2000 May;65(5):227-51 [10751636.001]
  • [Cites] Mol Cell. 2000 Jun;5(6):939-48 [10911988.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Aug 1;97(16):9042-6 [10908655.001]
  • [Cites] Nature. 2000 Aug 17;406(6797):747-52 [10963602.001]
  • [Cites] Nature. 2000 Sep 28;407(6803):538-41 [11029009.001]
  • [Cites] EMBO J. 2000 Oct 16;19(20):5406-17 [11032808.001]
  • [Cites] Cancer. 2000 Oct 15;89(8):1732-8 [11042568.001]
  • [Cites] Cell. 2000 Dec 8;103(6):843-52 [11136970.001]
  • [Cites] J Steroid Biochem. 1986 Jan;24(1):77-83 [2422449.001]
  • [Cites] J Biol Chem. 1986 Oct 15;261(29):13754-9 [3093483.001]
  • [Cites] Mol Endocrinol. 1988 Sep;2(9):785-91 [2459605.001]
  • [Cites] Br J Cancer. 1988 Nov;58(5):600-5 [2851309.001]
  • [Cites] Cell. 1989 Nov 3;59(3):477-87 [2805068.001]
  • [Cites] J Steroid Biochem Mol Biol. 1990 Dec 20;37(6):811-4 [2285594.001]
  • [Cites] EMBO J. 1992 Mar;11(3):1025-33 [1372244.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 May 15;89(10):4658-62 [1584801.001]
  • [Cites] Oncogene. 1993 Jun;8(6):1501-9 [8502476.001]
  • [Cites] Mol Endocrinol. 1993 Jun;7(6):743-52 [7689695.001]
  • [Cites] J Natl Cancer Inst. 1995 Mar 15;87(6):446-51 [7861463.001]
  • [Cites] J Steroid Biochem Mol Biol. 1995 Feb;52(2):159-71 [7873451.001]
  • [Cites] Mol Endocrinol. 1995 Jan;9(1):24-33 [7539106.001]
  • [Cites] Biochem Biophys Res Commun. 1995 Aug 4;213(1):24-31 [7639742.001]
  • [Cites] Science. 1995 Dec 1;270(5241):1491-4 [7491495.001]
  • [Cites] Breast Cancer Res Treat. 1995;36(3):267-85 [8573710.001]
  • [Cites] EMBO J. 1996 Jan 2;15(1):110-24 [8598193.001]
  • [Cites] EMBO J. 1996 Mar 15;15(6):1292-300 [8635462.001]
  • [Cites] EMBO J. 1996 May 1;15(9):2174-83 [8641283.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):5925-30 [8650195.001]
  • [Cites] FEBS Lett. 1996 Aug 19;392(1):49-53 [8769313.001]
  • [Cites] Mol Endocrinol. 1996 Nov;10(11):1388-98 [8923465.001]
  • [Cites] Mol Endocrinol. 1997 Jan;11(1):48-53 [8994187.001]
  • [Cites] Am J Pathol. 1997 May;150(5):1563-70 [9137083.001]
  • [Cites] Annu Rev Cell Dev Biol. 1997;13:513-609 [9442882.001]
  • [Cites] Crit Rev Oncog. 1997;8(1):29-46 [9516085.001]
  • [Cites] Mol Cell Biol. 1998 Apr;18(4):1978-84 [9528769.001]
  • [Cites] Lancet. 1998 May 16;351(9114):1451-67 [9605801.001]
  • [Cites] Mol Cell Biol. 1999 Feb;19(2):1182-9 [9891052.001]
  • [Cites] Oncogene. 1999 Feb 4;18(5):1227-37 [10022129.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Mar 2;96(5):1858-62 [10051559.001]
  • [Cites] Breast Cancer Res Treat. 1998;52(1-3):65-77 [10066073.001]
  • [Cites] J Biol Chem. 1999 Mar 19;274(12):8335-43 [10075741.001]
  • [Cites] Science. 1999 May 21;284(5418):1354-6 [10334989.001]
  • [Cites] Mol Endocrinol. 1999 Sep;13(9):1522-34 [10478843.001]
  • [Cites] Oncogene. 2004 Nov 25;23(55):8920-30 [15467744.001]
  • [Cites] Mol Endocrinol. 2005 Mar;19(3):732-48 [15528270.001]
  • [Cites] Mol Cell Proteomics. 2005 Apr;4(4):346-55 [15671044.001]
  • [Cites] Mol Cancer Ther. 2006 Oct;5(10):2512-21 [17041095.001]
  • [Cites] Cancer Cell. 2006 Oct;10(4):309-19 [17045208.001]
  • [Cites] Mol Endocrinol. 2006 Dec;20(12):3120-32 [16945990.001]
  • [Cites] Breast Cancer Res. 2000;2(5):360-6 [11250729.001]
  • [Cites] Oncogene. 2001 Mar 22;20(12):1465-75 [11313890.001]
  • [Cites] Genes Dev. 2001 May 1;15(9):1045-50 [11331599.001]
  • [Cites] Mol Biol Cell. 2001 May;12(5):1431-43 [11359933.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Feb 16;281(1):259-65 [11178989.001]
  • [Cites] EMBO J. 2001 Nov 1;20(21):6050-9 [11689445.001]
  • (PMID = 17627304.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; 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 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Neoplasm Proteins; 0 / Protein Kinase Inhibitors; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / Ubiquitin; EC 2.7.10.2 / src-Family Kinases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Other-IDs] NLM/ PMC1906730
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23. Swami S, Raghavachari N, Muller UR, Bao YP, Feldman D: Vitamin D growth inhibition of breast cancer cells: gene expression patterns assessed by cDNA microarray. Breast Cancer Res Treat; 2003 Jul;80(1):49-62
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  • [Title] Vitamin D growth inhibition of breast cancer cells: gene expression patterns assessed by cDNA microarray.
  • 1,25-Dihydroxyvitamin D3 [1,25(OH)2D3], the active metabolite of vitamin D, is a potent inhibitor of breast cancer cell growth.
  • Although it is evident that 1,25(OH)2D3 inhibits growth of both estrogen receptor alpha-positive [ER alpha(+)] and -negative [ER alpha(-)] breast cancer cells, the cellular pathways contributing to these effects remain unclear.
  • We studied the gene expression patterns in ER alpha(+) MCF-7 and ER alpha(-) MDA MB 231 human breast cancer cells following 1,25(OH)2D3 treatment, using cDNA expression arrays.
  • Some of these results were confirmed by real-time PCR.
  • In conclusion, the gene expression profiles of the two cell lines studied were different with a few overlapping genes suggesting that different cellular pathways might be regulated by 1,25(OH)2D3 to exert its growth inhibitory effects in ER alpha(+) and ER alpha(-) cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Calcitriol / pharmacology. Oligonucleotide Array Sequence Analysis
  • [MeSH-minor] DNA, Neoplasm / analysis. Down-Regulation / drug effects. Female. Gene Expression Regulation, Neoplastic / drug effects. Humans. Polymerase Chain Reaction. Tumor Cells, Cultured. Up-Regulation / drug effects


24. Tanaka H, Nakamura M, Kameda C, Kubo M, Sato N, Kuroki S, Tanaka M, Katano M: The Hedgehog signaling pathway plays an essential role in maintaining the CD44+CD24-/low subpopulation and the side population of breast cancer cells. Anticancer Res; 2009 Jun;29(6):2147-57
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  • [Title] The Hedgehog signaling pathway plays an essential role in maintaining the CD44+CD24-/low subpopulation and the side population of breast cancer cells.
  • The side population (SP) and the CD44(+)/CD24(-/low) population have been reported in separate studies to include more tumorigenic cells than other populations, and to have the ability to form new tumors and undergo heterogeneous differentiation in breast cancer tissue.
  • However, the relationship between these two populations has not yet been explored in breast cancer cells.
  • Here it is shown that the SP and the CD44(+)/CD24(-/low) populations are overlapping.
  • These data suggest that the Hh signaling pathway is essential for the proliferation of the tumorigenic population of breast cancer cells, and that this pathway might represent a new candidate for breast cancer therapy targeting cancer stem cells.
  • [MeSH-major] Antigens, CD24 / metabolism. Antigens, CD44 / metabolism. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Hedgehog Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Animals. Antineoplastic Agents, Phytogenic / therapeutic use. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Carcinoma, Pancreatic Ductal / drug therapy. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / secondary. Cell Line, Tumor. Cell Proliferation / drug effects. Colonic Neoplasms / drug therapy. Colonic Neoplasms / metabolism. Colonic Neoplasms / pathology. Drug Resistance, Neoplasm. Female. Flow Cytometry. Humans. Mice. Mice, Inbred NOD. Mice, SCID. Paclitaxel / therapeutic use. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Trans-Activators / antagonists & inhibitors. Trans-Activators / genetics. Trans-Activators / metabolism. Transcription Factors / antagonists & inhibitors. Transcription Factors / genetics. Transcription Factors / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 19528475.001).
  • [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 / Antigens, CD24; 0 / Antigens, CD44; 0 / Antineoplastic Agents, Phytogenic; 0 / CD24 protein, human; 0 / CD44 protein, human; 0 / GLI1 protein, human; 0 / Hedgehog Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Trans-Activators; 0 / Transcription Factors; P88XT4IS4D / Paclitaxel
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25. Susnjar S, Bosnjak S, Radulovic S, Stevanovic J, Gajic-Dobrosavljevic M, Kreacic M: Dose-finding study of capecitabine in combination with weekly paclitaxel for patients with anthracycline-pretreated metastatic breast cancer. J BUON; 2007 Apr-Jun;12(2):189-96
Hazardous Substances Data Bank. FLUOROURACIL .

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  • [Title] Dose-finding study of capecitabine in combination with weekly paclitaxel for patients with anthracycline-pretreated metastatic breast cancer.
  • PURPOSE: Capecitabine and paclitaxel show high efficacy, non-overlapping toxicity profiles and preclinical synergism, providing the rationale for their combination in metastatic breast cancer (MBC).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Breast Neoplasms / drug therapy. Deoxycytidine / analogs & derivatives. Fluorouracil / analogs & derivatives. Paclitaxel / administration & dosage
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Anthracyclines / therapeutic use. Antibiotics, Antineoplastic / therapeutic use. Capecitabine. Drug Administration Schedule. Female. Humans. Maximum Tolerated Dose. Middle Aged. Neoplasm Metastasis

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  • (PMID = 17600871.001).
  • [ISSN] 1107-0625
  • [Journal-full-title] Journal of B.U.ON. : official journal of the Balkan Union of Oncology
  • [ISO-abbreviation] J BUON
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antibiotics, Antineoplastic; 0W860991D6 / Deoxycytidine; 6804DJ8Z9U / Capecitabine; P88XT4IS4D / Paclitaxel; U3P01618RT / Fluorouracil
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26. Del Barco S, Colomer R, Calvo L, Tusquets I, Adrover E, Sánchez P, Rifà J, De la Haba J, Virizuela JA: Non-pegylated liposomal doxorubicin combined with gemcitabine as first-line treatment for metastatic or locally advanced breast cancer. Final results of a phase I/II trial. Breast Cancer Res Treat; 2009 Jul;116(2):351-8
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  • [Title] Non-pegylated liposomal doxorubicin combined with gemcitabine as first-line treatment for metastatic or locally advanced breast cancer. Final results of a phase I/II trial.
  • Doxorubicin and gemcitabine are active as single agents in breast cancer, have different mechanisms of action, and mainly have non-overlapping side effects.
  • This open, multicenter, single-arm phase I/II study assessed the safety and activity of gemcitabine in combination with non-pegylated liposomal doxorubicin (Myocet), a more cardiac-friendly anthracycline, in the first-line treatment of patients with advanced breast cancer.
  • The principal toxicity observed was hematological, and 48% of patients developed grade 3-4 neutropenia.
  • There were no symptomatic cardiac events despite the fact that 36% of the patients had received prior treatment with adjuvant anthracyclines.
  • The combination of Myocet and gemcitabine at the RD is safe and has encouraging clinical activity in patients with advanced breast cancer, without apparent cardiac toxicity in anthracycline-pretreated patients.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Deoxycytidine / administration & dosage. Deoxycytidine / adverse effects. Deoxycytidine / analogs & derivatives. Disease-Free Survival. Dose-Response Relationship, Drug. Doxorubicin / administration & dosage. Doxorubicin / adverse effects. Humans. Kaplan-Meier Estimate. Liposomes. Middle Aged. Neoplasm Staging. Treatment Outcome

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  • (PMID = 18941891.001).
  • [ISSN] 1573-7217
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Clinical Trial, Phase III; Journal Article; Multicenter Study
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Liposomes; 0W860991D6 / Deoxycytidine; 80168379AG / Doxorubicin; B76N6SBZ8R / gemcitabine
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27. Mehta K, Osipo C: Trastuzumab resistance: role for Notch signaling. ScientificWorldJournal; 2009;9:1438-48
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Epidermal growth factor receptor-2 (ErbB-2/HER2) is a potent breast oncogene that has been shown to be amplified in 20% of breast cancers.
  • Overexpression of ErbB-2 predicts for aggressive tumor behavior, resistance to some cytotoxic and antihormonal therapies, and poor overall survival.
  • Trastuzumab, the humanized, monoclonal antibody directed against ErbB-2 has shown tremendous efficacy and improved overall survival for women when combined with a taxane-based chemotherapy.
  • However, resistance to trastuzumab remains a major concern, most notably in women with metastatic breast cancer.
  • Here we review the many possible mechanisms of action that could contribute to resistance, and novel therapies to prevent or reverse the resistant phenotype.
  • Moreover, we provide a critical role for Notch signaling cross-talk with overlapping or new signaling networks in trastuzumab-resistant breast.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Breast Neoplasms / drug therapy. Receptors, Notch / physiology
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Drug Resistance, Neoplasm. Female. Humans. Receptor, ErbB-2 / drug effects. Receptor, ErbB-2 / physiology. Signal Transduction / drug effects. Trastuzumab


28. Kudoh K, Ramanna M, Ravatn R, Elkahloun AG, Bittner ML, Meltzer PS, Trent JM, Dalton WS, Chin KV: Monitoring the expression profiles of doxorubicin-induced and doxorubicin-resistant cancer cells by cDNA microarray. Cancer Res; 2000 Aug 1;60(15):4161-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Drug resistance in cancer is a major obstacle to successful chemotherapy.
  • Cancer cells exposed to antitumor drugs may be directly induced to express a subset of genes that could confer resistance, thus allowing some cells to escape killing and form the relapsed resistant tumor.
  • Alternatively, some cancer cells may be expressing an array of genes that could confer intrinsic resistance, and exposure to cytotoxic drugs select for the survival of these cells that form the relapsed tumor.
  • Our results showed that transient treatment with doxorubicin altered the expression of a diverse group of genes in a time-dependent manner.
  • This distinct set of overlapping genes may represent the signature profile of doxorubicin-induced gene expression and resistance in cancer cells.
  • Our studies demonstrate the feasibility of obtaining potential molecular profile or fingerprint of anticancer drugs in cancer cells by cDNA microarray, which might yield further insights into the mechanisms of drug resistance and suggest alternative methods of treatment.
  • [MeSH-major] Antineoplastic Agents / pharmacology. DNA, Complementary / genetics. DNA, Neoplasm / genetics. Doxorubicin / pharmacology. Gene Expression / drug effects. Gene Expression Profiling
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Breast Neoplasms / metabolism. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic / drug effects. Humans. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Messenger / metabolism. Tumor Cells, Cultured

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  • (PMID = 10945624.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA67722
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Complementary; 0 / DNA, Neoplasm; 0 / RNA, Messenger; 80168379AG / Doxorubicin
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29. Boettcher M, Fredebohm J, Gholami AM, Hachmo Y, Dotan I, Canaani D, Hoheisel JD: Decoding pooled RNAi screens by means of barcode tiling arrays. BMC Genomics; 2010;11:7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: We synthesized DNA microarrays with six overlapping 25 nt long tiling probes complementary to each unique 60 nt molecular barcode sequence associated with every shRNA expression construct.
  • Out of a pool of 305 shRNAs, we identified 28 candidate shRNAs to fully or partially impair the viability of the breast carcinoma cell line MDA-MB-231.
  • Our experimental approach, coupled with commercially available lentiviral vector shRNA libraries, has the potential to greatly facilitate the discovery of putative targets for cancer therapy as well as sensitizers of drug toxicity.
  • [MeSH-minor] Breast Neoplasms / genetics. Cell Line, Tumor. Humans. Nucleic Acid Probes. RNA, Neoplasm / genetics. Recoverin. Reproducibility of Results

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  • [Cites] Nat Methods. 2006 Sep;3(9):701-6 [16929315.001]
  • [Cites] Nat Methods. 2006 Sep;3(9):715-9 [16929317.001]
  • [Cites] Nat Rev Cancer. 2008 Jan;8(1):61-70 [18075512.001]
  • [Cites] Science. 2008 Feb 1;319(5863):617-20 [18239125.001]
  • [Cites] Science. 2008 Feb 1;319(5863):620-4 [18239126.001]
  • [Cites] Cell Cycle. 2008 Sep 1;7(17):2647-53 [18728395.001]
  • [Cites] Cell Cycle. 2008 Oct;7(19):2987-90 [18818511.001]
  • [Cites] Clin Cancer Res. 2008 Dec 15;14(24):7988-99 [19088015.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20380-5 [19091943.001]
  • [Cites] Biochem Biophys Res Commun. 2009 Feb 27;380(1):166-70 [19166812.001]
  • [Cites] Br J Cancer. 2009 Apr 21;100(8):1213-8 [19319136.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10781-6 [11535808.001]
  • [Cites] Nature. 2002 Jan 31;415(6871):530-6 [11823860.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10393-8 [12917485.001]
  • [Cites] Nucleic Acids Res. 2003 Dec 1;31(23):e151 [14627841.001]
  • [Cites] Science. 2004 Feb 6;303(5659):832-5 [14764878.001]
  • [Cites] Nature. 2004 Mar 25;428(6981):427-31 [15042091.001]
  • [Cites] Nature. 2004 Mar 25;428(6981):431-7 [15042092.001]
  • [Cites] Clin Chem. 2004 Nov;50(11):1986-93 [15364883.001]
  • [Cites] Nat Genet. 1995 Apr;9(4):444-50 [7795653.001]
  • [Cites] Nat Genet. 1996 Mar;12(3):298-302 [8589721.001]
  • [Cites] Genes Chromosomes Cancer. 1995 Dec;14(4):227-51 [8605112.001]
  • [Cites] Genes Dev. 2005 Mar 1;19(5):570-82 [15741319.001]
  • [Cites] BMC Biol. 2005;3:16 [16029492.001]
  • [Cites] Nat Genet. 2005 Nov;37(11):1281-8 [16200065.001]
  • [Cites] Biosci Rep. 2005 Oct-Dec;25(5-6):299-307 [16307378.001]
  • [Cites] Nat Rev Cancer. 2006 May;6(5):382-91 [16633366.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4952-60 [16651453.001]
  • [Cites] Nature. 2006 May 4;441(7089):106-10 [16572121.001]
  • (PMID = 20051122.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Nucleic Acid Probes; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 135844-11-0 / Recoverin
  • [Other-IDs] NLM/ PMC2824726
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30. Chinn P, Braslawsky G, White C, Hanna N: Antibody therapy of non-Hodgkin's B-cell lymphoma. Cancer Immunol Immunother; 2003 May;52(5):257-80
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antibody therapy of non-Hodgkin's B-cell lymphoma.
  • Engineering antibodies with reduced immunogenicity and enhanced effector functions, and selecting antigen targets with the appropriate specificity, density, and/or functionality, have contributed to the recent clinical successes in using unconjugated "naked" antibody therapies of B-cell lymphoma (rituximab) and breast carcinoma (Herceptin).
  • The non-overlapping toxicities of naked antibodies and chemotherapy, together with their potential synergy, which is based on unique and complementary mechanisms of action, have contributed to the creation of new standards of care in cancer therapy and management.
  • Furthermore, the exquisite specificity of antibodies renders them ideal vehicles for selective delivery of toxic payloads such as drugs or radionuclides.
  • Although successful in therapy of hematological cancers (Zevalin, Mylotarg), the broader application of these technologies to carcinomas still remains to be proven in clinical testing.
  • With the advent of genomics and proteomics, new membrane-associated tumor antigens are being discovered and will provide novel targets for future antibody therapy of cancer.
  • [MeSH-major] Immunotherapy / methods. Lymphoma, B-Cell / immunology. Lymphoma, B-Cell / therapy
  • [MeSH-minor] Animals. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. Antigens, Neoplasm / immunology. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Lymphoma / immunology. Mice. Rituximab. Time Factors

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  • (PMID = 12700943.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 197
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31. Ejendal KF, Hrycyna CA: Differential sensitivities of the human ATP-binding cassette transporters ABCG2 and P-glycoprotein to cyclosporin A. Mol Pharmacol; 2005 Mar;67(3):902-11
Hazardous Substances Data Bank. CYCLOSPORIN A .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The half-transporter ABCG2 and the widely studied P-glycoprotein (P-gp) are two ABC transporters that, when overexpressed, are capable of extruding a variety of structurally unrelated chemotherapy agents from cells.
  • In this study, we demonstrate that human ABCG2 and P-glycoprotein, despite overlapping substrate specificities, differ in sensitivity to the immunomodulator cyclosporin A.
  • In this study, we used human ABCG2 and human P-gp, each expressed separately in drug-selected MCF-7 sublines and transiently transfected HeLa cells.
  • We also demonstrated, for the first time, that [125I]iodoarylazidoprazosin, a photoaffinity analog of the substrate prazosin, labels multiple variants of ABCG2 specifically and that this labeling, although competed by some ABCG2 substrates, is unaffected by cyclosporin A.
  • These labeling data also suggest the presence of multiple drug binding sites in ABCG2.
  • [MeSH-major] ATP-Binding Cassette Transporters / metabolism. ATP-Binding Cassette, Sub-Family B, Member 1 / metabolism. Cyclosporine / pharmacology. Neoplasm Proteins / metabolism
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. Acridines / pharmacology. Breast Neoplasms. Cell Line, Tumor. Female. HeLa Cells. Humans. Intracellular Membranes / metabolism. Kinetics. Microsomes / metabolism. Recombinant Proteins / metabolism. Substrate Specificity. Tetrahydroisoquinolines / pharmacology. Transfection

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  • (PMID = 15598974.001).
  • [ISSN] 0026-895X
  • [Journal-full-title] Molecular pharmacology
  • [ISO-abbreviation] Mol. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / ATP-Binding Cassette, Sub-Family B, Member 1; 0 / Acridines; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; 0 / Tetrahydroisoquinolines; 83HN0GTJ6D / Cyclosporine; N488540F94 / Elacridar
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32. Scaltriti M, Verma C, Guzman M, Jimenez J, Parra JL, Pedersen K, Smith DJ, Landolfi S, Ramon y Cajal S, Arribas J, Baselga J: Lapatinib, a HER2 tyrosine kinase inhibitor, induces stabilization and accumulation of HER2 and potentiates trastuzumab-dependent cell cytotoxicity. Oncogene; 2009 Feb 12;28(6):803-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Lapatinib is a human epidermal growth factor receptor 2 (HER2) tyrosine kinase inhibitor (TKI) that has clinical activity in HER2-amplified breast cancer.
  • In vitro studies have shown that lapatinib enhances the effects of the monoclonal antibody trastuzumab suggesting partially non-overlapping mechanisms of action.
  • Lapatinib, given alone or in combination with trastuzumab to HER2-overexpressing breast cancer cells SKBR3 and MCF7-HER2, inhibited HER2 phosphorylation, prevented receptor ubiquitination and resulted in a marked accumulation of inactive receptors at the cell surface.
  • Lapatinib-induced accumulation of HER2 and trastuzumab-mediated downregulation of HER2 was also observed in vivo, where the combination of the two agents triggered complete tumor remissions in all cases after 10 days of treatment.
  • We propose that this is a novel mechanism of action of the combination that may be clinically relevant and exploitable in the therapy of patients with HER2-positive tumors.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Breast Neoplasms / drug therapy. Drug Synergism. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology. Receptor, ErbB-2 / antagonists & inhibitors
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Cell Line, Tumor. Cell Membrane / metabolism. Gene Expression Regulation, Neoplastic. Humans. Mice. Neoplasm Transplantation. Remission Induction. Signal Transduction. Trastuzumab


33. Davies AM, Ho C, Metzger AS, Beckett LA, Christensen S, Tanaka M, Lara PN, Lau DH, Gandara DR: Phase I study of two different schedules of bortezomib and pemetrexed in advanced solid tumors with emphasis on non-small cell lung cancer. J Thorac Oncol; 2007 Dec;2(12):1112-6
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  • INTRODUCTION: Bortezomib and pemetrexed are approved anticancer agents with non-overlapping mechanisms of action and toxicity.
  • Tumor types included lung (n = 16), adenoid cystic carcinoma (n = 2), prostate (n = 2), sarcoma (n = 2), breast (n = 1), thymus (n = 1), head and neck (n = 1), and gastrointestinal(n = 2).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / mortality. Lung Neoplasms / drug therapy. Lung Neoplasms / mortality
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Boronic Acids / administration & dosage. Boronic Acids / adverse effects. Bortezomib. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Glutamates / administration & dosage. Glutamates / adverse effects. Guanine / administration & dosage. Guanine / adverse effects. Guanine / analogs & derivatives. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Staging. Neoplasms / drug therapy. Neoplasms / mortality. Neoplasms / pathology. Pemetrexed. Pyrazines / administration & dosage. Pyrazines / adverse effects. Survival Analysis

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  • (PMID = 18090584.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Boronic Acids; 0 / Glutamates; 0 / Pyrazines; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; 69G8BD63PP / Bortezomib
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