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1. Murialdo R, Boy D, Musizzano Y, Tixi L, Murelli F, Ballestrero A: Squamous cell carcinoma of the breast: a case report. Cases J; 2009;2:7336

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  • [Title] Squamous cell carcinoma of the breast: a case report.
  • INTRODUCTION: Pure primary squamous cell carcinoma of the breast is uncommon and it's debated the correct management of this disease.
  • CASE PRESENTATION: A 54-years-old woman presented with signs and symptoms of mastitis of left breast.
  • She underwent antibiotic therapy without benefit.
  • She performed an ultrasound and mammographic scan of the left breast.
  • Fine needle aspiration cytology revealed an infiltrative poorly differentiated squamous cell carcinoma.
  • Subsequently wide local excision of the left breast with ipsilateral axillary lymph nodes dissection was performed.
  • The pathological examination revealed an infiltrative poorly differentiated squamous cell carcinoma of the breast.
  • Adjuvant chemotherapy cisplatin and 5-fluorouracil based was administered.
  • CONCLUSIONS: Pure primary squamous cell carcinoma of the breast is a rare and aggressive disease often treatment-refractory.
  • An optimal systemic treatment is needed to improve patient's outcome.

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  • [Cites] Acta Cytol. 1989 Mar-Apr;33(2):201-4 [2929222.001]
  • [Cites] Ann Surg Oncol. 1996 Jul;3(4):367-74 [8790849.001]
  • [Cites] ANZ J Surg. 2002 Jan;72(1):65-7 [11906428.001]
  • [Cites] Cancer Radiother. 2002 Dec;6(6):366-8 [12504775.001]
  • [Cites] Eur J Surg Oncol. 2003 May;29(4):386-9 [12711295.001]
  • [Cites] Eur J Obstet Gynecol Reprod Biol. 2008 Apr;137(2):222-6 [17481802.001]
  • [Cites] Breast. 2000 Dec;9(6):315-9 [14965754.001]
  • [Cites] Clin Breast Cancer. 2005 Aug;6(3):270-2 [16137440.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):7827-35 [16258085.001]
  • [Cites] Breast Cancer. 2007;14(1):109-12 [17245005.001]
  • [Cites] Gan To Kagaku Ryoho. 2007 Mar;34(3):443-6 [17353640.001]
  • [Cites] Am J Clin Oncol. 2003 Dec;26(6):571-3 [14663374.001]
  • (PMID = 19829944.001).
  • [ISSN] 1757-1626
  • [Journal-full-title] Cases journal
  • [ISO-abbreviation] Cases J
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2740227
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2. Zhang C, Chakravarty D, Sakabe I, Mewani RR, Boudreau HE, Kumar D, Ahmad I, Kasid UN: Role of SCC-S2 in experimental metastasis and modulation of VEGFR-2, MMP-1, and MMP-9 expression. Mol Ther; 2006 May;13(5):947-55
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  • [Title] Role of SCC-S2 in experimental metastasis and modulation of VEGFR-2, MMP-1, and MMP-9 expression.
  • SCC-S2/GG2-1/NDED (approved gene symbol TNFAIP8) is a transcription factor NF-kappaB-inducible, antiapoptotic, and oncogenic molecule.
  • In this study, we examined the role of SCC-S2 in invasion and experimental metastasis.
  • We demonstrate that expression of SCC-S2 cDNA in MDA-MB 435 human breast cancer cells is associated with enhanced invasion in vitro and increased frequency of pulmonary colonization of tumor cells in athymic mice.
  • Systemic treatment of athymic mice with a cationic liposomal formulation of SCC-S2 antisense oligo led to decreased incidence of pulmonary metastasis and inhibition of SCC-S2 expression in vivo.
  • Antisense inhibition of endogenous SCC-S2 expression correlated with decreased expression of VEGF receptor-2 in tumor cells and human lung microvascular endothelial cells and loss of endothelial cell viability.
  • In addition, downregulation of SCC-S2 expression in tumor cells was associated with decreased expression of known metastasis-related molecules MMP-1 and MMP-9.
  • These results demonstrate a novel role for SCC-S2 in tumor progression, involving multiple effectors, and provide a basis for SCC-S2-targeted cancer gene therapy.
  • [MeSH-major] Breast Neoplasms / pathology. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Metalloproteases / metabolism. Proteins / metabolism. Vascular Endothelial Growth Factor Receptor-2 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Humans. Liposomes. Lung Neoplasms / drug therapy. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Lung Neoplasms / secondary. Matrix Metalloproteinase 1 / genetics. Matrix Metalloproteinase 1 / metabolism. Matrix Metalloproteinase 9 / genetics. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Invasiveness. Neoplasm Metastasis / drug therapy. Neoplasm Transplantation. Oligonucleotides, Antisense / therapeutic use. Transplantation, Heterologous

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  • (PMID = 16455304.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GG2-1 protein, human; 0 / Liposomes; 0 / Oligonucleotides, Antisense; 0 / Proteins; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.4.- / Metalloproteases; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1
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3. Marini P, Schmid A, Jendrossek V, Faltin H, Daniel PT, Budach W, Belka C: Irradiation specifically sensitises solid tumour cell lines to TRAIL mediated apoptosis. BMC Cancer; 2005 Jan 14;5:5
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  • [Title] Irradiation specifically sensitises solid tumour cell lines to TRAIL mediated apoptosis.
  • BACKGROUND: TRAIL (tumor necrosis factor related apoptosis inducing ligand) is an apoptosis inducing ligand with high specificity for malignant cell systems.
  • Combined treatment modalities using TRAIL and cytotoxic drugs revealed highly additive effects in different tumour cell lines.
  • Little is known about the efficacy and underlying mechanistic effects of a combined therapy using TRAIL and ionising radiation in solid tumour cell systems.
  • Additionally, little is known about the effect of TRAIL combined with radiation on normal tissues.
  • METHODS: Tumour cell systems derived from breast- (MDA MB231), lung--(NCI H460) colorectal--(Colo 205, HCT-15) and head and neck cancer (FaDu, SCC-4) were treated with a combination of TRAIL and irradiation using two different time schedules.
  • Normal tissue cultures from breast, prostate, renal and bronchial epithelia, small muscle cells, endothelial cells, hepatocytes and fibroblasts were tested accordingly.
  • RESULTS: The combined treatment of TRAIL with irradiation strongly increased apoptosis induction in all treated tumour cell lines compared to treatment with TRAIL or irradiation alone.
  • Upregulation of TRAIL receptor DR5 after irradiation was observed in four of six tumour cell lines but did not correlate to tumour cell sensitisation to TRAIL.
  • TRAIL did not show toxicity in normal tissue cell systems.
  • In addition, pre-irradiation did not sensitise all nine tested human normal tissue cell cultures to TRAIL.
  • Sequential application of ionising radiation followed by TRAIL is associated with an synergistic induction of cell death in a large panel of solid tumour cell lines.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis. Membrane Glycoproteins / therapeutic use. Neoplasms / therapy. Radiation, Ionizing. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Apoptosis Regulatory Proteins. Caspase 8. Caspases / metabolism. Cell Line, Tumor. Cells, Cultured. Combined Modality Therapy. Humans. Poly(ADP-ribose) Polymerases / metabolism. Receptors, Tumor Necrosis Factor / metabolism. TNF-Related Apoptosis-Inducing Ligand

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  • [Cites] Curr Biol. 1997 Dec 1;7(12):1003-6 [9382840.001]
  • [Cites] Cell. 1997 Nov 14;91(4):479-89 [9390557.001]
  • [Cites] Immunity. 1997 Dec;7(6):813-20 [9430226.001]
  • [Cites] FEBS Lett. 1998 Mar 6;424(1-2):41-5 [9537512.001]
  • [Cites] Cancer Res. 1998 Apr 15;58(8):1593-8 [9563466.001]
  • [Cites] J Biol Chem. 1998 Jun 5;273(23):14363-7 [9603945.001]
  • [Cites] J Biol Chem. 2001 Dec 7;276(49):46639-46 [11583996.001]
  • [Cites] Clin Cancer Res. 2001 Dec;7(12):3874-83 [11751478.001]
  • [Cites] Neoplasia. 2001 Nov-Dec;3(6):535-46 [11774036.001]
  • [Cites] J Immunol. 2002 Feb 1;168(3):1356-61 [11801676.001]
  • [Cites] J Exp Med. 2002 Jan 21;195(2):161-9 [11805143.001]
  • [Cites] Blood. 2002 Mar 15;99(6):2162-71 [11877293.001]
  • [Cites] Drug Resist Updat. 2001 Aug;4(4):243-52 [11991679.001]
  • [Cites] Int J Cancer. 2002 Jun 1;99(4):491-504 [11992538.001]
  • [Cites] Cancer Chemother Pharmacol. 2002 Jul;50(1):46-52 [12111111.001]
  • [Cites] Apoptosis. 2002 Oct;7(5):449-59 [12207178.001]
  • [Cites] Oncogene. 2002 Dec 12;21(57):8786-803 [12483532.001]
  • [Cites] Cancer Res. 2003 Mar 1;63(5):1059-66 [12615723.001]
  • [Cites] Cell Death Differ. 2003 Jan;10(1):66-75 [12655296.001]
  • [Cites] Br J Cancer. 2003 Jun 2;88(11):1800-7 [12771998.001]
  • [Cites] Cytokine Growth Factor Rev. 2003 Jun-Aug;14(3-4):337-48 [12787570.001]
  • [Cites] FASEB J. 2003 Aug;17(11):1547-9 [12824303.001]
  • [Cites] Radiother Oncol. 2003 Aug;68(2):189-98 [12972315.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5390-400 [14500373.001]
  • [Cites] Essays Biochem. 2003;39:73-88 [14585075.001]
  • [Cites] Clin Cancer Res. 2004 Feb 15;10(4):1463-70 [14977850.001]
  • [Cites] Int J Oncol. 2004 May;24(5):1133-40 [15067334.001]
  • [Cites] Oncogene. 2004 Apr 12;23(16):2797-808 [15077143.001]
  • [Cites] Prostate. 2004 Sep 15;61(1):35-49 [15287092.001]
  • [Cites] Oncogene. 2004 Oct 28;23(50):8320-32 [15467752.001]
  • [Cites] J Infect Dis. 1978 Feb;137(2):122-30 [627734.001]
  • [Cites] Cell. 1993 Sep 24;74(6):957-67 [8402885.001]
  • [Cites] Cell. 1998 Aug 21;94(4):481-90 [9727491.001]
  • [Cites] Cell. 1998 Aug 21;94(4):491-501 [9727492.001]
  • [Cites] Cell Death Differ. 1998 Dec;5(12):997-1000 [9894605.001]
  • [Cites] EMBO J. 1999 Feb 1;18(3):632-43 [9927423.001]
  • [Cites] Nat Med. 1999 Feb;5(2):157-63 [9930862.001]
  • [Cites] Mol Cell. 1999 Feb;3(2):159-67 [10078199.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1754-9 [10677530.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):847-53 [10706092.001]
  • [Cites] Oncogene. 2000 Feb 24;19(9):1181-90 [10713706.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3100-5 [10737788.001]
  • [Cites] Nat Cell Biol. 2000 Apr;2(4):241-3 [10783243.001]
  • [Cites] Nat Med. 2000 May;6(5):564-7 [10802713.001]
  • [Cites] J Biol Chem. 2000 Jul 28;275(30):23319-25 [10770955.001]
  • [Cites] J Clin Invest. 1999 Jul;104(2):155-62 [10411544.001]
  • [Cites] J Biol Chem. 1999 Oct 22;274(43):30603-10 [10521444.001]
  • [Cites] Prostate. 2005 Feb 1;62(2):165-86 [15389801.001]
  • [Cites] Oncogene. 2005 Jan 6;24(1):130-40 [15531922.001]
  • [Cites] Cell Death Differ. 1999 Nov;6(11):1087-98 [10578178.001]
  • [Cites] Biochemistry. 2000 Feb 1;39(4):633-40 [10651627.001]
  • [Cites] Oncogene. 2000 Sep 21;19(40):4563-73 [11030145.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):7149-55 [11156424.001]
  • [Cites] Cancer Res. 2001 Jan 15;61(2):759-63 [11212279.001]
  • [Cites] Blood. 2001 Mar 1;97(5):1378-87 [11222383.001]
  • [Cites] Nat Med. 2001 Apr;7(4):383-5 [11283636.001]
  • [Cites] Nat Cell Biol. 2001 Apr;3(4):409-16 [11283615.001]
  • [Cites] Blood. 2001 May 1;97(9):2596-603 [11313247.001]
  • [Cites] Oncogene. 2001 Apr 19;20(17):2190-6 [11360204.001]
  • [Cites] Gynecol Oncol. 2001 Jun;81(3):380-90 [11371126.001]
  • [Cites] Hepatology. 2001 Jul;34(1):3-6 [11431726.001]
  • [Cites] Cell. 1995 May 19;81(4):505-12 [7538907.001]
  • [Cites] Cell. 1996 Jun 14;85(6):817-27 [8681377.001]
  • [Cites] Science. 1997 Apr 4;276(5309):111-3 [9082980.001]
  • [Cites] Science. 1997 Aug 8;277(5327):815-8 [9242610.001]
  • [Cites] Science. 1997 Aug 8;277(5327):818-21 [9242611.001]
  • [Cites] Curr Biol. 1997 Sep 1;7(9):693-6 [9285725.001]
  • [Cites] EMBO J. 1997 Sep 1;16(17):5386-97 [9311998.001]
  • [Cites] J Exp Med. 1997 Oct 6;186(7):1165-70 [9314565.001]
  • [Cites] J Biol Chem. 1997 Oct 10;272(41):25417-20 [9325248.001]
  • (PMID = 15651986.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC547906
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4. Chung MS, Ha TK, Lee KG, Paik SS: A case of long survival in poorly differentiated small cell carcinoma of the pancreas. World J Gastroenterol; 2008 Aug 21;14(31):4964-7
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  • [Title] A case of long survival in poorly differentiated small cell carcinoma of the pancreas.
  • Small cell carcinoma (SCC) of the pancreas is rare.
  • It has similar histological features to pulmonary small cell carcinoma and is equally aggressive.
  • Most patients with SCC in the pancreas reported in case studies died within 1 year after diagnosis.
  • We present a case of unusually long-term survival after surgery and combined chemotherapy for SCC of the pancreas.
  • Computed tomography revealed dilated common bile duct caused by external compression of the mass in the pancreatic head.
  • Exploratory laparotomy and pancreaticoduodenectomy (PPPD) was performed with histopathological analysis confirming a primary small cell carcinoma of the pancreas.
  • After an uneventful postoperative recovery, the patient was treated with 6 cycles of combined chemotherapy consisting of cisplantin and ectoposide.
  • During the follow-up, there was no evidence of recurrence and the patient has remained in a good health condition for 36 mo since the diagnosis.
  • [MeSH-major] Carcinoma, Small Cell / pathology. Cell Differentiation. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Cholangiopancreatography, Magnetic Resonance. Disease-Free Survival. Female. Humans. Middle Aged. Pancreatectomy. Time Factors. Tomography, X-Ray Computed. Treatment Outcome

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  • [Cites] Jpn J Clin Oncol. 2004 May;34(5):250-4 [15231859.001]
  • [Cites] Breast Cancer. 2009;16(1):68-71 [18504641.001]
  • [Cites] Cancer. 1973 Jun;31(6):1523-7 [4350960.001]
  • [Cites] Pathol Annu. 1974;9(0):27-41 [4154097.001]
  • [Cites] Cancer Res. 1976 Jul;36(7 PT 2):2690-8 [1277176.001]
  • [Cites] Cancer. 1981 May 15;47(10):2500-2 [6268272.001]
  • [Cites] Cancer. 1984 Apr 1;53(7):1552-4 [6321009.001]
  • [Cites] Medicine (Baltimore). 1987 Nov;66(6):457-71 [2824968.001]
  • [Cites] Cancer. 1989 Nov 15;64(10):2007-9 [2553237.001]
  • [Cites] Cancer. 1990 Feb 1;65(3):422-4 [1688727.001]
  • [Cites] Med Pediatr Oncol. 1992;20(2):89-99 [1310345.001]
  • [Cites] Cancer. 1992 Sep 15;70(6):1514-9 [1325274.001]
  • [Cites] Cancer Invest. 1996;14(4):335-9 [8689428.001]
  • [Cites] Cancer. 1997 May 1;79(9):1729-36 [9128989.001]
  • [Cites] Cancer. 1997 Oct 15;80(8):1366-72 [9338459.001]
  • [Cites] Pancreatology. 2004;4(6):521-6 [15334003.001]
  • [Cites] Acta Oncol. 2007;46(6):846-51 [17653910.001]
  • [Cites] Breast Cancer. 2007;14(4):414-9 [17986808.001]
  • [Cites] Yonsei Med J. 2007 Dec 31;48(6):1066-71 [18159605.001]
  • [Cites] J Gastroenterol Hepatol. 2004 Sep;19(9):1087-91 [15304133.001]
  • (PMID = 18756608.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
  • [Other-IDs] NLM/ PMC2739953
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5. Ku TK, Crowe DL: Coactivator-mediated estrogen response in human squamous cell carcinoma lines. J Endocrinol; 2007 Apr;193(1):147-55
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  • [Title] Coactivator-mediated estrogen response in human squamous cell carcinoma lines.
  • Estrogen signaling in non-reproductive tract tissues such as skin is less well characterized and the effectiveness of anti-estrogen therapy for cancer arising from these tissues is unknown.
  • We show that tamoxifen (TAM) treatment inhibited cell cycle progression and proliferation of human cancer lines derived from stratified squamous epithelium squamous cell carcinoma (SCC).
  • The E2 treatment promoted displacement of the NCoR from ERalpha and recruitment of CBP to the receptor.
  • SRC-1 expression was not detected in these SCC lines; however, transient transfection of SRC-1, CBP, or both coactivators enhanced transactivation of an estrogen responsive promoter in cancer cells treated with E2 or TAM.
  • SRC-1 expression restored the E2-mediated proliferative response to human SCC lines.
  • We concluded that SRC-1 was a key molecular determinant of estrogen-mediated proliferation in human SCC lines.
  • [MeSH-major] Carcinoma, Squamous Cell / metabolism. Estrogen Antagonists / pharmacology. Estrogen Receptor alpha / metabolism. Estrogens / pharmacology. Histone Acetyltransferases / metabolism. Tamoxifen / pharmacology. Transcription Factors / metabolism
  • [MeSH-minor] Blotting, Western / methods. Breast Neoplasms. CREB-Binding Protein / genetics. CREB-Binding Protein / metabolism. Cell Cycle / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Chromatin Immunoprecipitation. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Lipids / administration & dosage. Lipids / genetics. Nuclear Receptor Coactivator 1. Reverse Transcriptase Polymerase Chain Reaction. Transfection / methods

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  • (PMID = 17400812.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CREBBP protein, human; 0 / Estrogen Antagonists; 0 / Estrogen Receptor alpha; 0 / Estrogens; 0 / Lipids; 0 / Lipofectamine; 0 / Transcription Factors; 094ZI81Y45 / Tamoxifen; EC 2.3.1.48 / CREB-Binding Protein; EC 2.3.1.48 / Histone Acetyltransferases; EC 2.3.1.48 / NCOA1 protein, human; EC 2.3.1.48 / Nuclear Receptor Coactivator 1; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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6. Skipper JB, McNally LR, Rosenthal EL, Wang W, Buchsbaum DJ: In vivo efficacy of marimastat and chemoradiation in head and neck cancer xenografts. ORL J Otorhinolaryngol Relat Spec; 2009;71(1):1-5
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  • OBJECTIVE: To assess the effect of combining a synthetic matrix metalloprotease inhibitor and chemoradiation therapy on tumor growth in a murine model of head and neck squamous-cell carcinoma (SCC).
  • METHODS: Athymic, nude mice bearing SCC-1 xenografts were used to comprise 4 treatment groups:.
  • Radiotherapy was given in 4 fractions of 8 Gy divided over days 8, 12, 16 and 20 with 4 intraperitoneal doses of cisplatin (3 mg/kg) 1 h before each fraction of radiation.
  • RESULTS: Animals receiving triple treatment had delayed growth, measured as lengthened tumor doubling time, compared to the cisplatin + radiation combination (p = 0.03).
  • Also, compared to control, the triple-treatment group (p = 0.005) had delayed growth in terms of doubling time.
  • Factor VIII immunohistochemistry to assess microvessel density did not demonstrate a reduction in neovascularization between the triple-treatment and cisplatin + radiation combination groups.
  • CONCLUSIONS: Chemoradiation + marimastat therapy had delayed tumor growth, compared to the chemoradiation alone.
  • Based on these results, marimastat may work in combination with chemotherapy and radiation to inhibit tumor growth.

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  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • [Cites] J Natl Cancer Inst. 1997 Sep 3;89(17):1260-70 [9293916.001]
  • [Cites] J Biol Chem. 1996 Nov 29;271(48):30375-80 [8939999.001]
  • [Cites] Ann Med. 1999 Feb;31(1):34-45 [10219712.001]
  • [Cites] J Clin Invest. 1999 May;103(9):1237-41 [10225966.001]
  • [Cites] Cancer Chemother Pharmacol. 1999;43 Suppl:S42-51 [10357558.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14):3374-8 [10416597.001]
  • [Cites] J Clin Oncol. 2004 Dec 1;22(23):4683-90 [15570070.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3193-9 [15833850.001]
  • [Cites] Mol Cancer Ther. 2005 Nov;4(11):1717-28 [16275993.001]
  • [Cites] N Engl J Med. 2006 Feb 9;354(6):567-78 [16467544.001]
  • [Cites] Invest New Drugs. 2006 Mar;24(2):135-40 [16502351.001]
  • [Cites] J Neurooncol. 2006 Jul;78(3):295-302 [16636750.001]
  • [Cites] Cancer Res. 2006 Sep 1;66(17):8511-9 [16951163.001]
  • [Cites] Clin Cancer Res. 2001 Jul;7(7):1912-22 [11448904.001]
  • [Cites] Cancer Res. 2000 Mar 1;60(5):1326-31 [10728694.001]
  • [Cites] Nat Clin Pract Oncol. 2007 Feb;4(2):86-100 [17259930.001]
  • [Cites] Cancer Res. 2001 Jul 15;61(14):5453-60 [11454691.001]
  • [Cites] Neoplasia. 2002 Mar-Apr;4(2):164-70 [11896571.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):1223-7 [11948136.001]
  • [Cites] Semin Radiat Oncol. 2003 Jan;13(1):13-21 [12520460.001]
  • [Cites] Clin Exp Metastasis. 2002;19(8):697-702 [12553375.001]
  • [Cites] Nature. 1985 Nov 7-13;318(6041):66-9 [3903517.001]
  • [Cites] Genomics. 1994 Jan 1;19(1):86-90 [8188246.001]
  • [Cites] EMBO J. 1995 Mar 1;14(5):908-17 [7534227.001]
  • [Cites] Int J Cancer. 1995 May 29;61(5):732-7 [7768649.001]
  • [Cites] Breast Cancer Res Treat. 1995;36(2):227-36 [8534870.001]
  • [Cites] Nature. 1998 Jul 16;394(6690):287-91 [9685160.001]
  • (PMID = 18931526.001).
  • [ISSN] 1423-0275
  • [Journal-full-title] ORL; journal for oto-rhino-laryngology and its related specialties
  • [ISO-abbreviation] ORL J. Otorhinolaryngol. Relat. Spec.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K08 CA102154-04; United States / NCI NIH HHS / CA / NIH T32CA075930; United States / NCI NIH HHS / CA / NCI K08CA102154; United States / NCI NIH HHS / CA / T32 CA075930; United States / NCI NIH HHS / CA / CA102154-04; United States / NCI NIH HHS / CA / K08 CA102154
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Hydroxamic Acids; 0 / Matrix Metalloproteinase Inhibitors; 0 / Protease Inhibitors; D5EQV23TDS / marimastat; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS110571; NLM/ PMC2700630
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7. Siegelmann-Danieli N, Murphy TJ, Meschter SC, Stein ME, Prichard J: Primary pure squamous cell carcinoma of the breast. Clin Breast Cancer; 2005 Aug;6(3):270-2
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  • [Title] Primary pure squamous cell carcinoma of the breast.
  • Primary squamous cell carcinoma (SCC) of the breast is an extremely rare tumor.
  • It is diagnosed when the malignant cells are entirely of squamous type, the tumor is independent from overlying skin, and other primary SCC sites are excluded.
  • This report presents clinical, radiologic, and histologic correlative findings of a patient diagnosed with pure SCC of the breast.
  • Literature review suggests that primary SCC tumors of the breast are large, often cystic lesions, with a low rate of nodal involvement, no expression of estrogen and progesterone receptors, and resistance to the chemotherapy regimens commonly used in breast cancer.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma, Squamous Cell / diagnosis

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  • [CommentIn] Clin Breast Cancer. 2006 Jun;7(2):180 [16800983.001]
  • (PMID = 16137440.001).
  • [ISSN] 1526-8209
  • [Journal-full-title] Clinical breast cancer
  • [ISO-abbreviation] Clin. Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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8. Aparicio I, Martínez A, Hernández G, Hardisson D, De Santiago J: Squamous cell carcinoma of the breast. Eur J Obstet Gynecol Reprod Biol; 2008 Apr;137(2):222-6
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  • [Title] Squamous cell carcinoma of the breast.
  • OBJECTIVE: Pure squamous cell carcinoma (SCC) of the breast is a rare tumour and its clinical behaviour is not correctly known.
  • The aim of the study is to evaluate the prevalence, epidemiological and clinical characteristics of the cases of SCC studied in our institution.
  • STUDY DESIGN: The breast department's database was searched for patients diagnosed with breast SCC between September 1979 and June 2006.
  • RESULTS: Eleven patients were identified (0.19%) between 5771 cases of breast cancer.
  • Mean survival from the time recurrent disease was recognized was 9 (1-16) months.
  • CONCLUSIONS: SCC of the breast is aggressive and often treatment-refractory.
  • The role of different new chemotherapy regimens need to be explored.
  • [MeSH-major] Breast Neoplasms / diagnosis. Breast Neoplasms / therapy. Carcinoma, Squamous Cell / diagnosis. Carcinoma, Squamous Cell / therapy
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Combined Modality Therapy. Female. Humans. Mastectomy. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Prevalence. Prognosis. Radiotherapy, Adjuvant. Retrospective Studies. Survival Analysis. Treatment Outcome

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  • (PMID = 17481802.001).
  • [ISSN] 0301-2115
  • [Journal-full-title] European journal of obstetrics, gynecology, and reproductive biology
  • [ISO-abbreviation] Eur. J. Obstet. Gynecol. Reprod. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
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9. Bhatt L, Fernando I: Primary squamous cell carcinoma of the breast: achieving long-term control with cisplatin-based chemotherapy. Clin Breast Cancer; 2009 Aug;9(3):187-8
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  • [Title] Primary squamous cell carcinoma of the breast: achieving long-term control with cisplatin-based chemotherapy.
  • Pure primary squamous cell carcinoma (SCC) of the breast is rare and difficult to treat.
  • Published series suggest a poor response to conventional breast chemotherapy.
  • A 66-year-old woman with locally advanced SCC of the breast received combined-modality treatment with high-dose radiation therapy (59 Gy in 22 fractions); mastectomy; and chemotherapy with cisplatin 50 mg/m(2), mitomycin-C 6 mg/m(2), and ifosfamide 3 g/m(2) given in 21-day cycles.
  • We would suggest that this case lends support to the use of high-dose radiation therapy and platinum-based chemotherapy in the management of this difficult condition.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Breast Neoplasms / drug therapy. Carcinoma, Squamous Cell / drug therapy. Cisplatin / administration & dosage
  • [MeSH-minor] Aged. Combined Modality Therapy. Disease-Free Survival. Female. Humans. Ifosfamide / administration & dosage. Mastectomy. Mitomycin / administration & dosage

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  • (PMID = 19661044.001).
  • [ISSN] 1938-0666
  • [Journal-full-title] Clinical breast cancer
  • [ISO-abbreviation] Clin. Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 50SG953SK6 / Mitomycin; Q20Q21Q62J / Cisplatin; UM20QQM95Y / Ifosfamide
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10. Uchida N, Ishiguro K, Suda T, Nishimura M: [A case of aggressive primary squamous cell carcinoma of the breast refractory to preoperative neoadjuvant chemotherapy]. Gan To Kagaku Ryoho; 2009 Dec;36(13):2619-22
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  • [Title] [A case of aggressive primary squamous cell carcinoma of the breast refractory to preoperative neoadjuvant chemotherapy].
  • A 42-year-old woman came to our hospital complaining of an enlarging tumor in her right breast.
  • A core needle biopsy of the involved area demonstrated primary squamous cell carcinoma (SCC) of the breast.
  • Although postoperative adjuvant chemotherapy consisting of carboplatin (CBDCA) +etoposide (VP-16) was administered, the patient died three months after surgery.
  • SCC of the breast is generally treated according to clinical stage using protocol for common types of breast cancer.
  • However, effective regimens have not been established for SCC, because it tends to be treatment-refractory.
  • Therefore, in patients with SCC, it is important to consider surgery at an earlier stage than would be considered for a common breast cancer requiring preoperative neoadjuvant chemotherapy.
  • [MeSH-major] Breast Neoplasms / therapy. Carcinoma, Squamous Cell / therapy
  • [MeSH-minor] Adult. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Epirubicin / administration & dosage. Fatal Outcome. Female. Fluorouracil / administration & dosage. Humans. Lung Neoplasms / secondary. Neoadjuvant Therapy. Organoplatinum Compounds / administration & dosage. Paclitaxel / administration & dosage. Vinblastine / administration & dosage. Vinblastine / analogs & derivatives

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  • (PMID = 20009466.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Alkylating; 0 / Antineoplastic Agents, Phytogenic; 0 / Organoplatinum Compounds; 3Z8479ZZ5X / Epirubicin; 5V9KLZ54CY / Vinblastine; 8N3DW7272P / Cyclophosphamide; 8UQ3W6JXAN / nedaplatin; P88XT4IS4D / Paclitaxel; Q6C979R91Y / vinorelbine; U3P01618RT / Fluorouracil
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11. Takahashi T, Akashi-Tanaka S, Fukutomi T, Watanabe T, Katsumata N, Miyakawa K, Hasegawa T, Tsuda H: Two special types of breast cancer presenting as progressive disease after neoadjuvant chemotherapy with docetaxel plus doxorubicin. Breast Cancer; 2001;8(3):234-7
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  • [Title] Two special types of breast cancer presenting as progressive disease after neoadjuvant chemotherapy with docetaxel plus doxorubicin.
  • Seventy-eight patients with primary breast cancer over 3 cm in diameter in stages II A, II B, III A and III B according to the UICC classification received neoadjuvant chemotherapy from August 1, 1998 to June 30, 2000 at the Breast Division of the National Cancer Center Hospital.
  • Neoadjuvant chemotherapy consisted of doxorubicin (Adriamycin: ADM) 50 mg/m(2) and docetaxel (Taxotere: DOC) 60 mg/m(2) every three weeks.
  • Although neoadjuvant chemotherapy with this regimen achieved good responses in patients with breast cancer, 2 patients presented with progressive disease (PD) after treatment.
  • One patient had inflammatory breast cancer (IBC) and the other had primary squamous cell carcinoma (SCC) of the breast.
  • There were 4 cases of IBC and one case of SCC of the breast who received neoadjuvant chemotherapy in this series.
  • Our observations suggest that this regimen might not be effective for these types of breast cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Neoplasms / secondary. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / drug therapy. Carcinoma, Ductal, Breast / secondary. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / secondary. Neoadjuvant Therapy. Paclitaxel / analogs & derivatives. Taxoids

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  • (PMID = 11668246.001).
  • [ISSN] 1340-6868
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; 80168379AG / Doxorubicin; P88XT4IS4D / Paclitaxel
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12. Behranwala KA, Nasiri N, Abdullah N, Trott PA, Gui GP: Squamous cell carcinoma of the breast: clinico-pathologic implications and outcome. Eur J Surg Oncol; 2003 May;29(4):386-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Squamous cell carcinoma of the breast: clinico-pathologic implications and outcome.
  • AIMS: Pure squamous cell carcinoma (SCC) of the breast is a rare tumour and little is known about long-term outcome.
  • METHODS: All patients with SCC treated at our institution between 1970 and 2001 were included.
  • There were seven poorly differentiated and three moderately differentiated SCC.
  • Primary treatment was mastectomy in six patients, wide local excision in four patients and radiotherapy in one patient.
  • Adjuvant chemotherapy was given to three patients and five patients received adjuvant radiotherapy.
  • Two patients developed local recurrence at 5 and 12 months and three patients developed distant metastasis at 2, 36 and 306 months.
  • Three patients were treated with chemotherapy at recurrence.
  • The 2- and 5-year overall survival was 80% (SE=13%) and 67% (SE=16%) respectively.
  • CONCLUSION: SCC of the breast adopts an aggressive course with outcome comparable to poorly differentiated breast adenocarcinoma.
  • [MeSH-major] Breast Neoplasms / diagnosis. Carcinoma, Squamous Cell / diagnosis
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Female. Humans. Lymphatic Metastasis / diagnosis. Mastectomy, Modified Radical. Mastectomy, Segmental. Medical Records. Middle Aged. Neoplasm Recurrence, Local / diagnosis. Radiotherapy, Adjuvant. Retrospective Studies. Treatment Outcome

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  • (PMID = 12711295.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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13. Tao Z, Chen FZ: [Clinical analysis of primary squamous cell carcinoma of the breast]. Zhonghua Wai Ke Za Zhi; 2003 Mar;41(3):183-5
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  • [Title] [Clinical analysis of primary squamous cell carcinoma of the breast].
  • OBJECTIVE: To study the clinicopathological features of primary squamous cell carcinoma (SCC) of breast and the diagnosis and treatment of the disease.
  • METHODS: The clinical, operative and pathological data from 7 cases of SCC of breast were retrospectively analysed.
  • All patients were diagnosed as having SCC by fine-needle aspiration before operation.
  • Pathological examination showed primary squamous cell carcinoma of the breast with metastasis to axlliary lymph nodes in one patient.
  • CONCLUSION: The diagnosis of primary squamous cell carcinoma of the breast is dependent on pathological results.
  • Radical mastectomy including modified radical mastectomy is most effective in the treatment of mammary SCC.
  • Postoperative chemotherapy and radiation are necessary auxiliary therapy.
  • [MeSH-major] Breast Neoplasms / therapy. Carcinoma, Squamous Cell / therapy

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  • (PMID = 12887775.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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14. Sharma R, Usmani S, Siegel R: Primary squamous cell carcinoma of breast in background of phyllodes tumor--a case report. Conn Med; 2009 Jun-Jul;73(6):341-3
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  • [Title] Primary squamous cell carcinoma of breast in background of phyllodes tumor--a case report.
  • Primary squamous cell carcinoma of the breast (PSCCB) is a rare and generally aggressive malignancy constituting < 0.1% of invasive breast cancers.
  • This report describes a case of primary squamous cell carcinoma of the breast that emerged in association with a phyllodes tumor.
  • Our patient, a 59-year-old female, presented with a rapidly growing 9x12 cm breast mass.
  • She underwent modified radical mastectomy followed by chemotherapy with carboplatin and docetaxel.
  • She is free of disease one year after diagnosis.
  • Clinicians should be aware of the aggressive behavior of this tumor, and adequate investigation should be done to rule out metastasis from another primary site.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Squamous Cell / pathology. Phyllodes Tumor / pathology

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  • (PMID = 19637664.001).
  • [ISSN] 0010-6178
  • [Journal-full-title] Connecticut medicine
  • [ISO-abbreviation] Conn Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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15. Tayeb K, Saâdi I, Kharmash M, Hadadi K, El Omari-Alaoui H, El Ghazi E, Mansouri A, Errihani H, Benjaafar N, El Gueddari BK: [Primary squamous cell carcinoma of the breast. Report of three cases]. Cancer Radiother; 2002 Dec;6(6):366-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Primary squamous cell carcinoma of the breast. Report of three cases].
  • Primary squamous cell carcinoma of the breast is a rare neoplasma included in metaplastic breast cancer.
  • The treatment is based on surgery associated to radiation therapy and chemotherapy.
  • Prognosis seems to be similar to others breast carcinoma.
  • We report three cases of primary squamous cell carcinoma of the breast recruited at National Institute of Oncology with review of the literature.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Squamous Cell / pathology
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Combined Modality Therapy. Female. Humans. Middle Aged. Prognosis. Radiotherapy, Adjuvant

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  • (PMID = 12504775.001).
  • [ISSN] 1278-3218
  • [Journal-full-title] Cancer radiothérapie : journal de la Société française de radiothérapie oncologique
  • [ISO-abbreviation] Cancer Radiother
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
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16. Hiramatsu K, Kato K, Hirata A, Matsuba H, Hara T, Ito T, Miyata T, Akagawa T, Kutsuna Y, Machiki Y, Fujioka S: [A resected case of squamous cell carcinoma of the breast successfully treated by FU plus cisplatin (CDDP) adjuvant therapy against recurrent metastases]. Gan To Kagaku Ryoho; 2007 Mar;34(3):443-6
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  • [Title] [A resected case of squamous cell carcinoma of the breast successfully treated by FU plus cisplatin (CDDP) adjuvant therapy against recurrent metastases].
  • A resected case of squamous cell carcinoma associated with ductal carcinoma in the hemilateral breast successfully treated by FU plus cisplatin (CDDP) adjuvant therapy against recurrent metastases is reported with some discussion.
  • A 42-year-old woman was admitted to our hospital because of right breast tumor.
  • By physical examination, mammography, ultrasound examination and aspirated cytology, we diagnosed squamous cell carcinoma of the right breast.
  • Before operation SCC antigen was elevated.
  • Standard mastectomy was performed, and SCC antigen was decreased within normal range.
  • Then, a standard regimen of chemotherapy using docetaxel with anti-hormonal therapy by LH-RH analog and tamoxifen was done as first-line adjuvant therapy.
  • Four months after operation the SCC antigen level was elevated again, and recurrence of cancer (skin and liver metastases) was recognized.
  • Next, we tried 5-FU/UFT plus CDDP for squamous cell carcinoma of other organs such as the esophagus.
  • These anti-tumor drugs proved effective, and no metastasis of the skin was detected thereafter, and liver metastatic lesion was decreased in ten months.
  • The SCC antigen level was within the normal range again.
  • Based on the present findings,we recommend adjuvant chemotherapy by FU plus CDDP for squamous cell carcinoma of the breast.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Breast Neoplasms / drug therapy. Carcinoma, Squamous Cell / drug therapy
  • [MeSH-minor] Adult. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Combined Modality Therapy. Drug Administration Schedule. Drug Combinations. Female. Fluorouracil / administration & dosage. Humans. Mastectomy. Neoplasm Invasiveness. Oxonic Acid / administration & dosage. Skin Neoplasms / pathology. Tegafur / administration & dosage. Uracil / administration & dosage

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  • (PMID = 17353640.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 56HH86ZVCT / Uracil; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil; FP protocol
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17. Bharthuar A, Khoury T, Haas KN, Mashtare T, Black J, Baer M, Yang G, Khushalani N, Iyer RV: Expression of breast cancer resistance protein (BCRP) in esophageal cancers (EC). J Clin Oncol; 2009 May 20;27(15_suppl):e13529

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of breast cancer resistance protein (BCRP) in esophageal cancers (EC).
  • Median survival remains 15-18 months despite platinum, fluropyrimidine & irinotecan based therapy.
  • BCRP is an ATP-dependent efflux protein associated with chemotherapy (CT) (e.g. irinotecan) resistance.
  • Baseline demographics, therapy given & OS data were collected and correlated with BCRP expression.
  • RESULTS: Baseline patient and tumor characteristics: Gender: M 35, F 5; Histology: 37 Adenoca & 3 SCC; Stage 1-III 27, Stage IV 10, unknown 3; CT: cisplatin+irinotecan (n=16), oxaliplatin+fluoropyrimidine (n=8), other (n=16); IHC: 30 of 40 cancers (75%) expressed BCRP [strong (n=28) & intermediate (n=3); membranous (n=17), cytoplasmic (n=27) & both (n=14)].
  • Response rates to irinotecan based therapies are seen in 30-40 % of EC, whether the 40% with low tumor BCRP constitute a majority of the responders needs to be prospectively validated in a larger dataset & should include markers that predict response to 5-FU & platinum based CT to allow individualizing therapy for this cancer.

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  • (PMID = 27961291.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Miura H, Taira O, Hiraguri S, Maeda J, Kato H: Recurrent squamous cell carcinoma of the breast with undifferentiated features: report of a case. Surg Today; 2002;32(10):891-5
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  • [Title] Recurrent squamous cell carcinoma of the breast with undifferentiated features: report of a case.
  • Squamous cell carcinoma of the breast is a rare type of cancer, the origin of which is still uncertain.
  • We report a case of squamous cell carcinoma of the breast with a recurrent tumor that showed undifferentiated features.
  • The patient was a 55-year-old woman who originally presented with a left breast mass in the upper outer quadrant.
  • Echography showed a 46 x 29 x 23-mm mass with cavity formation, and aspiration cytology confirmed a diagnosis of squamous cell carcinoma.
  • Pathologically, the tumor was composed of squamous cell carcinoma and noninvasive ductal carcinoma.
  • Despite intensive therapy including chemotherapy (CEF: cyclophosphamide, epirubicin, 5-fluorouracil) and irradiation (50 Gy), the patient died from pulmonary and skin metastases 20 months after her initial operation.
  • The squamous cell carcinoma of the breast in this patient grew rapidly and her prognosis was poor.
  • Immunohistochemical findings indicated the possibility that the squamous cell carcinoma developed from noninvasive ductal carcinoma of the comedo type, and that the undifferentiated cells from the site of recurrence developed from dedifferentiation of the squamous cell carcinoma.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Squamous Cell / pathology. Neoplasm Recurrence, Local / pathology
  • [MeSH-minor] Combined Modality Therapy. Fatal Outcome. Humans. Lung Neoplasms / secondary. Lymph Node Excision. Male. Mastectomy, Modified Radical. Middle Aged. Skin Neoplasms / secondary

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  • (PMID = 12376787.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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19. Maksimović S: [Primary squamous cell carcinoma of the breast: rare form carcinoma]. Med Arh; 2009;63(2):114-6
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  • [Title] [Primary squamous cell carcinoma of the breast: rare form carcinoma].
  • Primary squamous cell carcinoma (SCC) is a rare form of breast carcinoma.
  • We report a case of a young woman, 37-year-old, with history of a lump in the upper outer quadrant of the left breast with ulceration of the skin surface.
  • Diagnosis of the tumour of the breast was made at the Department of surgery in General Hospital in Bijeljina in September 2007.
  • Ultrasonogram of the left breast tumor identified an irregularly shaped hypoechoic lesion.
  • After clinical staging of the disease, we performed incision biopsy of the skin and tumour of the left breast with histopathology examination (standard hematoxylin and eosin).
  • After histopathology, patient's case was presented to the working group for breast tumors which decided to start with the neoadjuvant chemotherapy using platinum.
  • After six cycles of neoadjuvant chemotherapy, regression of breast tumor was confirmed.
  • Working group decided that radical mastectomy of left breast should be performed.
  • [MeSH-major] Breast Neoplasms. Carcinoma, Squamous Cell


20. Uchida N, Tsuzuki Y, Ando T, Mochida Y, Yoshikawa M, Sekihara M, Kobayashi M, Ide M, Ohno Y, Kuwano H: Malignant proliferating trichilemmal tumor in the skin over the breast: a case report. Breast Cancer; 2000 Jan;7(1):79-82
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  • [Title] Malignant proliferating trichilemmal tumor in the skin over the breast: a case report.
  • It is composed of multiple cysts consisting of squamous epithelium with trichilemmal keratinization without granular layer interposition.
  • We describe a 67-year-old woman with a malignant proliferating trichilemmal tumor in the skin over the breast.
  • We first misdiagnosed the disease as a primary squamous cell carcinoma of the breast with a metastatic lymph node in the axilla because of the disease site and our unfamiliarity with the disease.
  • To the best of our knowledge, only one case of a proliferating trichilemmal tumor occurring in the skin over the breast has been reported.
  • [MeSH-major] Breast Neoplasms / pathology. Hair Diseases / pathology. Hair Follicle / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Axilla. Carcinoma, Squamous Cell / diagnosis. Combined Modality Therapy. Cyclophosphamide / administration & dosage. Diagnostic Errors. Doxorubicin / administration & dosage. Fadrozole / administration & dosage. Female. Fluorouracil / administration & dosage. Humans. Lymphatic Metastasis. Mastectomy, Radical. Mitomycin / administration & dosage. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / surgery

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  • (PMID = 11029776.001).
  • [ISSN] 1340-6868
  • [Journal-full-title] Breast cancer (Tokyo, Japan)
  • [ISO-abbreviation] Breast Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 50SG953SK6 / Mitomycin; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; H3988M64PU / Fadrozole; U3P01618RT / Fluorouracil
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21. Chen YY, Chiang SY, Lin JG, Yang JS, Ma YS, Liao CL, Lai TY, Tang NY, Chung JG: Emodin, aloe-emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 human tongue cancer cells. Anticancer Res; 2010 Mar;30(3):945-51
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  • [Title] Emodin, aloe-emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 human tongue cancer cells.
  • In our primary studies, we have shown that emodin, aloe-emodin and rhein induced cytotoxic effects, including cell cycle arrest and apoptosis in SCC-4 human tongue cancer cells.
  • However, details regarding their effects on DNA damage and repair gene expression in SCC-4 cells are not clear.
  • We investigated whether or not emodin, aloe-emodin and rhein induced DNA damage and inhibited DNA repair gene expression in SCC-4 cells.
  • Comet assay (single cell electrophoresis) indicated that incubation of SCC-4 cells with 0, 20, 30 and 40 microM of emodin, 0, 25, 50 and 100 microM of aloe-emodin or rhein led to a longer DNA migration smear (comet tail).
  • This means that all examined agents induced DNA damage in SCC-4 cells and these effects are dose-dependent but emodin is stronger than that of aloe-emodin or rhein.
  • The results from real-time PCR assay demonstrated that 30 microM of emodin or aloe-emodin used for 24 and 48 h treatment in SCC-4 cells significantly inhibited expression of genes associated with DNA damage and repair [ataxia telangiectasia mutated (ATM); ataxia-telangiectasia and Rad3-related (ATR); 14-3-3sigma (14-3-3sigma); breast cancer 1, early onset (BRCA1); and DNA-dependent serine/threonine protein kinase (DNA-PK)]; only rhein suppressed the expression of O(6)-methylguanine-DNA methyltransferase (MGMT) mRNA with 48 h treatment, but had no effect on ATM expression.
  • On 24 h treatment, only aloe-emodin significantly affected ATM expression.
  • In conclusion, these agents induced DNA damage followed by the inhibition of DNA repair-associated gene expressions, including ATM, ATR, 14-3-3sigma, BRCA1, DNA-PK and MGMT in SCC-4 human tongue cancer cells.
  • [MeSH-major] Anthraquinones / pharmacology. DNA Repair Enzymes / antagonists & inhibitors. Emodin / pharmacology. Tongue Neoplasms / drug therapy. Tongue Neoplasms / genetics. Tumor Suppressor Proteins / antagonists & inhibitors
  • [MeSH-minor] 14-3-3 Proteins. Ataxia Telangiectasia Mutated Proteins. BRCA1 Protein / biosynthesis. BRCA1 Protein / genetics. Biomarkers, Tumor / biosynthesis. Biomarkers, Tumor / genetics. Cell Cycle Proteins / biosynthesis. Cell Cycle Proteins / genetics. Cell Line, Tumor. Comet Assay. DNA Damage. DNA Modification Methylases / biosynthesis. DNA Modification Methylases / genetics. DNA Repair / drug effects. DNA Repair / genetics. DNA-Activated Protein Kinase / biosynthesis. DNA-Activated Protein Kinase / genetics. DNA-Binding Proteins / biosynthesis. DNA-Binding Proteins / genetics. Enzyme Inhibitors / pharmacology. Exonucleases / biosynthesis. Exonucleases / genetics. Exoribonucleases. Gene Expression / drug effects. Humans. Neoplasm Proteins / biosynthesis. Neoplasm Proteins / genetics. Polymerase Chain Reaction. Protein-Serine-Threonine Kinases / biosynthesis. Protein-Serine-Threonine Kinases / genetics

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  • (PMID = 20393018.001).
  • [ISSN] 1791-7530
  • [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 / 14-3-3 Proteins; 0 / Anthraquinones; 0 / BRCA1 Protein; 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / DNA-Binding Proteins; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Proteins; C8IYT9CR7C / aloe emodin; EC 2.1.1.- / DNA Modification Methylases; EC 2.1.1.63 / MGMT protein, human; EC 2.7.11.1 / ATM protein, human; EC 2.7.11.1 / ATR protein, human; EC 2.7.11.1 / Ataxia Telangiectasia Mutated Proteins; EC 2.7.11.1 / DNA-Activated Protein Kinase; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 3.1.- / Exonucleases; EC 3.1.- / Exoribonucleases; EC 3.1.- / SFN protein, human; EC 6.5.1.- / DNA Repair Enzymes; KA46RNI6HN / Emodin; YM64C2P6UX / rhein
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22. Misra AK, Mishra A, Agrawal G, Agarwal A, Mishra SK: Occult breast carcinoma: a report of four cases and review of literature. Indian J Cancer; 2001 Mar;38(1):49-54
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  • [Title] Occult breast carcinoma: a report of four cases and review of literature.
  • We report four occult carcinoma breast cases in which extensive axillary node metastases was the first manifestation.
  • Primary tumor could be found in three patients, one had squamous cell carcinoma (SCC) & two had infiltrating duct carcinoma (IDC).
  • However primary tumor was not detected in breast tissue of the fourth patient.
  • Extensive lymph node metastases were found in three out of 14,15 out of 15(SCC), 24 out of 24 and 1 out of three axillary nodes respectively.
  • All patient received postoperative radiotherapy and chemotherapy.
  • We have reviewed the literature and discussed the approach to diagnosis and management in female patients presenting with metastatic carcinoma in the axillary nodes with emphasis on the appropriate pre-treatment evaluation.
  • [MeSH-major] Breast Neoplasms / diagnosis

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  • (PMID = 14758886.001).
  • [ISSN] 0019-509X
  • [Journal-full-title] Indian journal of cancer
  • [ISO-abbreviation] Indian J Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] India
  • [Number-of-references] 13
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23. Lutsenko SV, Feldman NB, Severin SE: Cytotoxic and antitumor activities of doxorubicin conjugates with the epidermal growth factor and its receptor-binding fragment. J Drug Target; 2002 Nov;10(7):567-71
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  • The epidermal growth factor (EGF) receptor is expressed at high levels on many types of tumor cells, such as squamous carcinoma, breast cancer and endothelial cells.
  • We studied targeted delivery of the anticancer drug doxorubicin (DOX) using EGF and its receptor-binding fragment (EGFfr) to cells able to overexpress EGF receptors.
  • The cytotoxic activities (CTA) of the conjugates were studied in vitro in different tumor cell lines (MCF-7Wt, MCF-7AdrR, B16) and endothelial cells using MTT-test.
  • Besides, the conjugates effectively decreased the drug resistance of MCF-7AdrR cells.
  • CTA of the conjugates against endothelial cell cultures markedly exceeded that of free DOX.
  • [MeSH-minor] 3T3 Cells. Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Survival / drug effects. Cells, Cultured. Female. Fibroblasts. Humans. Melanoma, Experimental / drug therapy. Melanoma, Experimental / pathology. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Tumor Cells, Cultured

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  • (PMID = 12683724.001).
  • [ISSN] 1061-186X
  • [Journal-full-title] Journal of drug targeting
  • [ISO-abbreviation] J Drug Target
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 62229-50-9 / Epidermal Growth Factor; 80168379AG / Doxorubicin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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24. Reckova M, Mego M, Rejlekova K, Sycova-Mila Z, Obertova Z, Mardiak J: Small-cell carcinoma of the ovary with breast metastases: a case report. Klin Onkol; 2010;23(1):43-5
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  • [Title] Small-cell carcinoma of the ovary with breast metastases: a case report.
  • BACKGROUNDS: Small cell carcinoma (SCC) is characterised by high metastatic potential and the possibility to metastasize to practically any tissue.
  • Small cell carcinoma of the ovary (SCCO) has a very poor prognosis and patients usually die within one year of the initial diagnosis.
  • Breast metastases from SCCO are extremely rare.
  • CASE: We present a 67-year-old female patient with SCCO who initially presented with bone and bilateral breast metastases.
  • Considering the clinical presentation, the patient's age, the absence of hypercalcemia and histological characteristics, a diagnosis of pulmonary type SCCO was made.
  • There was no tumour present in the lungs at the time of the initial diagnosis and thus we ruled out pulmonary SCC.
  • RESULTS: Initially, the patient was treated with radiotherapy of the bone lesion and systemic chemotherapy (etoposide with carboplatin) with the result of partial remission.
  • Six months later she was diagnosed with progressive disease in the bone, soft tissue including the breast as well as new lesions in the right kidney, pelvis and lungs.
  • She was treated with 2nd line chemotherapy (topotecan with cisplatin) with the result of progressive disease.
  • Shortly after brain irradiation, her status deteriorated rapidly and she died two years after her initial SCCO diagnosis.
  • CONCLUSION: Extrapulmonary small cell carcinoma is a clinicopathological entity distinct from pulmonary small cell carcinoma.
  • It is very rare and therefore there is very little information available regarding treatment of this disease.
  • In contrast to experience in the treatment of pulmonary small cell cancers, prolonged survival is not common.
  • [MeSH-major] Breast Neoplasms / secondary. Carcinoma, Small Cell / secondary. Ovarian Neoplasms / pathology

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  • (PMID = 20192073.001).
  • [ISSN] 0862-495X
  • [Journal-full-title] Klinická onkologie : casopis Ceské a Slovenské onkologické spolecnosti
  • [ISO-abbreviation] Klin Onkol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Czech Republic
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25. Rodríguez-Cuevas S, Barroso-Bravo S, Almanza-Estrada J, Cristóbal-Martínez L, González-Rodríguez E: Electrochemotherapy in primary and metastatic skin tumors: phase II trial using intralesional bleomycin. Arch Med Res; 2001 Jul-Aug;32(4):273-6
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  • [Title] Electrochemotherapy in primary and metastatic skin tumors: phase II trial using intralesional bleomycin.
  • BACKGROUND: Surgery and/or radiotherapy are the elective therapies for most primary skin cancers.
  • Nevertheless, some patients develop recurrences, and chemotherapy has resulted in poor complete responses.
  • Permeabilization of the cell membrane by electric pulses allows bleomycin to enter into the cell, increasing possibility of cytotoxicity.
  • There were basal cell carcinomas (BCC) (nine lesions), in-transit metastasis of melanoma (MM) (two patients/13 nodules), squamous cell carcinomas (SCC) of the upper aerodigestive tract metastatic to the skin (two patients/two nodules), and skin metastases from breast cancer (two patients/14 nodules).
  • No complications were documented related to the treatment and tolerance was adequate.
  • CONCLUSIONS: Electrochemotherapy (ECT) is a new cancer modality of treatment that is effective in a variety of skin cancers.
  • This treatment represents an excellent alternative to standard surgery or radiotherapy, with an outpatient-based treatment applied in one to three sessions.
  • The major impact was obtained in BBC, but ECT is a useful palliative therapy in melanoma, breast cancer, or SCC.
  • [MeSH-major] Antibiotics, Antineoplastic / administration & dosage. Bleomycin / administration & dosage. Carcinoma, Basal Cell / drug therapy. Carcinoma, Ductal, Breast / secondary. Carcinoma, Squamous Cell / secondary. Electroporation. Melanoma / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Aged. Breast Neoplasms. Cell Membrane Permeability. Facial Neoplasms / drug therapy. Facial Neoplasms / secondary. Female. Humans. Injections, Intralesional. Male. Middle Aged. Muscle Contraction. Palliative Care. Remission Induction. Treatment Outcome

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  • (PMID = 11440782.001).
  • [ISSN] 0188-4409
  • [Journal-full-title] Archives of medical research
  • [ISO-abbreviation] Arch. Med. Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 11056-06-7 / Bleomycin
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26. Ye F, Xui L, Yi J, Zhang W, Zhang DY: Anticancer activity of Scutellaria baicalensis and its potential mechanism. J Altern Complement Med; 2002 Oct;8(5):567-72
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Scutellaria baicalensis is a widely used Chinese herbal medicine that historically is used in anti-inflammatory and anticancer therapy.
  • METHODS: Cell lines from the most common human cancers, including squamous cell carcinoma (SCC-25, KB), breast cancer (MCF-7), hepatocellular carcinoma (HepG2), prostate carcinoma (PC-3 and LNCaP), and colon cancer (KM-12 and HCT-15) were tested.
  • Percentage of viable cells after treatment was assessed using a trypan blue dye exclusion assay and the level of PGE(2) production was determined by enzyme immunoassay (EIA).
  • RESULTS: Scutellaria baicalensis demonstrated a strong dose-dependent growth inhibition in all cell lines.
  • Inhibition concentration at 50% (IC(50)) for HepG2, MCF-7, PC-3, LNCaP, KM-12, HCT-15, KB and SCC-25 cells was 1.1, 0.9, 0.52, 0.82, 1.1, 1.5, 1.0, and 1.2 mg/mL, respectively.
  • Three cell lines (KB, SCC-25, and HepG2) were assessed for the production of PGE(2) and a high level of extracellular (KB and SCC-25) and intracellular PGE(2) (HepG2) was noted.
  • CONCLUSIONS: Scutellaria baicalensis strongly inhibits cell growth in all cancer cell lines tested.
  • However, prostate and breast cancer cells (PC-3, LNCaP, and MCF-7) are slightly more sensitive than other type of cancer cells.
  • It also inhibits PGE(2) production, indicating that suppression of tumor cell growth may be due to its ability to inhibit COX-2 activity.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Dinoprostone / antagonists & inhibitors. Growth Inhibitors / pharmacology. Neoplasms / drug therapy. Phytotherapy / methods. Scutellaria baicalensis
  • [MeSH-minor] Arachidonic Acid / metabolism. Breast Neoplasms / drug therapy. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Squamous Cell / drug therapy. Colonic Neoplasms / drug therapy. Cyclooxygenase 2. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Female. Humans. In Vitro Techniques. Isoenzymes / metabolism. Liver Neoplasms / drug therapy. Male. Membrane Proteins. Prostaglandin-Endoperoxide Synthases / metabolism. Prostatic Neoplasms / drug therapy. Tumor Cells, Cultured / drug effects

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  • (PMID = 12470437.001).
  • [ISSN] 1075-5535
  • [Journal-full-title] Journal of alternative and complementary medicine (New York, N.Y.)
  • [ISO-abbreviation] J Altern Complement Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Growth Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 27YG812J1I / Arachidonic Acid; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; K7Q1JQR04M / Dinoprostone
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27. Wietrzyk J, Chodyński M, Fitak H, Wojdat E, Kutner A, Opolski A: Antitumor properties of diastereomeric and geometric analogs of vitamin D3. Anticancer Drugs; 2007 Apr;18(4):447-57
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  • Analogs of 1,25-dihydroxyvitamin D3 with a reversed configuration at C-1 or C-24 and E or Z geometry of the double bond at C-22 in the side chain or at C-5 in the triene system were examined for their antiproliferative activity in vitro against a spectrum of various human cancer cell lines.
  • The analogs coded PRI-2201 (calcipotriol), PRI-2202 and PRI-2205, such as calcitriol and tacalcitol (used as a referential agents), revealed antiproliferative activity against human HL-60, HL-60/MX2, MCF-7, T47D, SCC-25 and mouse WEHI-3 cancer cell lines.
  • Calcitriol and tacalcitol showed toxicity in the same protocol at 100 times lower doses.
  • [MeSH-minor] Animals. Antigens, CD11b / metabolism. Antigens, CD14 / metabolism. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Calcitriol / analogs & derivatives. Calcitriol / pharmacology. Calcium / blood. Carcinoma, Lewis Lung / drug therapy. Carcinoma, Lewis Lung / pathology. Cell Cycle / drug effects. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Coloring Agents. Female. Fibroblasts / metabolism. HL-60 Cells. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Inbred DBA. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / pathology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Rhodamines. Stereoisomerism. Tetrazolium Salts. Thiazoles

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  • (PMID = 17351397.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Antigens, CD14; 0 / Antineoplastic Agents; 0 / Coloring Agents; 0 / Rhodamines; 0 / Tetrazolium Salts; 0 / Thiazoles; 143NQ3779B / calcipotriene; 1C6V77QF41 / Cholecalciferol; 2609-88-3 / lissamine rhodamine B; 298-93-1 / thiazolyl blue; FXC9231JVH / Calcitriol; SY7Q814VUP / Calcium
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28. Gadducci A, Cosio S, Carpi A, Nicolini A, Genazzani AR: Serum tumor markers in the management of ovarian, endometrial and cervical cancer. Biomed Pharmacother; 2004 Jan;58(1):24-38
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  • CA 125 is the most reliable serum marker for ovarian carcinoma.
  • Whereas its role in the screening of the malignancy is controversial, serum CA 125 assay is very useful for both the differential diagnosis of ovarian masses, particularly in postmenopause, and the monitoring of the response to chemotherapy and follow-up of patients with histologically proven ovarian carcinoma.
  • Tumor-associated antigens other than CA 125, such as CA 19.9, CA 15.3 and TAG.72, firstly identified in gastro-intestinal or breast malignancies, have been detected also in tissue and serum samples from patients with ovarian carcinoma.
  • Serum CA 125 correlates with the clinical course of disease better than the other antigens, and in patients with positive CA 125 assay at diagnosis the concomitant evaluation of CA 19.9 or CA 72.4 or CA 15.3 does not offer any additional benefit for monitoring ovarian carcinoma.
  • Serum alphaFP and betaHCG are very useful in the preoperative evaluation and management of nondysgerminomatous ovarian germ cell tumors, whereas elevated serum inhibin levels can be detected in patients with granulosa cell tumors of the ovary.
  • As for endometrial carcinoma, preoperative serum CA 125 levels correlate with stage, depth of myometrial invasion, histologic grade, cervical invasion, peritoneal cytology, lymph node status and clinical outcome.
  • Moreover, serial CA 125 assay is a good indicator of disease activity and a useful biochemical tool for post-treatment surveillance of patients with endometrial carcinoma.
  • SCC is the most reliable serum marker for squamous cell cervical carcinoma, and in patients with this malignancy pretreatment SCC levels are related to tumor stage, tumor size, depth of cervical invasion, lymph-vascular space involvement, lymph node status and clinical outcome.
  • Serial SCC measurements parallel the response to radiotherapy and chemotherapy as well as the clinical course of disease after the completion of treatment.
  • Serum CYFRA 21.1 seems to be less sensitive than serum SCC for squamous cell cervical carcinoma.
  • [MeSH-major] Biomarkers, Tumor / blood. Endometrial Neoplasms / blood. Endometrial Neoplasms / therapy. Ovarian Neoplasms / blood. Ovarian Neoplasms / therapy. Uterine Cervical Neoplasms / blood. Uterine Cervical Neoplasms / therapy


29. Song W, Dong Z, Jin T, Mantellini MG, Núñez G, Nör JE: Cancer gene therapy with iCaspase-9 transcriptionally targeted to tumor endothelial cells. Cancer Gene Ther; 2008 Oct;15(10):667-75
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  • [Title] Cancer gene therapy with iCaspase-9 transcriptionally targeted to tumor endothelial cells.
  • Antiangiogenic therapies have shown varying results partly because each tumor type secretes a distinct panel of angiogenic factors to sustain its own microvascular network.
  • In addition, recent evidence demonstrated that tumors develop resistance to antiangiogenic therapy by turning on alternate angiogenic pathways when one pathway is therapeutically inhibited.
  • Here, we test the hypothesis that expression of a caspase-based artificial death switch in tumor-associated endothelial cells will disrupt tumor blood vessels and slow down tumor progression irrespective of tumor type.
  • Adenoviral vectors expressing inducible Caspase-9 (iCaspase-9) under transcriptional regulation with the endothelial cell-specific vascular endothelial growth factor receptor-2 (VEGFR2) promoter (Ad-hVEGFR2-iCaspase-9) induced apoptosis of proliferating human dermal microvascular endothelial cells (HDMECs), but not human tumor cells (UM-SCC-17B, head and neck squamous cell carcinoma; HepG2, hepatocellular carcinoma; PC-3, prostate adenocarcinoma; SLK, Kaposi's sarcoma; MCF-7, breast adenocarcinoma).
  • Notably, apoptosis was dependent upon activation of iCaspase-9 with the dimerizer drug AP20187.
  • We conclude that a cancer gene therapy strategy based on a transcriptionally targeted viral vector expressing an inducible caspase allows for selective and controlled ablation of microvessels of histopathologically diverse tumor types.

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  • [Cites] Carcinogenesis. 2000 Mar;21(3):505-15 [10688871.001]
  • [Cites] Gene Ther. 2000 Jan;7(2):110-4 [10673715.001]
  • [Cites] Science. 2000 Aug 18;289(5482):1197-202 [10947988.001]
  • [Cites] Cancer Res. 2000 Nov 1;60(21):6142-7 [11085538.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):2183-8 [11280784.001]
  • [Cites] Lab Invest. 2001 Apr;81(4):453-63 [11304564.001]
  • [Cites] Cancer Res. 2001 Sep 15;61(18):6795-804 [11559553.001]
  • [Cites] Gene Ther. 2002 Apr;9(7):444-51 [11938459.001]
  • [Cites] Int J Cancer. 1994 Nov 15;59(4):520-9 [7525492.001]
  • [Cites] Cancer Res. 1996 Apr 1;56(7):1615-20 [8603410.001]
  • [Cites] Sci Am. 1996 Sep;275(3):150-4 [8701285.001]
  • [Cites] Science. 1998 Jan 16;279(5349):377-80 [9430587.001]
  • [Cites] Hum Gene Ther. 1997 Dec 10;8(18):2239-47 [9449377.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3655-60 [9520421.001]
  • [Cites] Surg Oncol Clin N Am. 1998 Jul;7(3):505-36 [9624215.001]
  • [Cites] J Biol Chem. 1998 Dec 11;273(50):33489-94 [9837928.001]
  • [Cites] Curr Top Microbiol Immunol. 1999;237:1-30 [9893343.001]
  • [Cites] Hum Gene Ther. 1999 Sep 20;10(14):2273-85 [10515447.001]
  • [Cites] Exp Physiol. 2005 Jan;90(1):27-31 [15542621.001]
  • [Cites] Gene Ther. 2005 Feb;12(4):320-9 [15616606.001]
  • [Cites] Mol Ther. 2005 Aug;12(2):189-211 [15946903.001]
  • [Cites] Cancer Cell. 2005 Oct;8(4):299-309 [16226705.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 May;8(5):405-13 [17377525.001]
  • [Cites] Exp Cell Res. 2007 Oct 1;313(16):3645-57 [17720154.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):334-41 [10667585.001]
  • [Cites] Gene Ther. 2000 May;7(10):896-902 [10845728.001]
  • (PMID = 18566614.001).
  • [ISSN] 1476-5500
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] ENG
  • [Grant] United States / NIDCR NIH HHS / DE / R01-DE15948; United States / NIDCR NIH HHS / DE / R01 DE014601-01; United States / NIDCR NIH HHS / DE / R01 DE014601; United States / NIDCR NIH HHS / DE / R01 DE016586-01; United States / NIDCR NIH HHS / DE / R01-DE14601; United States / NIDCR NIH HHS / DE / R01 DE016586; United States / NIDCR NIH HHS / DE / R01 DE015948-01; United States / NIDCR NIH HHS / DE / R01-DE16586; United States / NIDCR NIH HHS / DE / R01 DE015948
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AP20187; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; EC 3.4.22.- / Caspase 9; WM0HAQ4WNM / Tacrolimus
  • [Other-IDs] NLM/ NIHMS96109; NLM/ PMC2665693
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30. Feng W, Duan X, Liu J, Xiao J, Brown RE: Morphoproteomic evidence of constitutively activated and overexpressed mTOR pathway in cervical squamous carcinoma and high grade squamous intraepithelial lesions. Int J Clin Exp Pathol; 2009;2(3):249-60
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  • [Title] Morphoproteomic evidence of constitutively activated and overexpressed mTOR pathway in cervical squamous carcinoma and high grade squamous intraepithelial lesions.
  • Preclinical in vitro and in vivo studies using HPV-containing human cervical carcinoma cell lines have shown that the mammalian target of rapamycin (mTOR) inhibitor, rapamycin, and epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor, erlotinib, can induce growth delay of xenografts.
  • Activation of Akt and mTOR are also observed in cervical squamous cell carcinoma and, the expression of phosphorylated mTOR was reported to serve as a marker to predict response to chemotherapy and survival of cervical cancer patients.
  • Therefore, we investigated: a) the expression level of EGFR in cervical squamous cell carcinoma (SCC) and high-grade squamous intraepithelial lesions (HSIL) versus non-neoplastic cervical squamous epithelium;.
  • b) the state of activation of the mTOR pathway in these same tissues; and c) any impact of these signal transduction molecules on cell cycle.
  • Formalin-fixed paraffin-embedded tissue microarray blocks containing 20 samples each of normal cervix, HSIL and invasive SCC, derived from a total of 60 cases of cervical biopsies and cervical conizations were examined.
  • Immunohistochemistry was utilized to detect the following antigens: EGFR; mTOR pathway markers, phosphorylated (p)-mTOR (Ser2448) and p-p70S6K (Thr389); and cell cycle associated proteins, Ki-67 and S phase kinase-associated protein (Skp)2.
  • We found that plasmalemmal EGFR expression was limited to the basal/parabasal cells (2-3+, EI = 67) in normal cervical epithelium (NL), but was diffusely positive in all HSIL (EI = 237) and SCC (EI 226).
  • The pattern of cytoplasmic p-mTOR and nuclear p-p70S6K expression was similar to that of EGFR; all showed a significantly increased EI in HSIL/SCC versus NL (p<0.02).
  • Nuclear translocation of p-mTOR was observed in all SCC lesions (EI = 202) and was significantly increased versus both HSIL (EI = 89) and NL (EI = 54) with p<0.015 and p<0.0001, respectively.
  • Concomitant increases in MI and proportion of nuclear Ki-67 and Skp2 expression were noted in HSIL and SCC.
  • In conclusion, morphoproteomic analysis reveals constitutive activation and overexpression of the mTOR pathway in HSIL and SCC as evidenced by: increased nuclear translocation of pmTOR and p-p70S6K, phosphorylated at putative sites of activation, Ser2448 and Thr389, respectively; correlative overexpression of the upstream signal transducer, EGFR, and increases in cell cycle correlates, Skp2 and mitotic indices.
  • These results suggest that the mTOR pathway plays a key role in cervical carcinogenesis and targeted therapies may be developed for SCC as well as its precursor lesion, HSIL.


31. Liu Z, Liu Y, Jia B, Zhao H, Jin X, Li F, Chen X, Wang F: Epidermal growth factor receptor-targeted radioimmunotherapy of human head and neck cancer xenografts using 90Y-labeled fully human antibody panitumumab. Mol Cancer Ther; 2010 Aug;9(8):2297-308
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  • Panitumumab (ABX-EGF or Vectibix), the first fully human monoclonal antibody targeting epidermal growth factor receptor (EGFR), was approved by the Food and Drug Administration for treatment of patients with metastatic colorectal cancer.
  • Here, we report for the first time the radioimmunotherapy (RIT) of EGFR-positive human head and neck cancer in a nude mouse model using pure beta(-) emitter (90)Y-labeled panitumumab.
  • The RIT efficacy of (90)Y-DOTA-panitumumab was evaluated in UM-SCC-22B tumor model.
  • CD31, Ki67, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and H&E staining were done on UM-SCC-22B tumor sections after treatment.
  • The tumor uptake of (111)In-DOTA-panitumumab in UM-SCC-22B tumor-bearing nude mice was 26.10 +/- 4.93, 59.11 +/- 7.22, 44.57 +/- 9.80, 40.38 +/- 7.76, and 14.86 +/- 7.23 % injected dose per gram of tissue at 4, 24, 72, 120, and 168 hours after injection, respectively.
  • RIT with a single dose of 100 microCi (90)Y-DOTA-panitumumab caused significant tumor growth delay and improved the survival in UM-SCC-22B tumor model.
  • A single dose of 200 microCi (90)Y-DOTA-panitumumab led to almost complete tumor regression (tumor volumes were 34.83 +/- 11.11 mm(3) and 56.02 +/- 39.95 mm(3) on days 0 and 46 after treatment, respectively).
  • Histopathologic analysis of tumors and normal organs further validated the therapeutic efficacy and limited systemic toxicity of (90)Y-DOTA-panitumumab.
  • The high tumor uptake and prolonged tumor retention, as well as effective therapy, reveal that (90)Y-DOTA-panitumumab may be a promising radioimmunotherapeutic agent to treat EGFR-positive solid tumors.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Head and Neck Neoplasms / drug therapy. Head and Neck Neoplasms / radiotherapy. Radioimmunotherapy / methods. Receptor, Epidermal Growth Factor / immunology. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Line, Tumor. Fluorescent Antibody Technique. Gamma Cameras. Humans. Mice. Organometallic Compounds / pharmacology. Organometallic Compounds / therapeutic use. Tissue Distribution / drug effects. Yttrium Radioisotopes

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  • [Copyright] (c) 2010 AACR.
  • [Cites] Invest New Drugs. 1999;17(3):259-69 [10665478.001]
  • [Cites] Clin Cancer Res. 2010 Apr 1;16(7):2095-105 [20215534.001]
  • [Cites] J Nucl Med. 2000 May;41(5):903-11 [10809207.001]
  • [Cites] Head Neck. 2001 Jul;23(7):559-65 [11400244.001]
  • [Cites] J Clin Oncol. 2001 Jul 1;19(13):3234-43 [11432891.001]
  • [Cites] J Nucl Med. 2001 Oct;42(10):1530-7 [11585869.001]
  • [Cites] Cancer. 2002 Mar 1;94(5):1593-611 [11920518.001]
  • [Cites] Cancer Res. 2002 Aug 1;62(15):4300-6 [12154033.001]
  • [Cites] Cancer Res. 2002 Dec 15;62(24):7350-6 [12499279.001]
  • [Cites] Bioconjug Chem. 2004 Mar-Apr;15(2):235-41 [15025518.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1201-8 [14993230.001]
  • [Cites] Nat Rev Drug Discov. 2004 Jun;3(6):488-99 [15173838.001]
  • [Cites] N Engl J Med. 2004 Jul 22;351(4):337-45 [15269313.001]
  • [Cites] Biochem Biophys Res Commun. 1978 Feb 28;80(4):849-57 [637870.001]
  • [Cites] N Engl J Med. 1993 Jan 21;328(3):184-94 [8417385.001]
  • [Cites] J Nucl Med. 1993 Nov;34(11):1953-63 [8229241.001]
  • [Cites] Head Neck. 1997 Sep;19(6):500-5 [9278758.001]
  • [Cites] Eur J Nucl Med. 1998 Nov;25(11):1562-5 [9799354.001]
  • [Cites] Cancer. 2004 Nov 15;101(10):2222-9 [15452834.001]
  • [Cites] J Nucl Med. 2005 Jan;46 Suppl 1:13S-7S [15653647.001]
  • [Cites] J Nucl Med. 2005 Jan;46 Suppl 1:141S-50S [15653662.001]
  • [Cites] Cancer Metastasis Rev. 2005 Jan;24(1):129-46 [15785877.001]
  • [Cites] Anticancer Drugs. 2006 Aug;17(7):855-7 [16926635.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9673-81 [17018625.001]
  • [Cites] J Clin Oncol. 2006 Oct 20;24(30):4914-21 [17050875.001]
  • [Cites] Anticancer Drugs. 2007 Jan;18(1):7-15 [17159497.001]
  • [Cites] Curr Cancer Drug Targets. 2006 Dec;6(8):691-710 [17168674.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2007 Jun;34(6):850-8 [17262214.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 15;104(20):8444-8 [17488826.001]
  • [Cites] Breast Cancer Res Treat. 2007 Jul;104(1):13-9 [17004106.001]
  • [Cites] N Engl J Med. 2008 Sep 11;359(11):1143-54 [18784104.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):6154-60 [18829494.001]
  • [Cites] Clin Cancer Res. 2008 Nov 15;14(22):7330-9 [19010848.001]
  • [Cites] Cancer Chemother Pharmacol. 2009 Feb;63(3):567 [18500520.001]
  • [Cites] J Nucl Med. 2009 Jan;50(1):123-31 [19091906.001]
  • [Cites] Cancer. 2009 Mar 1;115(5):922-35 [19156911.001]
  • [Cites] Cancer Biother Radiopharm. 2009 Feb;24(1):15-24 [19216631.001]
  • [Cites] J Nucl Med. 2009 Jul;50(7):1116-23 [19525473.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2009 Sep;36(9):1483-94 [19360404.001]
  • [Cites] J Nucl Med. 2009 Dec;50(12):2008-16 [19949026.001]
  • [Cites] Cancer Res. 2009 Dec 1;69(23):8941-8 [19920193.001]
  • [Cites] Mol Imaging. 2010 Feb;9(1):21-9 [20128995.001]
  • [Cites] Clin Cancer Res. 2000 Feb;6(2):701-8 [10690556.001]
  • (PMID = 20682654.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 EB999999; United States / Intramural NIH HHS / / ZIA EB000073-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Organometallic Compounds; 0 / Yttrium Radioisotopes; 0 / panitumumab; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ NIHMS454864; NLM/ PMC3629966
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32. Burns MR, Graminski GF, Weeks RS, Chen Y, O'Brien TG: Lipophilic lysine-spermine conjugates are potent polyamine transport inhibitors for use in combination with a polyamine biosynthesis inhibitor. J Med Chem; 2009 Apr 9;52(7):1983-93
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  • The attachment of a length-optimized C(16) lipophilic substituent to the epsilon-nitrogen atom of an earlier lead compound, D-Lys-Spm (5), has produced an analogue, D-Lys(C(16)acyl)-Spm (11) with several orders of magnitude more potent cell growth inhibition on a variety of cultured cancer cell types including breast (MDA-MB-231), prostate (PC-3), melanoma (A375), and ovarian (SK-OV-3), among others.
  • The resulting novel two-drug combination therapy targeting cellular polyamine metabolism has shown exceptional efficacy against cutaneous squamous cell carcinomas (SCC) in a transgenic ornithine decarboxylase (ODC) mouse model of skin cancer.
  • A majority (88%) of large, aggressive SCCs exhibited complete or nearly complete remission to this combination therapy, whereas responses to each agent alone were poor.
  • The availability of a potent polyamine transport inhibitor allows, for the first time, for a real test of the hypothesis that starving cells of polyamines will lead to objective clinical response.

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  • [Cites] Clin Dermatol. 1995 Nov-Dec;13(6):621-6 [8882774.001]
  • [Cites] Protein Sci. 1996 Oct;5(10):1984-90 [8897598.001]
  • [Cites] J Biol Chem. 1996 Nov 1;271(44):27556-63 [8910341.001]
  • [Cites] Cancer Res. 1997 Jan 15;57(2):234-9 [9000561.001]
  • [Cites] Cell. 1997 Jan 24;88(2):223-33 [9008163.001]
  • [Cites] Biophys J. 1997 May;72(5):2014-31 [9129805.001]
  • [Cites] J Med Chem. 1997 May 9;40(10):1475-94 [9154970.001]
  • [Cites] Cancer Res. 1997 Jul 1;57(13):2630-7 [9205069.001]
  • [Cites] Bioconjug Chem. 1997 Nov-Dec;8(6):891-5 [9404663.001]
  • [Cites] Trends Cell Biol. 1998 Feb;8(2):84-7 [9695814.001]
  • [Cites] J Drug Target. 1998;6(1):65-77 [9769022.001]
  • [Cites] J Biol Chem. 1999 Feb 5;274(6):3265-7 [9920864.001]
  • [Cites] Biochem J. 1999 Mar 1;338 ( Pt 2):317-23 [10024506.001]
  • [Cites] Biochem Soc Trans. 1998 Nov;26(4):595-601 [10047789.001]
  • [Cites] Antimicrob Agents Chemother. 1999 May;43(5):1267-9 [10223949.001]
  • [Cites] Chem Biol. 1999 Oct;6(10):717-29 [10508681.001]
  • [Cites] J Biol Chem. 2004 Nov 19;279(47):49355-66 [15208319.001]
  • [Cites] J Am Chem Soc. 2004 Dec 15;126(49):15930-1 [15584704.001]
  • [Cites] Bioorg Med Chem. 2005 Apr 1;13(7):2523-36 [15755654.001]
  • [Cites] Chembiochem. 2005 Dec;6(12):2126-42 [16254940.001]
  • [Cites] Eur Biophys J. 2006 Jan;35(2):92-103 [16217647.001]
  • [Cites] Int J Cancer. 2006 May 1;118(9):2344-9 [16331620.001]
  • [Cites] J Am Chem Soc. 2006 Sep 6;128(35):11463-70 [16939269.001]
  • [Cites] J Am Chem Soc. 2007 Jan 17;129(2):268-9 [17212394.001]
  • [Cites] Mol Cancer Ther. 2007 Feb;6(2):782-8 [17308074.001]
  • [Cites] Med Res Rev. 2007 Sep;27(5):696-722 [17022036.001]
  • [Cites] Bioorg Med Chem Lett. 2003 Oct 6;13(19):3267-71 [12951106.001]
  • [Cites] J Am Chem Soc. 2003 Nov 19;125(46):13984-7 [14611234.001]
  • [Cites] J Biol Chem. 2003 Nov 21;278(47):47181-9 [12972423.001]
  • [Cites] J Am Chem Soc. 2003 Nov 26;125(47):14348-56 [14624583.001]
  • [Cites] J Pept Sci. 2003 Nov-Dec;9(11-12):679-89 [14658789.001]
  • [Cites] Biochem J. 2004 Feb 15;378(Pt 1):93-103 [14609430.001]
  • [Cites] J Nat Prod. 2004 May;67(5):811-6 [15165142.001]
  • [Cites] Annu Rev Biochem. 2004;73:559-87 [15189153.001]
  • [Cites] J Am Chem Soc. 2004 Aug 11;126(31):9506-7 [15291531.001]
  • [Cites] J Cell Biol. 1976 Mar;68(3):512-20 [192729.001]
  • [Cites] J Antimicrob Chemother. 2003 May;51(5):1159-65 [12697647.001]
  • [Cites] J Med Chem. 2003 Jun 19;46(13):2672-82 [12801231.001]
  • [Cites] Cell Mol Biol. 1991;37(8):773-83 [1807787.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Feb 15;90(4):1354-8 [8433993.001]
  • [Cites] Eur Urol. 1993;24(1):124-31 [7689970.001]
  • [Cites] Am J Physiol. 1994 Mar;266(3 Pt 1):C776-83 [8166241.001]
  • [Cites] J Am Acad Dermatol. 1994 May;30(5 Pt 1):774-8 [8176018.001]
  • [Cites] Anticancer Res. 1994 Mar-Apr;14(2A):443-8 [8017845.001]
  • [Cites] J Med Chem. 1994 Oct 14;37(21):3464-76 [7932575.001]
  • [Cites] Science. 1994 Oct 21;266(5184):433-5 [7939682.001]
  • [Cites] Cancer Res. 1995 Oct 1;55(19):4205-9 [7671221.001]
  • [Cites] J Biol Chem. 1996 Apr 19;271(16):9519-25 [8621624.001]
  • [Cites] Glycobiology. 1996 Mar;6(2):121-9 [8727784.001]
  • [Cites] Int J Biochem Cell Biol. 1996 Aug;28(8):843-61 [8811834.001]
  • [Cites] Biochim Biophys Acta. 1978 Apr 6;473(3-4):241-93 [350276.001]
  • [Cites] Biochemistry. 1980 Jul 8;19(14):3307-14 [6250564.001]
  • [Cites] Biochem J. 1980 Dec 15;192(3):941-5 [6786285.001]
  • [Cites] Adv Cancer Res. 1981;35:151-268 [7041538.001]
  • [Cites] Adv Cancer Res. 1982;36:1-102 [6289636.001]
  • [Cites] Science. 1983 Mar 4;219(4588):1083-5 [6823570.001]
  • [Cites] Science. 1983 Aug 12;221(4611):673-5 [6603020.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5774-8 [2874556.001]
  • [Cites] J Chromatogr. 1986 Jul 11;380(1):19-32 [3745383.001]
  • [Cites] Cell. 1988 Dec 23;55(6):1189-93 [2849510.001]
  • [Cites] J Dermatol Surg Oncol. 1989 Mar;15(3):315-28 [2646336.001]
  • [Cites] Int J Biochem. 1990;22(3):211-8 [2110083.001]
  • [Cites] Pharm Res. 2007 Nov;24(11):1977-92 [17443399.001]
  • [Cites] Int J Oncol. 2008 Apr;32(4):749-56 [18360702.001]
  • [Cites] J Am Chem Soc. 2008 Aug 6;130(31):10064-5 [18613675.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Jun;1(1):32-8 [18841250.001]
  • [Cites] Cancer Res. 1990 Aug 15;50(16):5077-83 [2116224.001]
  • [Cites] Anticancer Res. 2000 Jan-Feb;20(1A):97-101 [10769640.001]
  • [Cites] Breast Cancer Res Treat. 2000 Mar;60(2):99-105 [10845272.001]
  • [Cites] J Am Chem Soc. 2001 Aug 8;123(31):7691-6 [11480993.001]
  • [Cites] Antimicrob Agents Chemother. 2001 Sep;45(9):2441-9 [11502512.001]
  • [Cites] Peptides. 2001 Oct;22(10):1675-81 [11587796.001]
  • [Cites] J Med Chem. 2001 Oct 25;44(22):3632-44 [11606128.001]
  • [Cites] Biochemistry. 2002 Feb 19;41(7):2254-63 [11841217.001]
  • [Cites] J Med Chem. 2002 Aug 15;45(17):3612-8 [12166934.001]
  • [Cites] Int J Antimicrob Agents. 2003 Jan;21(1):13-9 [12507833.001]
  • [Cites] Curr Protein Pept Sci. 2003 Apr;4(2):105-24 [12678850.001]
  • [Cites] Biochemistry. 2003 Apr 22;42(15):4311-20 [12693927.001]
  • (PMID = 19281226.001).
  • [ISSN] 1520-4804
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA094107-07; United States / NCI NIH HHS / CA / R01 CA094107; United States / NCI NIH HHS / CA / 5R01CA094107-07; United States / NCI NIH HHS / CA / R01 CA094107-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Polyamines; 0 / lysyl-epsilon-palmitoyl-N1-spermine; 2FZ7Y3VOQX / Spermine; EC 4.1.1.17 / Ornithine Decarboxylase; K3Z4F929H6 / Lysine; ZQN1G5V6SR / Eflornithine
  • [Other-IDs] NLM/ NIHMS103358; NLM/ PMC2714422
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