Common origins of MDA-MB-435 cells from various sources with those shown to have melonoma properties

Recently, the tissue origin of MDA-MB-435 cell line has been the subject of considerable debate. In this study, we set out to determine whether MDA-MB-435-DTP cells shown to express melanoma-specific genes were identical to various other MDA-MB-435 cell stocks worldwide. CGH-microarray, genetic polymorphism genotyping, microsatellite fingerprint analysis and/or chromosomal number confirmed that the MDA-MB-435 cells maintained at the Lombardi Comprehensive Cancer Center (MDA-MB-435-LCC) are almost identical to the MDA-MB-435-DTP cells, and showed a very similar profile to those obtained from the same original source (MD Anderson Cancer Center) but maintained independently (MDA-MB-435-PMCC). Gene expression profile analysis confirmed common expression of genes among different MDA-MB-435-LCC cell stocks, and identified some unique gene products in MDA-MB-435-PMCC cells. RT-PCR analysis confirmed the expression of the melanoma marker tyrosinase across multiple MDA-MB-435 cell stocks. Collectively, our results show that the MDA-MB-435 cells used widely have identical origins to those that exhibit a melanoma-like gene expression signature, but exhibit a small degree of genotypic and phenotypic drift.

[1]  G. Ellison,et al.  Further evidence to support the melanocytic origin of MDA-MB-435 , 2002, Molecular pathology : MP.

[2]  C Caldas,et al.  Molecular cytogenetic analysis of breast cancer cell lines , 2000, British Journal of Cancer.

[3]  G. Nicolson,et al.  Multiple phenotypic divergence of mammary adenocarcinoma cell clones , 1984, Clinical & Experimental Metastasis.

[4]  T. Shike,et al.  Animal models. , 2001, Contributions to nephrology.

[5]  Christian A. Rees,et al.  Systematic variation in gene expression patterns in human cancer cell lines , 2000, Nature Genetics.

[6]  G. Nicolson,et al.  Immunization with a vaccine that combines the expression of MUC1 and B7 co-stimulatory molecules prolongs the survival of mice and delays the appearance of mouse mammary tumors , 2004, Clinical & Experimental Metastasis.

[7]  J. Talmadge,et al.  Relationship of macrophage content, immunogenicity, and metastatic potential of a murine osteosarcoma of recent origin , 2005, Clinical & Experimental Metastasis.

[8]  J. Scheys,et al.  Genotyping for polymorphic drug metabolizing enzymes from paraffin-embedded and immunohistochemically stained tumor samples. , 2003, Pharmacogenetics.

[9]  T. Hsu,et al.  Cytogenetic analysis on eight human breast tumor cell lines: high frequencies of 1q, 11q and HeLa-like marker chromosomes. , 1981, Cancer genetics and cytogenetics.

[10]  G. Nicolson,et al.  Phenotypic drift and heterogeneity in response of metastatic mammary adenocarcinoma cell clones to Adriamycin, 5-fluoro-2′-deoxyuridine and methotrexate treatment in vitro , 1983, Clinical & Experimental Metastasis.

[11]  Nasreen S Jessani,et al.  Enzyme activity profiles of the secreted and membrane proteome that depict cancer cell invasiveness , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[12]  Jeffrey W. Smith,et al.  Gene expression profiling of tumor xenografts: In vivo analysis of organ‐specific metastasis , 2003, International journal of cancer.

[13]  M. Waltham,et al.  LCC15-MB Cells are MDA-MB-435: A Review of Misidentified Breast and prostate cell lines , 2004, Clinical & Experimental Metastasis.

[14]  T. Hirano,et al.  Examination of oncogene amplification by genomic DNA microarray in hepatocellular carcinomas: comparison with comparative genomic hybridization analysis. , 2001, Cancer genetics and cytogenetics.

[15]  J N Weinstein,et al.  A protein expression database for the molecular pharmacology of cancer , 1997, Electrophoresis.

[16]  M. Gottesman,et al.  MDA435/LCC6 and MDA435/LCC6MDR1: ascites models of human breast cancer. , 1996, British Journal of Cancer.

[17]  P. Drew,et al.  Karyotypic variation between independently cultured strains of the cell line MCF-7 identified by multicolour fluorescence in situ hybridization. , 2002, International journal of oncology.

[18]  G. Nicolson,et al.  Heterogeneous response and clonal drift of sensitivities of metastatic 13762NF mammary adenocarcinoma clones to gamma-radiation in vitro. , 1983, Cancer research.

[19]  J. Russo,et al.  In Vitro Models for Human Breast Cancer , 2004 .

[20]  J. Price,et al.  Studies of human breast cancer metastasis using nude mice , 1990, Cancer and Metastasis Reviews.

[21]  J. Price Analyzing the metastatic phenotype , 1994, Journal of cellular biochemistry.

[22]  A. Whittemore,et al.  BRCA1/2 mutation status influences somatic genetic progression in inherited and sporadic epithelial ovarian cancer cases. , 2003, Cancer research.

[23]  Gordon B Mills,et al.  Lineage Infidelity of MDA-MB-435 Cells , 2004, Cancer Research.

[24]  J. Thiery Epithelial–mesenchymal transitions in tumour progression , 2002, Nature Reviews Cancer.

[25]  J Piper,et al.  Optimizing comparative genomic hybridization for analysis of DNA sequence copy number changes in solid tumors , 1994, Genes, chromosomes & cancer.

[26]  D. Scudiero,et al.  Cell line designation change: multidrug-resistant cell line in the NCI anticancer screen. , 1998, Journal of the National Cancer Institute.

[27]  C. Gilles,et al.  The Epithelial to Mesenchymal Transition and Metastatic Progression in Carcinoma , 1996 .

[28]  D. Botstein,et al.  Cluster analysis and display of genome-wide expression patterns. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[29]  M. Waltham,et al.  Epidermal Growth Factor-Induced Epithelio-Mesenchymal Transition in Human Breast Carcinoma Cells , 2003, Laboratory Investigation.

[30]  M. Hendrix,et al.  Molecular biology of breast cancer metastasis Molecular expression of vascular markers by aggressive breast cancer cells , 2000, Breast Cancer Research.

[31]  J. Price,et al.  Tumorigenicity and metastasis of human breast carcinoma cell lines in nude mice. , 1990, Cancer research.