High-resolution chromosome 3p allelotyping of breast carcinomas and precursor lesions demonstrates frequent loss of heterozygosity and a discontinuous pattern of allele loss.

[1]  J. Minna,et al.  Epigenetic inactivation of RASSF1A in lung and breast cancers and malignant phenotype suppression. , 2001, Journal of the National Cancer Institute.

[2]  J. Minna,et al.  Promoter methylation and silencing of the retinoic acid receptor-beta gene in lung carcinomas. , 2001, Journal of the National Cancer Institute.

[3]  J. Minna,et al.  The 630-kb lung cancer homozygous deletion region on human chromosome 3p21.3: identification and evaluation of the resident candidate tumor suppressor genes. The International Lung Cancer Chromosome 3p21.3 Tumor Suppressor Gene Consortium. , 2000, Cancer research.

[4]  Y. Chen,et al.  Comparative genomic hybridization analysis of 38 breast cancer cell lines: a basis for interpreting complementary DNA microarray data. , 2000, Cancer research.

[5]  J. Minna,et al.  Two identical triplet sisters carrying a germline BRCA1 gene mutation acquire very similar breast cancer somatic mutations at multiple other sites throughout the genome , 2000, Genes, chromosomes & cancer.

[6]  R. Osborne,et al.  A genome-wide map showing common regions of loss of heterozygosity/allelic imbalance in breast cancer. , 2000, Cancer research.

[7]  C. Yue,et al.  Genome-wide search for loss of heterozygosity using laser capture microdissected tissue of breast carcinoma: an implication for mutator phenotype and breast cancer pathogenesis. , 2000, Cancer research.

[8]  J. Taubenberger,et al.  Loss of heterozygosity in fibrocystic change of the breast: genetic relationship between benign proliferative lesions and associated carcinomas. , 2000, The American journal of pathology.

[9]  Chun Xing Li,et al.  Epigenetic inactivation of a RAS association domain family protein from the lung tumour suppressor locus 3p21.3 , 2000, Nature Genetics.

[10]  M. Widschwendter,et al.  Methylation and silencing of the retinoic acid receptor-beta2 gene in breast cancer. , 2000, Journal of the National Cancer Institute.

[11]  Y. Nakamura,et al.  Loss of heterozygosity at 3p24-p25 as a prognostic factor in breast cancer. , 2000, Cancer letters.

[12]  S. Lam,et al.  High resolution chromosome 3p allelotyping of human lung cancer and preneoplastic/preinvasive bronchial epithelium reveals multiple, discontinuous sites of 3p allele loss and three regions of frequent breakpoints. , 2000, Cancer research.

[13]  B. Rampy,et al.  The expression of Fhit protein is related inversely to disease progression in patients with breast carcinoma , 2000, Cancer.

[14]  T. P. Pretlow,et al.  Loss of fragile histidine triad expression in colorectal carcinomas and premalignant lesions. , 2000, Cancer research.

[15]  J. Minna,et al.  The 630-kb Lung Cancer Homozygous Deletion Region on Human Chromosome 3 p 21 . 3 : Identification and Evaluation of the Resident Candidate Tumor Suppressor Genes 1 , 2000 .

[16]  A. Maitra,et al.  Use of archival fine‐needle aspirates for the allelotyping of tumors , 1999, Cancer.

[17]  Chen-Yang Shen,et al.  Breast cancer risk associated with genotype polymorphism of the estrogen-metabolizing genes CYP17, CYP1A1, and COMT: a multigenic study on cancer susceptibility. , 1999, Cancer research.

[18]  Y. Pekarsky,et al.  FHIT loss of function in human primary breast cancer correlates with advanced stage of the disease. , 1999, Cancer research.

[19]  C. Croce,et al.  The tumor-suppressor gene FHIT is involved in the regulation of apoptosis and in cell cycle control. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[20]  O. Kallioniemi,et al.  Reduced Fhit expression in sporadic and BRCA2-linked breast carcinomas. , 1999, Cancer research.

[21]  A. Maitra,et al.  Loss of heterozygosity at 3p in benign lesions preceding invasive breast cancer. , 1999, The Journal of surgical research.

[22]  J. Tischfield,et al.  A novel signature mutation for oxidative damage resembles a mutational pattern found commonly in human cancers. , 1999, Cancer research.

[23]  S. Wallace,et al.  In vitro repair of synthetic ionizing radiation-induced multiply damaged DNA sites. , 1999, Journal of molecular biology.

[24]  J. Minna,et al.  Comparison of features of human breast cancer cell lines and their corresponding tumors. , 1999, Clinical cancer research : an official journal of the American Association for Cancer Research.

[25]  K. Kinzler,et al.  Genetic instabilities in human cancers , 1998, Nature.

[26]  M. Westerfield,et al.  Characterization of paired tumor and non‐tumor cell lines established from patients with breast cancer , 1998, International journal of cancer.

[27]  J. Bergh,et al.  Homozygous deletions at 3p12 in breast and lung cancer , 1998, Oncogene.

[28]  H R Garner,et al.  Computerized polymorphic marker identification: experimental validation and a predicted human polymorphism catalog. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[29]  J. Minna,et al.  Cloning of a breast cancer homozygous deletion junction narrows the region of search for a 3p21.3 tumor suppressor gene , 1998, Oncogene.

[30]  J. Minna,et al.  Comparison of molecular changes in lung cancers in HIV-positive and HIV-indeterminate subjects. , 1998, JAMA.

[31]  I. Bièche,et al.  Location of several putative genes possibly involved in human breast cancer progression. , 1998, Cancer research.

[32]  P. O’Connell,et al.  Analysis of loss of heterozygosity in 399 premalignant breast lesions at 15 genetic loci. , 1998, Journal of the National Cancer Institute.

[33]  J. Minna,et al.  Allelotyping demonstrates common and distinct patterns of chromosomal loss in human lung cancer types , 1998, Genes, chromosomes & cancer.

[34]  E. Zabarovsky,et al.  Human/mouse microcell hybrid based elimination test reduces the putative tumor suppressor region at 3p21.3 to 1.6 cM , 1997, Genes, chromosomes & cancer.

[35]  Robert F. Bonner,et al.  Laser Capture Microdissection: Molecular Analysis of Tissue , 1997, Science.

[36]  M. Emi,et al.  Detailed deletion mapping of chromosome arm 3p in breast cancers: A 2‐cM region on 3p14.3‐21.1 and a 5‐cM region on 3p24.3‐25.1 commonly deleted in tumors , 1997, Genes, chromosomes & cancer.

[37]  Y. Miller,et al.  Widely dispersed p53 mutation in respiratory epithelium. A novel mechanism for field carcinogenesis. , 1997, The Journal of clinical investigation.

[38]  K. Patil,et al.  Molecular origin of cancer: catechol estrogen-3,4-quinones as endogenous tumor initiators. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[39]  J. Minna,et al.  Precise localization of the FHIT gene to the common fragile site at 3p14.2 (FRA3B) and characterization of homozygous deletions within FRA3B that affect FHIT transcription in tumor cell lines , 1997, Genes, chromosomes & cancer.

[40]  J. Minna,et al.  Analysis of the FHIT gene and FRA3B region in sporadic breast cancer, preneoplastic lesions, and familial breast cancer probands. , 1997, Cancer research.

[41]  M. Jasin,et al.  Loss of heterozygosity induced by a chromosomal double-strand break. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[42]  J. Minna,et al.  Deletions of chromosome 3p are frequent and early events in the pathogenesis of uterine cervical carcinoma. , 1997, Cancer research.

[43]  F. Mitelman,et al.  Deletion of the short arm of chromosome 3 in breast tumors , 1997, Genes, chromosomes & cancer.

[44]  E. Zabarovsky,et al.  A 3p21.3 region is preferentially eliminated from human chromosome 3/mouse microcell hybrids during tumor growth in SCID mice , 1997, Genes, chromosomes & cancer.

[45]  H. Klinger,et al.  Chromosome 3p14 homozygous deletions and sequence analysis of FRA3B. , 1997, Human molecular genetics.

[46]  F. Mitelman,et al.  Karyotypic abnormalities in fibroadenomas of the breast , 1997, International journal of cancer.

[47]  A. Thor,et al.  Loss of Heterozygosity in Normal Tissue Adjacent to Breast Carcinomas , 1996, Science.

[48]  M. Wigler,et al.  Evaluation of the FHIT gene in colorectal cancers. , 1996, Cancer research.

[49]  C. Cordon-Cardo,et al.  Chromosome 3 allelic losses and microsatellite alterations in transitional cell carcinoma of the urinary bladder. , 1996, The American journal of pathology.

[50]  J. Minna,et al.  Construction of a 600-kilobase cosmid clone contig and generation of a transcriptional map surrounding the lung cancer tumor suppressor gene (TSG) locus on human chromosome 3p21.3: progress toward the isolation of a lung cancer TSG. , 1996, Cancer research.

[51]  W. Franklin,et al.  Distinct 3p21.3 deletions in lung cancer and identification of a new human semaphorin. , 1996, Oncogene.

[52]  N. Phillips,et al.  Allelotyping of ductal carcinoma in situ of the breast: deletion of loci on 8p, 13q, 16q, 17p and 17q. , 1995, Cancer research.

[53]  A. Gerdes,et al.  Chromosome abnormalities in benign hyperproliferative disorders of epithelial and stromal breast tissue , 1995, International journal of cancer.

[54]  D. Easton,et al.  Breast and ovarian cancer incidence in BRCA1-mutation carriers. Breast Cancer Linkage Consortium. , 1995, American journal of human genetics.

[55]  J. Minna,et al.  Allele-specific chromosome 3p deletions occur at an early stage in the pathogenesis of lung carcinoma. , 1995, JAMA.

[56]  Steven E. Bayer,et al.  A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. , 1994, Science.

[57]  S. Seal,et al.  Localization of a breast cancer susceptibility gene, BRCA2, to chromosome 13q12-13. , 1994, Science.

[58]  K. Kok,et al.  A homozygous deletion in a small cell lung cancer cell line involving a 3p21 region with a marked instability in yeast artificial chromosomes. , 1994, Cancer research.

[59]  B. Ljung,et al.  Deletion of two separate regions on chromosome 3p in breast cancers. , 1994, Cancer research.

[60]  D. Buchhagen,et al.  Homozygous deletion, rearrangement and hypermethylation implicate chromosome region 3p14.3‐3p21.3 in sporadic breast‐cancer development , 1994, International journal of cancer.

[61]  M. Slattery,et al.  A comprehensive evaluation of family history and breast cancer risk. The Utah Population Database. , 1993, JAMA.

[62]  J. Minna,et al.  A homozygous deletion on chromosome 3 in a small cell lung cancer cell line correlates with a region of tumor suppressor activity. , 1993, Oncogene.

[63]  J. Gnarra,et al.  Identification of the von Hippel-Lindau disease tumor suppressor gene. , 1993, Science.

[64]  Y. Nakamura,et al.  Accumulation of genetic alterations and progression of primary breast cancer. , 1991, Cancer research.

[65]  G. Wahl,et al.  A central role for chromosome breakage in gene amplification, deletion formation, and amplicon integration. , 1991, Genes & development.

[66]  W D Dupont,et al.  Risk factors for breast cancer in women with proliferative breast disease. , 1985, The New England journal of medicine.

[67]  J. Minna,et al.  A nonrandom chromosomal abnormality, del 3p(14-23), in human small cell lung cancer (SCLC). , 1982, Cancer genetics and cytogenetics.

[68]  J. Minna,et al.  Specific chromosome defect associated with human small-cell lung cancer; deletion 3p(14-23). , 1982, Science.

[69]  Bernice W. Polemis.  Nonparametric Statistics for the Behavioral Sciences , 1959 .