V
Vicki L. Hopwood
Researcher at University of Texas MD Anderson Cancer Center
Publications - 26
Citations - 1142
Vicki L. Hopwood is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Cytogenetics & Cancer. The author has an hindex of 11, co-authored 26 publications receiving 1113 citations.
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Journal Article
Androgen-independent cancer progression and bone metastasis in the LNCaP model of human prostate cancer.
George N. Thalmann,Ploutarchos E. Anezinis,Shi Ming Chang,Haiyen E. Zhau,E. Edmund Kim,Vicki L. Hopwood,Sen Pathak,Andrew C. von Eschenbach,Leland W.K. Chung +8 more
TL;DR: It is demonstrated that one of the LNCaP sublines derived from C4-2 tumors that metastasized to the lymph node and bone acquired metastatic potential.
Journal Article
Involvement of Chromosome 7 in Primary Lung Tumor and Nonmalignant Normal Lung Tissue
Jin S. Lee,Sen Pathak,Vicki L. Hopwood,Barbara Tomasovic,Tedd D. Mullins,Fraser L. Baker,Gary Spitzer,James A. Neidhart +7 more
TL;DR: The cytogenetic data suggest that chromosome 7 may be associated with lung cancer development and that trisomy 6 may be the hallmark of premalignant changes, at least in a subgroup of patients with non-small cell lung cancer.
Journal Article
Genetic susceptibility to lung cancer as determined by lymphocytic chromosome analysis.
TL;DR: The data on lymphocytic chromosomal rearrangements in lung cancer patients not only indicates the importance of specific genetic changes in the etiology of lung cancer but also emphasizes the putative role of such analysis in determining primary genetic abnormalities in the large heterogeneous group of lung cancers.
Journal Article
Chromosome anomalies in human breast cancer: evidence for specific involvement of 1q region in lymphocyte cultures.
TL;DR: It is concluded that chromosome 1q rearrangement might be one of the primary lesions specifically associated with the development of breast cancer.
Journal Article
Dna repair and mutagen sensitivity in patients with triple primary cancers
TL;DR: Findings support the concept of diminished DNA repair capacity as an underlying feature in the development of a mutator phenotype in individuals with multiple primary cancers.