Zobrazeno 1 - 7
of 7
pro vyhledávání: '"W E, Pierceall"'
Publikováno v:
Oncogene. 11(7)
Alterations in intercellular junction and membrane cytoskeletal proteins may underlie some of the morphological, invasive and metastatic properties of cancer. E-cadherin, a transmembrane protein that functions in epithelial cell-cell interactions at
Autor:
E R, Fearon, W E, Pierceall
Publikováno v:
Cancer surveys. 24
Chromosome 18q is among the regions thought to harbour a tumour suppressor gene(s) that is frequently inactivated by LOH during the development of several cancer types, including those of the gastrointestinal tract. In addition, colorectal cancers wi
Publikováno v:
Cancer research. 53(13)
Exposure to UV radiation has long been associated with the development of skin cancers. To identify the molecular targets in UV carcinogenesis, we analyzed 11 UV-induced murine skin cancers for mutations in the p53 tumor suppressor gene and found a 1
Publikováno v:
Cancer research. 52(14)
UV radiation is a potent DNA-damaging agent and a known inducer of skin cancer in experimental animals. To elucidate the role of oncogenes in UV carcinogenesis, we analyzed UV-induced murine skin tumors for mutations in codon 12, 13, or 61 of Ha-ras,
Autor:
H N, Ananthaswamy, W E, Pierceall
Publikováno v:
Progress in clinical and biological research. 376
Several genetic alterations that perturb normal cellular growth control mechanisms can cause cancers. These include point mutations, deletions, translocations, amplifications and gene rearrangements and occur primarily in two classes of interacting g
Autor:
W E, Pierceall, H N, Ananthaswamy
Publikováno v:
Oncogene. 6(11)
Our previous studies have shown that human skin cancers occurring on sun-exposed body sites frequently contain G----T mutations at the second position of Ha-ras codon 12. In this study, we investigated whether the c-Ha-ras-1 proto-oncogene could be a
Publikováno v:
Cancer research. 50(11)
Skin cancers induced in mice by UV radiation often exhibit a regressor phenotype. In order to determine how tumors escape the immune defenses of the normal immunocompetent host, we sought to isolate progressor variants from a UV radiation-induced C3H