Showing papers on "Cyclin-dependent kinase 8 published in 1996"
TL;DR: Endocytic trafficking of activated EGFR plays a critical role not only in attenuating EGFR signaling but also in establishing and controlling specific signaling pathways.
Abstract: Epidermal growth factor receptor (EGFR) signaling was analyzed in mammalian cells conditionally defective for receptor-mediated endocytosis. EGF-dependent cell proliferation was enhanced in endocytosis-defective cells. However, early EGF-dependent signaling events were not uniformly up-regulated. A subset of signal transducers required the normal endocytic trafficking of EGFR for full activation. Thus, endocytic trafficking of activated EGFR plays a critical role not only in attenuating EGFR signaling but also in establishing and controlling specific signaling pathways.
1,024 citations
TL;DR: The p53 mutations in nonmelanoma skin cancer of the head and neck: molecular evidence for field cancerization and the role of oncogenes and tumor suppressor genes in UV carcinogenesis are studied.
Abstract: 35. Kenna, H. P. Baden, A. J. Halperin and J. Poten (1991) A role for sunlight in skin cancer: UV-induced p53 mutations in squamous cell carcinoma. Proc. Natl. Acad. Sci. USA 88, 1012410128. Ziegler, A,, D. J. Leffell, S. Kunala, H. W. Sharma, M. Gailani, J . A. Simon, A. J. Halperin, H. P. Baden, P. E. Shapiro, A. E. Bale and D. E. Brash (1993) Mutation hotspots due to sunlight in the p53 gene of nonmelanoma skin cancers. Proc. Natl. Acad. Sci. USA 90, 421W220. Ziegler, A,, A. S. Jonason, D. J. Leffell, J. A. Simon, H. W. Sharma, J. Kimmelmann, L. Remington, T. Jacks and D. E. Brash (1994) Sunburn and p53 in the onset of skin cancer. Nature 372, 773-776. Nelson, M. A., J. G . Einspahr, D. S. Alberts, C. A. Balfour, J. A. Wymer, K. L. Welch, S. J. Salasche, J. L. Bangert, T. M. Grogan and P. 0. Bozzo (1994) Analysis of p53 gene in human precancerous actinic keratosis lesions and squamous cell cancers. Cancer Lett. 85, 23-29. Kanjilal, S. and H. N. Ananthaswamy (1994) The role of oncogenes and tumor suppressor genes in UV carcinogenesis. In Skin cancer: Mechanisms and Human Relevance (Edited by H. Mukhtar), pp. 305-316. CRC Press, Boca Raton, FL. Kanjilal, S., S. S. Strom, G. L. Clayman, R. S. Weber, A. K. ElNagger, K. K. Cummings, L. A. Hill, V. Kapur, M. R. Spitz, M. L. Kripke and H. N. Ananthaswamy (1995) p53 mutations in nonmelanoma skin cancer of the head and neck: molecular evidence for field cancerization. Cancer Res. 55, 3604-3609. Nataraj. A. J., J. C. Trent and H. N. Ananthaswamy (1995) p53 gene mutations and photocarcinogenesis. Photochem. Phorobiol. 62, 218-230. Nakazawa, H., D. English, P. L. Randell, K. Nakazawa, N. Martel, B. K. Armstrong and H. Yamasaki (1994) UV and skin cancer: specific p53 gene mutation in normal skin as a biologically relevant exposure measurement. Proc. Natl. Acad. Sci.
60 citations
TL;DR: GSTMl and CYP2D6 genotype frequencies in patients with pituitary tumours: effects on P53, RAS and GSP and Curcinogenesis 16, 16431645.
Abstract: skin. Histologic study with special reference to Bowen's disease. Cancer 21, 3 12-3 19. 23. Ryberg, D., E. Kure, S. Lystad, V. Skaug, L. Stangeland, I. Mercy, A,-L. Bfrresen and A. Haugen (1994) p53 mutations in lung tumours: relationship to putative susceptibility markers for cancer. Cancer Res. 54, 1551-1555. 24. Perrett, C. W., R. N. Clayton, M. Pistorello, M. Boscaro, M. Scanarini, A. Bates, N. Buckley, P. Jones, A. A. Fryer, J . Gilford, J. Alldersea and R. C. Strange (1995) GSTMl and CYP2D6 genotype frequencies in patients with pituitary tumours: effects on P53, RAS and GSP. Curcinogenesis 16, 16431645.
22 citations
TL;DR: Small GTP-binding proteins of the Rho-subfamily, including Cdc42, Rac1 and RhoA, are key control molecules in the reorganization of the actin cytoskeleton induced by growth factors, and Aberrations in signaling pathways controlled by RHo-like GTPases may have consequences for tumor progression and metastasis.
Abstract: Small GTP-binding proteins of the Rho-subfamily, including Cdc42, Rac1 and RhoA, are key control molecules in the reorganization of the actin cytoskeleton induced by growth factors. Recent studies indicate that signal transduction pathways regulated by Rho-like GTPases are interconnected with the Ras-Raf-MAPkinase pathway, and play a role in several kinase pathways that lead to transcriptional activation and oncogenic transformation. Moreover, pathways regulated by Rac are involved in the acquisition of invasive and metastatic capacity of tumor cells. Aberrations in signaling pathways controlled by Rho-like GTPases may thus have consequences for tumor progression and metastasis.
19 citations
Patent•
06 Dec 1996
TL;DR: In this article, the authors present methods for making and using tumor suppressor genes and proteins and peptides, and nucleic acids encoding these and related tumor suppressors proteins and proteins.
Abstract: The invention provides tumor suppressor genes, methods for making and using these and related tumor suppressor genes and proteins and peptides, and nucleic acids encoding these and related tumor suppressor proteins and peptides.
18 citations
TL;DR: Examination of the entire coding region of the p21 gene by SSCP analysis and direct DNA sequencing did not detect mutations in the coding domains, indicating that mutations of the SDI1/WAF1/CIP1/p21 gene are not present in cultured PC cells and suggest that defects in the p 21 gene are infrequent in prostate cancers.
Abstract: The SDI1/WAF1/CIP1 gene encodes a M(r) 21,000 protein (p21) that can arrest cell growth by associating with and inhibiting cyclin-dependent kinase complexes necessary for cells to exit G(1). It is a critical downstream effector in the p53 growth control pathway and can be transcriptionally upregulated by increasing levels of wild-type p53 protein. Somatic mutations in the p21 gene have been detected in 17% of primary prostate cancers. In the current study, we examined four prostate cancer cell lines for expression of and mutations in the p21 gene. Transcripts for p21 mRNA were present in all PC cell lines; p21 protein was detected in androgen-dependent LNCaP cells, as well as in androgen-independent DU-145 and TSU-Pr1 cells but not in androgen-independent PC-3 cells. Examination of the entire coding region of the p21 gene by SSCP analysis and direct DNA sequencing did not detect mutations in the coding domains of the p21 gene. These data indicate that mutations of the SDI1/WAF1/CIP1/p21 gene are not present in cultured PC cells and suggest that defects in the p21 gene are infrequent in prostate cancers.
7 citations
Journal Article•
TL;DR: Alterations of p53 tumor suppressor gene are the most common genetic change detected in human cancers, and it is likely that many of the biological functions of p 53 are a result of transcriptional regulation of downstream genes which involve in these functions.
Abstract: Alterations of p53 tumor suppressor gene are the most common genetic change detected in human cancers. Several biological functions of p53 have been described, including the induction of G1 arrest and apoptosis following DNA damage or other cellular insults. Biochemical activity of p53 has been proposed as a transcriptional regulator; p53 gene product can bind DNA in a sequence-specific manner and regulate transcription from promoters containing a consensus binding site. It is likely that many of the biological functions of p53 are a result of transcriptional regulation of downstream genes which involve in these functions.
3 citations
2 citations
TL;DR: A total of 71 primary sporadic ovarian carcinomas were analyzed for the presence of mutations in the exon 2 and 3 of the VHL tumor suppressor gene using the polymerase chain reaction with single strand conformation polymorphism analysis.
Abstract: The von Hippel-Lindau (VHL) tumor suppressor gene has been shown to be mutated frequently not only in neoplasms from von Hippel-Lindau disease, but also in sporadic clear cell renal carcinoma. In order to reveal the possible role of the VHL tumor suppressor gene in the development of ovarian carcinoma, a total of 71 primary sporadic ovarian carcinomas were analyzed for the presence of mutations in the exon 2 and 3 of the VHL tumor suppressor gene, using the polymerase chain reaction with single strand conformation polymorphism analysis. No mutations in the VHL gene were found in any of the tumors analyzed. This result shows that the VHL tumor suppressor gene does not play a major role in the tumorigenesis of sporadic ovarian carcinoma.
2 citations