Tumor Suppressor Genes

Weinberg, Robert A.

doi:10.1126/science.1659741

Cited by 1,484 publications

(645 citation statements)

References 190 publications

(40 reference statements)

Supporting

Mentioning

608

Contrasting

Unclassified

Order By: Relevance

“…p53 proteins encoded by mutant alleles are often more stable than wildtype p53. resulting in a dramatic increase in p53 expression and inactivation of wild-type p53 by a dominant-negative mechanism (Levine, 1990;Weinberg, 1991). In addition to genetic change.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis

Koh

Cho²,

Kong³

et al. 1998

Br J Cancer

View full text Add to dashboard Cite

Summary Forty-two oral squamous cell carcinomas (SCCs) were analysed for p53 mutations and human papillomavirus (HPV) (Regezi et al. 1993). W'hereas the epidemiology has been w-ell described so far. the molecular steps involsed in the pathogenesis of these common neoplasms are poorly understood. The role of human papillomas-irus (HPV) in the development of anogenital cancers has been widely studied. and current evidence shows that HPV infection is necessars for the desvelopment of most cervical cancers (zur Hausen. 1994). Approximately 80-90% of cervical carcinomas contain HPV DNA. and the predominant or high-risk types appear to be HPV-16. -18 and -33 (Yoshikawa et al. 1991). HPV E6 and E7 proteins. consistentlv expressed in HPV-transformed and HPVpositive tumours. can exert their oncogenic potential bv inactivating the products of the p53 tumour-suppressor cene (Lemine. 1990: zur Hausen. 1994) and the retimoblastoma (Rb) grene (Dy-son et al. 1989). In oral malignant lesions. the state of HPV infection has been reported to be as high as 76%c (Snijders et al. 1994). although there are still conflicting results in infection rate and role of HPV in oral carcinorenesis.

show abstract

Section: Discussionmentioning

confidence: 99%

“…In oral malignant lesions. the state of HPV infection has been reported to be as high as 76%c (Snijders et al 1994 (Weinberg. 1991: Smith et al 1995.…”

mentioning

confidence: 99%

p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis

Koh

Cho²,

Kong³

et al. 1998

Br J Cancer

View full text Add to dashboard Cite

show abstract

“…Allelic loss analysis is therefore a standard method to locate the regions carrying tumor suppressor genes (Knudson, 1985;Weinberg, 1991;Vogelstein and Kinzler, 1993). Identi®cation of novel tumor suppressor genes is important for understanding the molecular mechanism underlying carcinogenesis, but only about 25 suppressor genes have been identi®ed.…”

Section: Introductionmentioning

confidence: 99%

Allelic loss mapping and physical delineation of a region harboring a putative thymic lymphoma suppressor gene on mouse chromosome 12

et al. 1999

View full text Add to dashboard Cite

“…The phosphorylation of pRb, a tumor suppressor gene product, has been attributed to cyclin/CDK complexes and implicated in a proliferation-regulation mechanism in keratinocytes as well as other cell types (Demers et al, 1994;Koike et al, 1994). Loss of Rb function contributes to the loss of cell growth control in various tumors (Weinberg, 1991). There is considerable evidence that the E2F transcription factors are a critical target for pRb and pRb-related proteins (Bagchi et al, 1991;Bandara et al, 1991;Chellappan et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Deregulated expression of cell-cycle proteins during premalignant progression in SENCAR mouse skin

et al. 1998

View full text Add to dashboard Cite

It is now evident that several genes encoding regulatory activities that control the mammalian cell cycle, particularly some that control the progression of quiescent cells through G1 and into S phase, are targets for alterations that underlie the development of neoplasms. Here, we made a sequential study of alterations in cell cycle protein expression and complex formation among cyclin, cyclin dependent kinases (CDKs) and CDK inhibitors (CKIs) during premalignant progression in SENCAR mouse skin tumors. Changes in the level of expression were observed in positive (cyclin D1, D2, and E2F family members) and negative regulators (p16 Ink4a , p57 Kip2 ) of the cell cycle. Also, we observed the formation of cyclin/CDK/CKI complexes. The amounts of these proteins and complexes increased substantially at speci®c times during promotion but not during malignant conversion to carcinomas. These data show that deregulation of growth control occurs in benign tumors and that subsequent mutations not involved cell-cycle regulation are probably necessary to induce invasive behavior.

show abstract

Tumor Suppressor Genes

Cited by 1,484 publications

References 190 publications

p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis

p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis

Allelic loss mapping and physical delineation of a region harboring a putative thymic lymphoma suppressor gene on mouse chromosome 12

Deregulated expression of cell-cycle proteins during premalignant progression in SENCAR mouse skin

Contact Info

Product

Resources

About