Involvement of the Ink4a gene (p16 and p19arf) in murine tumorigenesis.

Orlow, Irene; Rabbani, Farhang; Chin, Lena J.; Pomerantz, Jason H.; Ligeois, N; Dudás, Mária; DePinho, Ronald A.; Cordon‐Cardo, Carlos

doi:10.3892/ijo.15.1.17

Cited by 4 publications

(3 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In particular, concerning the susceptibility to skin neoplasms, p16 INK4a −/− mice do not show a greater frequency of DMBA‐induced skin papillomas than p16 INK4a +/+ mice sharing the same genetic background [19]. In addition, molecular analysis of two SCCs which developed in ARF+/− mice show that p16 INK4a is neither mutated nor deleted [20]. Yet, a specific role for p16 INK4a in murine keratinocyte carcinogenesis was suspected from our results, as in two tumors we found INK4a‐ARF mutations affecting only the p16 INK4a transcript (Table 2).…”

Section: Discussionmentioning

confidence: 99%

INK4a‐ARF mutations in skin carcinomas from UV irradiated hairless mice

Soufir

Queillé

Mollier

et al. 2004

Molecular Carcinogenesis

View full text Add to dashboard Cite

To characterize further the role of the INK4a-ARF locus in the multistep process of skin carcinogenesis, we performed a mutational analysis of this locus in skin lesions from hairless mice either irradiated with UVB alone or with a solar simulator delivering UVA + B. INK4a-ARF mutations were present in five of 57 squamous cell carcinomas (9%), but no mutation was detected in precancerous lesions. All mutations were C:G > T:A transitions located at dipyrimidic sites, the hallmark of UVB mutagenesis. Three mutations affected only the p19(ARF) reading frame, whereas two mutations affected only the p16(INK4a) transcript. This study demonstrates for the first time UV-induced mutations of INK4a-ARF that occur in a small percentage in late stages skin tumors.

show abstract

Section: Discussionmentioning

confidence: 99%

INK4a‐ARF mutations in skin carcinomas from UV irradiated hairless mice

Soufir

Queillé

Mollier

et al. 2004

Molecular Carcinogenesis

View full text Add to dashboard Cite

show abstract

“…Forty percent of these tumors exhibit LOH at the Ink4a locus. 120 Deletion of exon 1β specific to Arf is also seen in some of these tumors, suggesting that in these cases it is a deficiency of Arf and not p16 Ink4a that leads to tumor development in mice. Susceptibility to tumorigenesis induced by the carcinogen DMBA alone or in combination with ultraviolet B irradiation is only slightly increased in Ink4a/Arf ex2-3 heterozygous mice compared to controls.…”

Section: Knockout Models For Ink4a/arfmentioning

confidence: 98%

“…Mice heterozygous for the Ink4a/Arf ex2–3 mutation show a moderate increase in fibrosarcomas, lymphomas, squamous cell carcinomas, and angiosarcomas. Forty percent of these tumors exhibit LOH at the Ink4a locus 120. Deletion of exon 1β specific to Arf is also seen in some of these tumors, suggesting that in these cases it is a deficiency of Arf and not p16 Ink4a that leads to tumor development in mice.…”

Section: Introductionmentioning

confidence: 99%

Transgenic and Knockout Mice Models to Reveal the Functions of Tumor Suppressor Genes

Taneja

Zhu

Maglic

et al. 2011

Clin Med Insights Oncol

View full text Add to dashboard Cite

Cancer is caused by multiple genetic alterations leading to uncontrolled cell proliferation through multiple pathways. Malignant cells arise from a variety of genetic factors, such as mutations in tumor suppressor genes (TSGs) that are involved in regulating the cell cycle, apoptosis, or cell differentiation, or maintenance of genomic integrity. Tumor suppressor mouse models are the most frequently used animal models in cancer research. The anti-tumorigenic functions of TSGs, and their role in development and differentiation, and inhibition of oncogenes are discussed. In this review, we summarize some of the important transgenic and knockout mouse models for TSGs, including Rb, p53, Ink4a/Arf, Brca1/2, and their related genes.

show abstract