The differential impact of p16(INK4a) or p19(ARF) deficiency on cell growth and tumorigenesis. (Q47264647)

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:14724566%20AND%20SRC:MED&resulttype=core&format=json

17 November 2019

title

The differential impact of p16(INK4a) or p19(ARF) deficiency on cell growth and tumorigenesis (English)

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17 November 2019

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17 November 2019

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17 November 2019

Ronald A DePinho

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17 November 2019

author name string

Periasamy Balasubramanian

series ordinal

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17 November 2019

Diego H Castrillon

series ordinal

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17 November 2019

language of work or name

English

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publication date

1 January 2004

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17 November 2019

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17 November 2019

volume

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17 November 2019

issue

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17 November 2019

page(s)

379-385

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Constitutive telomerase expression promotes mammary carcinomas in aging mice

17 November 2019

cites work

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Increased p16 expression with first senescence arrest in human mammary epithelial cells and extended growth capacity with p16 inactivation

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INK4a-deficient human diploid fibroblasts are resistant to RAS-induced senescence

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Biallelic mutations in p16(INK4a) confer resistance to Ras- and Ets-induced senescence in human diploid fibroblasts

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A cell cycle regulator potentially involved in genesis of many tumor types

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Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

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Both Rb/p16INK4a inactivation and telomerase activity are required to immortalize human epithelial cells.

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ARF function does not require p53 stabilization or Mdm2 relocalization

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Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice

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The Ink4a tumor suppressor gene product, p19Arf, interacts with MDM2 and neutralizes MDM2's inhibition of p53

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A germline deletion of p14(ARF) but not CDKN2A in a melanoma-neural system tumour syndrome family

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A two-stage, p16(INK4A)- and p53-dependent keratinocyte senescence mechanism that limits replicative potential independent of telomere status

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Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a

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Loss of p16Ink4a with retention of p19Arf predisposes mice to tumorigenesis

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7 January 2021

Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions

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7 January 2021