Loss of p16Ink4a confers susceptibility to metastatic melanoma in mice

By P. Krimpenfort, K. Quon, W. Mooi, Ate Loonstra, A. Berns. Nature, 2001

596 citations recorded by the source corpus.

Subfields: Biotechnology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/95afaec1d58d500a054a5f46bd1674c7a1a5aaa6

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Citations in the corpus

Guidelines for the welfare and use of animals in cancer research (2010, background): “…carcinoma Familial melanoma, sporadic pancreatic, brain tumours Crossed with Arf+/ mice Metastatic melanoma, sarcoma, carcinoma, lymphoma (Krimpenfort et al, 2001) Brca1 No tumour susceptibility Breast ovary Conditional mammaryspecific inactivation of Brca1 Mammary tumours (Xu et al,…”
The RB and p53 pathways in cancer. (2002, background): “Yet, mice lacking p16Ink4a, in particular, are tumor prone and develop a wide spectrum of cancers, particularly after exposure to chemical carcinogens or X-rays (Serrano et al., 1996; Krimpenfort et al., 2001; Sharpless et al., 2001).”
Regulation of the INK4b–ARF–INK4a tumour suppressor locus: all for one or one for all (2006, background): “Mice that are defective for any one of the genes have increased susceptibility to spontaneous or carcinogen-induced tumours, albeit to different degree”
The essence of senescence. (2010, background): “Genetic disruption of the gene encoding p16INK4A predisposes mice and humans to tumorigenesis, includ- ing melanoma (Gruis et al. 1995; Krimpenfort et al. 2001; Sharpless et al. 2001).”
The INK4a/ARF network in tumour suppression (2001, background): “Recently derived Ink4a -null mice (retaining a functional Arf ) are prone to tumour developmen”
Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15INK4B tumor suppressor gene (2010, background): “…website (http://www.nature.com/onc) N IH -PA Author M anuscript N IH -PA Author M anuscript mutations targeting each gene individually support the tumor suppression function for all three genes (Serrano et al., 1996; Kamijo et al., 1997; Krimpenfort et al., 2001, 2007; Sharpless et al., 2001).”
Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. (2003, background): “Mice with constitutive deletion of both or either component of the Ink4a/Arf locus do not develop spontaneous pancreatic adenocarcinoma; however, the rapid onset of lymphomas and sarcomas in these mice may preclude the study of more latent effects of deletions of this locus on pancreatic neoplasia (”
Species- and cell type-specific requirements for cellular transformation. (2004, background): “…transformation or p53 (Harvey et al., 1993; Kamijo et al., 1997), but not Ink4a in the two species and from different tissue compartments and or Rb (Krimpenfort et al., 2001; Sage et al., 2000; Sharpless et al., suggest possible limitations of some rodent experimental sys- 2001), have been…”
Cellular senescence in cancer and aging. (2007, unknown): “On the other hand, mice with decreased levels of p16INK4a are tumor prone, and this precludes the analysis of aging (Krimpenfort et al., 2001; Sharpless et al., 2001).”
Cellular senescence and the senescent secretory phenotype: therapeutic opportunities. (2013, unknown): “Interfering with pathways that can induce senescence-associated replicative arrest are likely to promote cancer, as occurs when p16 INK4a , the retinoblastoma (Rb) protein, or p53 is diminished or inactivated (67, 103).”
Pathways of apoptotic and non-apoptotic death in tumour cells (2004, background): “For example, mutant mice carrying cells that are incapable of entering senescence develop cancer at an early ag”
Comparative biology of mouse versus human cells: modelling human cancer in mice (2003, background): “Senescent MEFs also show an increase in the levels of Ink4a; however, MEFs from Ink4a -null or Rb -null embryos succumb to both culture- and RAS -induced senescenc”
Pancreatic cancer biology and genetics (2002, background): “The INK4A transcript displays a highly restricted expression pattern and is dispensable for normal development and homeostasi”