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The deletions that include the CDKN2A region also include the MTAP region.
our findings indicate that TP53 changes and CDKN2A deletions tend to coexist in LGG, suggesting that they are early events in progression of these tumors, as well as CDKN2A and PTEN deletions, since a significant association was observed, with CDKN2A changes preceding PTEN deletions, that are involved with malignant progression of gliomas.
Study report that p16 immunoreactivity in stromal cells of pleural mesothelioma (MPM) had significant relation with patients' high asbestos exposure, suggesting that the biology of MPM in highly exposed individuals differed from that of mesotheliomas in subjects with low exposure. Also, abnormal copy number of CDKN2A in MPM cells associated with high pulmonary asbestos fiber counts. a biological difference betwe
The prognostic role of CDKN2A RNA expression in muscle invasive bladder cancer (MIBC) is under discussion. CDKN2A RNA expression-based risk stratification of MIBC allows the identification of a CDKN2A(high) poor prognosis group with low expression of drug target genes.
Alterations in CDKN2A/ARF/CDKN2B were detected in 35/64 patients (55%). Most of them consisted of 9p21 losses involving homozygous deletions of the CDKNA/ARF gene (26/64), as confirmed by single nucleotide polymorphism (SNP) arrays and interphase fluorescence in situ hybridization (iFISH).
an unusual case of CML progressing to BP in a 1.6-year-old child, harboring IKZF1, PAX5, CDKN2A, and ETV6 deletions at diagnosis. It remains to be addressed whether distinct mechanisms might account for CML pathogenesis in early childhood.
In acquired sorafenib-resistant cells, ID1 low expression, p16/IL6 axis up-regulation, and AKT phosphorylation activation were observed.
P16 is significantly deficient in rectal cancer tissues.
Cholangiocarcinoma is a genetically diverse cancer. Alterations in CDKN2A/B and ERBB2 are associated with negative prognostic implications in patients with advanced disease. Somatic alterations with therapeutic implications were identified in almost half of patients
The combination of low budding, low stromal FOXP3 counts, presence of tertiary lymphoid tissue (TLT), and absence of CDKN2A mutations confers significant survival advantage in patients with pancreatic ductal adenocarcinoma (PDAC)
RXRalpha provokes tumor suppression through p53/p21/p16 and PI3K-AKT signaling pathways during stem cell differentiation and in cancer cells.
Biomarker p16 is the strongest predictor for anal low-grade squamous intraepithelial lesion-to-high-grade squamous intraepithelial lesions, outperforming other risk factors.
Case Report/Review: p16/Ink4a-positive cystic squamous cell carcinoma in midline neck arising from thyroglossal duct cyst.
CBX7 positively regulates stem cell-like characteristics of gastric cancer cells by inhibiting p16 and activating AKT-NF-kappaB-miR-21 pathway.
9p21.3 (CDKN2A) loss and PIK3CA mutation characterize a subgroup of metaplastic breast cancers with myoepithelial and spindle cell differentiation.
These data identify leukemia-generated NOX2-derived superoxide as a driver of protumoral p16INK4a-dependent senescence in bone marrow stromal cells. These findings reveal the importance of a senescent microenvironment for the pathophysiology of leukemia.
Our findings support the hypothesis that p16 has a similar prognostic role in both nonoropharyngeal and oropharyngeal cancer. Consideration should be given to increased testing for p16 in laryngeal, hypopharyngeal, and oral cavity primaries.
Study in Dutch CDKN2A-p16-Leiden mutation carriers revealed that patients with and without a pancreatic cystic lesion have a similar risk of pancreatic ductal adenocarcinoma (PDAC). However, cystic precursor lesions between 10 and 20 mm increase the risk of PDAC substantially. In view of the large size of the screen-detected tumors, a shorter interval of screening might be recommended for all patients.
CDKN2A + families had significantly higher percentages of pediatric patients with melanoma compared with CDKN2A- families.
The results show a family with melanoma-astrocytoma syndrome associated with a CDKN2A exon 1beta splice mutation. Our data also suggest that phenotypic variability in this family, and others with CDKN2A mutations, may arise from modifiers in genes other than MC1R.
results not only implicate a biological role for AR expression and p16Ink4a deletion in the pathogenesis of prostatic signet ring cell carcinoma (SRCC), but also provide a new and unique genetically engineered mouse (GEM) model for investigating the molecular mechanisms for SRCC development.
Ink4c-/- testes shown in double knockout mice partial reversal of the morphologic abnormalities, including testes size and Leydig cell differentiation defect.
The elimination of p19(ARF) -expressing cells prevented lung tissue from elastase-induced lung dysfunction.
Study report that the Slug is highly expressed in quiescent mouse satellite cell (SCs) and functions as a direct transcriptional repressor of p16Ink4a. Loss of Slug promotes de-repression of p16Ink4a in SCs and accelerates the entry of SCs into a fully senescent state upon damage-induced stress. p16Ink4a depletion partially rescues defects in Slug-deficient SCs.
results indicate that cells harboring activation of the p16 (INK4a) promoter accumulate with aging and inflammation in vivo, and display characteristics of senescence
Here we show that loss of Ezh2 resulted in altered expression of several key cyclin-dependent kinase inhibitors including Cdkn2a (p16 and Arf) and Cdkn1c (p57) in naive CD8+ T cells after activation, which explained the cell cycle impairment of Ezh2-deficient naive CD8+ T cells in response to antigenic stimulation.
These results point to a critical role of the Cdkn2ab locus in keeping the oncogenic potential of physiological levels of WNT signaling in check.
16Ink4a prevents the proliferation of stem cells during aging in the neurogenic niche of the dentate gyrus, after a neurogenic stimulus such as running. This indicates that P16Ink4a plays a role in the maintenance of dentate gyrus stem cells after stimulus, by keeping a reserve of their self-renewal capacity during aging.
Ezh2 deploys H3K27me3 to repress Cdkn2a expression in T follicular helper (TFH) cells, where aberrantly upregulated p19Arf, a Cdkn2a protein product, triggers TFH cell apoptosis and antagonizes Bcl6 function via protein-protein interaction.
P16INK4a deletion ameliorated renal tubulointerstitial injury in a stress-induced premature senescence model of Bmi1 deficiency.
Cdkn2a controls adipose tissue browning. Cdkn2a modulates gene networks involved in energy production and lipid metabolism.
INK4a role in the clear cell renal cell carcinoma
The high expression of p19(ARF) correlated with mutant p53 accumulation and tumor progression.
Pancreatic cancer was induced in adult mice by the combination of KRASG12D overexpression and loss of Tp53 and Cdkn2a only if Cdkn2b was concomitantly inactivated. inactivation of both Cdkn2b and Cdkn2a was necessary for Rb phosphorylation and to encompass oncogene-induced cellular senescence.
Study reveal that p16Ink4a and p21Waf1/Cip1 upregulate CX3CR1 expression by preventing CDK-mediated phosphorylation and inactivation of SMAD3 in monocytic myeloid-derived suppressor cells promoting tumor growth through chemotaxis.
In summary, our study employing INK4a/Arf -/- mice indicates that INK4a/Arf protects against UVB-induced carcinogenesis. INK4a/Arf was found to restrict the generation of ROS and to inhibit COX-2 expression, PGE2 synthesis and production of proinflammatory cytokines, all of which contribute to UV-induced inflammation.
5-Aza-2'-deoxycytidine partly protected against emphysema in mice via suppressing p16(Ink4a) expression in endothelial progenitor cells and lung tissue.
Arf (smArf) protein corrects p53-independent developmental defects of Arf tumor suppressor-deficient mice
This study shows that H3.3K27M mutation and PDGF signaling act in concert to accelerate gliomagenesis in a genetic mouse model and identifies repression of p16 tumor suppressor as a target of H3.3K27M.
This gene generates several transcript variants which differ in their first exons. At least three alternatively spliced variants encoding distinct proteins have been reported, two of which encode structurally related isoforms known to function as inhibitors of CDK4 kinase. The remaining transcript includes an alternate first exon located 20 Kb upstream of the remainder of the gene\; this transcript contains an alternate open reading frame (ARF) that specifies a protein which is structurally unrelated to the products of the other variants. This ARF product functions as a stabilizer of the tumor suppressor protein p53 as it can interact with, and sequester, the E3 ubiquitin-protein ligase MDM2, a protein responsible for the degradation of p53. In spite of the structural and functional differences, the CDK inhibitor isoforms and the ARF product encoded by this gene, through the regulatory roles of CDK4 and p53 in cell cycle G1 progression, share a common functionality in cell cycle G1 control. This gene is frequently mutated or deleted in a wide variety of tumors, and is known to be an important tumor suppressor gene.
, Cyclin dependent kinase inhibitor 2A (p16, inhibits CDK4)
, cell cycle inhibitor
, cell cycle regulator
, cyclin-dependent kinase 4 inhibitor A
, cyclin-dependent kinase inhibitor 2a p16Ink4a
, cyclin-dependent kinase inhibitor 2a p19Arf
, CDK4 inhibitor p16-INK4
, cell cycle negative regulator beta
, cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4)
, multiple tumor suppressor 1
, cyclin-dependent kinase inhibitor 2A (p16, inhibits CDK4)
, cyclin-dependent kinase inhibitor 2A, isoforms 1/2
, cyclin-dependent kinase inhibitor protein
, mitochondrial smARF