• Here we refine these evolutionary studies and expand them to the p16/Ink4a gene. (nih.gov)
  • also known as CDK4I, Cyclin-dependent kinase 4 inhibitor A, Multiple tumor suppressor 1, MTS-1, p16-INK4, p16-INK4a, p16INK4A) is encoded by the CDKN2A (also known as CDKN2, MTS1) gene (Gene ID 1029) in human. (sigmaaldrich.com)
  • No. MABE1451, is a highly specific mouse monoclonal antibody that targets INK4a (p16) and has been tested in Immunocytochemistry and Western Blotting. (sigmaaldrich.com)
  • The most well-studied are the p16(INK4A) and the p14(ARF) proteins. (medlineplus.gov)
  • The p16(INK4A) protein attaches (binds) to two other proteins called CDK4 and CDK6. (medlineplus.gov)
  • However, binding of p16(INK4A) blocks CDK4's or CDK6's ability to stimulate cell cycle progression. (medlineplus.gov)
  • In this way, p16(INK4A) controls cell division. (medlineplus.gov)
  • Cells begin to produce p16(INK4A) when they are no longer able to undergo cell division. (medlineplus.gov)
  • Most of these mutations lead to production of little or no functional p16(INK4A) protein. (medlineplus.gov)
  • Without p16(INK4A) to regulate cell growth and division (proliferation), cells can continue to grow and divide without control, which can lead to tumor formation. (medlineplus.gov)
  • A different type of alteration involving the CDKN2A gene can result in reduced amounts or an absence of the p16(INK4A) or p14(ARF) protein. (medlineplus.gov)
  • This alteration, known as promoter hypermethylation, turns off the production of p16(INK4A) or p14(ARF). (medlineplus.gov)
  • The CDKN2A gene mutations found in melanoma result in a nonfunctional p16(INK4A) protein. (medlineplus.gov)
  • CDKN2A gene mutations involved in cancer impair production of functional p16(INK4A) or, less commonly, p14(ARF), which can result in uncontrolled cell growth and tumor formation. (medlineplus.gov)
  • In this model, the senescence-sensitive promoter from the cyclin-dependent kinase inhibitor 2A ( Cdkn2a ) gene, also known as p16 INK4a , drives expression of 3MR, a fusion protein that is composed of luciferase and red fluorescent protein (RFP) reporters and herpes simplex virus-1 thymidine kinase, which converts ganciclovir (GCV) into an apoptosis inducer. (jax.org)
  • Although the senescent cells remain viable, they show typical changes with enlarged and flattened cell bodies, apoptosis resistance, increased activity of senescence-associated β -galactosidase (SA- β -gal), and upregulation of cyclin-dependent kinase (CDK) inhibitors including p16 INK4A , ARF proteins, and p21 [ 13 - 16 ]. (hindawi.com)
  • Mice lacking the tumor suppressors p16(Ink4a) (Cdkn2a, cyclin-dependent kinase inhibitor 2a), p19(Arf) (an alternative reading frame product of Cdkn2a,), and p27(Kip1) (Cdkn1b, cyclin-dependent kinase inhibitor 1b) result in malignant progression of epithelial cancers, sarcomas, and melanomas, respectively. (koreamed.org)
  • The p16(Ink4a) and p19(Arf) knockout mice were generated via transcription activator-like effector nucleases (TALENs), and p27(Kip1) knockout mice via clustered regularly interspaced short palindromic repeats/CRISPR-associated nuclease 9 (CRISPR/Cas9). (koreamed.org)
  • The CDKN2A/B locus contains genes encoding cell cycle inhibitors, including p16 Ink4a , which have not yet been implicated in the control of hepatic glucose homeostasis. (diabetesjournals.org)
  • Here, we show that p16 Ink4a deficiency enhances fasting-induced hepatic glucose production in vivo by increasing the expression of key gluconeogenic genes. (diabetesjournals.org)
  • p16 Ink4a downregulation leads to an activation of PKA-CREB-PGC1α signaling through increased phosphorylation of PKA regulatory subunits. (diabetesjournals.org)
  • Taken together, these results provide evidence that p16 Ink4a controls fasting glucose homeostasis and could as such be involved in T2D development. (diabetesjournals.org)
  • SnCs exhibit irreversible growth arrest accompanied by increased expression of cyclin-dependent kinase inhibitors (CDKi) such as p16 INK4a , and p21 Cip1 , accumulation of DNA damages, and secretion of diverse bioactive molecules known as the senescence-associated secretory phenotype (SASP). (aging-us.com)
  • Status of p16(INK4a) and E-cadherin gene promoter methylation in Moroccan patients with cervical carcinoma. (hal.science)
  • Transcriptional silencing, as a main consequence of hypermethylation of CpG islands, is the predominant mechanism of p16(INK4a) and E-cadherin gene inactivation in malignant epithelial tumors. (hal.science)
  • This study was conducted to evaluate the promoter methylation status of p16(INK4a) and E-cadherin genes in 22 specimens of cervical carcinomas, four cervical cancer cell lines (HeLa, SiHa, Caski, C33A), and 20 human papillomavirus negative specimens, obtained from normal cervical swabs, using the methylation-specific PCR approach. (hal.science)
  • Hypermethylation of the 5' CpG island of the p16(INK4a) and E-cadherin genes were found in 13 (59.1%) and 10 (45.5%) of 22 cervical cancer samples, respectively. (hal.science)
  • Furthermore, our findings did not show any correlation between promoter methylation of p16(INK4a) and E-cadherin genes and clinicopathological parameters, including HPV infection, phenotypic distribution, and stage of the disease. (hal.science)
  • However, hypermethylation of E-cadherin gene promoter appears to be age related in cervical cancer, whereas the frequency of aberrant methylation of p16(INK4a) gene promoter is unchanged according to the age of patients. (hal.science)
  • The defining characteristic of senescence is a highly stable cell cycle arrest, triggered by the up-regulation of cyclin-dependent kinase inhibitors such as p16 INK4a and p21 CIP1a . (rupress.org)
  • The tumor-suppressor gene CDKN2 (p16/INK4A/MTSI) is frequently altered in human gastric-cancer cell lines. (tmu.edu.tw)
  • lt;div class="textblock">Oncogenic Ras induces two products of the INK4a/ARF tumor suppressor locus (p16(INK4a) and p19(ARF)) in primary human and rodent fibroblasts, ultimately leading to a permanent state of cell cycle arrest resembling replicative senescence. (ku.dk)
  • Whereas p16(INK4a) antagonizes the activities of cyclin D-dependent kinases, p19(ARF) activates the p53 transcription factor. (ku.dk)
  • Although early passage primary fibroblast strains that lack both p21(Cip1) and p27(Kip1) fail to assemble cyclin D-dependent kinases, oncogenic Ras retained its ability to induce p19(ARF), but not p16(INK4a), protecting Cip/Kip-null cells from proliferating and undergoing transformation. (ku.dk)
  • Therefore, in the absence of p16(INK4a), p21(Cip1), and p27(Kip1), oncogenic Ras affects the functions of genes required for completion of the cell cycle. (ku.dk)
  • p15 INK4b and p16 INK4a are closely related proteins and both act on the Rb-pathway through the inhibition of the proliferation-promoting cyclin-dependent kinases CDK4 and CDK6. (biomedcentral.com)
  • p14 ARF is structurally and functionally unrelated to p15 INK4b or p16 INK4a and works primarily through activation of the p53 pathway. (biomedcentral.com)
  • A) Organization of the human INK4b-ARF-INK4a locus (not drawn to scale), encoding three distinct proteins, p15 INK4b , p14 ARF and p16 INK4a . (biomedcentral.com)
  • The untranslated regions (yellow boxes), the coding sequences of p15 INK4b (green), p14 ARF (blue) and p16 INK4a (red) are indicated. (biomedcentral.com)
  • Expression of p16INK4a (p16 positive) is highly correlated with human papilloma virus (HPV) infection in head and neck squamous cell carcinomas (HNSCC). (neobiotechnologies.com)
  • The protein p16INK4a is a potent cell cycle inhibitor and is a relatively selective CDK inhibitor. (foxchase.org)
  • In these transgenic mice, the nucleic acid sequence encoding human p16INK4a has been linked to an inducible promoter or an operon capable of activation by the reverse tetracycline-controlled transactivator (rtTA), mediating p16 transcription. (foxchase.org)
  • We hypothesized that BMP4 might exert beneficial effects through modulation of p16 and p18 expression in transduced MDSCs since the cyclin-dependent kinase inhibitors p16INK4A (p16) and p18INK4C (p18) cause early G1-phase cell cycle blockade. (pitt.edu)
  • The p16INK4A protein is a cell-cycle inhibitor that acts by inhibiting activated cyclin D:CDK4/6 complexes, which play a crucial role in the control of the cell cycle by phosphorylating Rb protein. (medscape.com)
  • CAOV3 cells, which are atRA sensitive, have been shown to express p16INK4a (p16), a cyclin dependent kinase inhibitor regulating the G1 checkpoint. (temple.edu)
  • Cyclin-dependent kinase inhibitors (CDKIs) are proteins that bind to and inhibit the activity of CDKs. (biomedcentral.com)
  • Cyclin-dependent kinase inhibitor proteins are essential in the regulation of the cell cycle. (wikipedia.org)
  • Cyclin-dependent kinase inhibitor proteins work by inactivating the CDKs by degradation. (wikipedia.org)
  • Cyclin-dependent kinase inhibitor proteins use ATP as a phosphate contributor to phosphorylate serine and threonine residues. (wikipedia.org)
  • Seven cyclin-dependent kinase inhibitor proteins have been identified. (wikipedia.org)
  • The discovery of Cyclin-dependent kinase inhibitor proteins in 1990 opened the door in how we think about cell cycle control. (wikipedia.org)
  • The active cyclin/CDK complex then phosphorylates proteins, activates them, and sends the cell into the next phase of the cell cycle. (wikipedia.org)
  • The G1 checkpoint is regulated by a multitude of molecules such as the retinoblastoma family of proteins, cyclins, cyclin dependent kinases (CDKs) and cyclin dependent kinase inhibitors (CDKis). (temple.edu)
  • Cystatin A (Cys A), a cysteine protease inhibitor, is a precursor of proteins involves in keratinocyte keratinization, and is expressed during the late phase of differentiation of these cells. (bvsalud.org)
  • In particular, the p16/cyclin-dependent kinase inhibitor 2A (CDKN2A) gene located on chromosomal region 9p21 frequently is altered in several types of cancer. (iiarjournals.org)
  • The tumor suppressor gene p16/cyclin-dependent kinase inhibitor-2A (CDKN2A) is located within the chromosomal region 9p21 and encodes a cell-cycle protein that is an inhibitor of cyclin-dependent kinases (CDK)-4 and -6. (iiarjournals.org)
  • A number of studies have shown that p16/CDKN2A is frequently altered in melanoma ( 9 ), pancreatic ( 10 ), urinary bladder ( 11 ) and lung cancer ( 12 ). (iiarjournals.org)
  • Genes necessary for cell cycle progression, such as E2F-dependent genes, are incorporated into the SAHF and are thereby silenced, contributing to the stability of the growth arrest. (rupress.org)
  • Primary mouse embryo fibroblasts lacking Cip1 and Kip1 genes encoding inhibitors of cyclin-dependent kinase-2 were used to further explore the effects of oncogenic Ras on arrest of the cell division cycle. (ku.dk)
  • Another important class of tumor suppressor genes involved in cell cycle control and in the generation of human cancers is the cyclin-dependent kinase (CDK) inhibitors. (medscape.com)
  • Conclusão: Os resultados suportam a investigação revelando que os genes MIG, CK14, p63, Cal A e Cys A se apresentam fortemente evidentes nos tumores de cavidade oral e o p16 suprimido, sugerindo que esta proteína pode exercer um papel de regulador negativo do ciclo celular. (bvsalud.org)
  • CDKs are under inhibitory control of cyclin dependent kinase inhibitors (CDKIs). (biomedcentral.com)
  • In this study we tested the expression of CDKIs p15, p16, p21 and p27 by immunohistochemistry to determine the role of CDKIs in the initiation of primordial follicle growth. (biomedcentral.com)
  • p15, p16, p21 and p27 in mouse ovaries by immunohistochemistry to assess whether the initiation of primordial follicle growth was associated with the expression of CDKIs. (biomedcentral.com)
  • A cyclin-dependent kinase inhibitor protein (also known as CKIs, CDIs, or CDKIs) is a protein which inhibits the enzyme cyclin-dependent kinase (CDK) and Cyclin activity by stopping the cell cycle if there are unfavorable conditions, therefore, acting as tumor suppressors. (wikipedia.org)
  • The INK and CIP/KIP families of cyclin dependent kinase inhibitors (CDKis) protect cells from oncogenic signals-initiated cellular transformation. (sigmaaldrich.com)
  • The p16 family (p15, p16, p18 and p19) binds to and inhibits the activities of CDK4 and CDK6. (biomedcentral.com)
  • Because of the positive correlation between P16 activity and cellular senescence , the possibility of senescence stimulation by DHA is proposed. (bvsalud.org)
  • Figure 2: Telomere-dependent senescence. (nature.com)
  • Figure 4: Senescence controlled by the p53 and p16-pRB pathways. (nature.com)
  • Increasing evidence indicates that senescent cells could be a promising new target for therapeutic intervention known as senotherapy, which includes depleting senescent cells, modulating SASP and restoration of senescence inhibitors. (frontiersin.org)
  • Several hallmarks of cellular senescence, such as cell cycle arrest, expression of cyclin-dependent kinase inhibitors, DNA damages, and senescence-associated secretory profile were evaluated. (aging-us.com)
  • Cyclins regulate the cell cycle in association with cyclin dependent kinases (CDKs). (biomedcentral.com)
  • The progression of cells through the cell cycle is regulated by a family of protein kinases known as the cyclin-dependent kinases (CDKs). (biomedcentral.com)
  • Cyclins function as the positive regulators of CDKs. (biomedcentral.com)
  • D-type and E-type cyclins assemble with CDKs during the G1 phase and these holoenzymes act as rate-limiting controllers to regulate passage through the restriction point and the subsequent onset of DNA replication [ 2 , 3 ]. (biomedcentral.com)
  • Cyclins and CDKs assemble into complexes with one another as cells progress through G1 phase, cyclins being required to activate the serine-threonine kinase activity of their catalytic partners. (biomedcentral.com)
  • Furthermore, CDK-activating kinase (CAK) phosphorylates cyclin-bound CDKs on a single threonine residue, a modification that is essential for their activity [ 6 - 9 ]. (biomedcentral.com)
  • Human cells contain many different cyclins binding to different CDKs. (wikipedia.org)
  • CDKs and cyclins appear and activate at specific cell cycle phases. (wikipedia.org)
  • Further research has demonstrates that Cdks, cyclins and CKIs play essential roles in processes such as transcription, epigenetic regulation, metabolism, stem cell self-renewal, neuronal functions and spermatogenesis. (wikipedia.org)
  • The cyclin-dependent kinase (CDK) inhibitors p21 and p16 inhibit the activity of CDKs, such as CDK4. (medscape.com)
  • We examined the expression of p16 and Rb protein by means of immunohistochemistry in 61 non-small cell lung cancers and have demonstrated an inverse relationship between the expression of p16 and Rb protein: 28/30 specimens that did not stain for p16 stained for Rb and 21/31 p16-positive specimens did not stain for Rb. (nih.gov)
  • p16 expression was studied and compared in these three groups using the immunohistochemistry technique. (advbiores.net)
  • Cell cycle progression is stopped by Cyclin-dependent kinase inhibitor protein at the G1 phase. (wikipedia.org)
  • As a result, it negatively regulates cyclin-D-dependent phosphorylation of the retinoblastoma (pRb) gene product, thus blocking cell-cycle progression from G 1 -to S-phase ( 2 - 4 ). (iiarjournals.org)
  • Deletion or mutation of the p16 gene leads to tumor development or tumor progression. (umich.edu)
  • Conclusion: p63, p16, MIB, Cal A, Cys A are markedly expressed and p16 is strongly suppressed in oral cavity tumors, which suggests that the latter protein may play a role in negative regulation of cell cycle progression. (bvsalud.org)
  • The various markers that enable assessment of the progression of preneoplastic lesions to spindle cell carcinoma include the p16 protein, which halts the cell cycle and induces apoptosis by pRb-mediated phosphorylation of cyclin-dependent kinase 4 (CDK4). (bvsalud.org)
  • PCNA is a co-factor of cyclin-D and it makes a complex with cyclin-D, a cyclin dependent kinase (CDK), and a cyclin dependent kinase inhibitor (CDKI). (biomedcentral.com)
  • Role in cancer: Cyclin-dependent kinase inhibitors (CKIs) mutants are frequent in human cancers. (wikipedia.org)
  • Fusions involving the tropomyosin-related kinase (TRK) family of neurotrophin receptor tyrosine kinases have been identified in various human cancers and suggested to function as oncogenic drivers. (aacrjournals.org)
  • p16 is a cyclin-dependent kinase inhibitor that has shown prognostic utility in some human cancers. (umich.edu)
  • Nevertheless, these results show that p16 plays a role in atRA mediated growth inhibition in ovarian carcinoma cells and that modulation of p16 expression can determine the growth response to atRA. (temple.edu)
  • In contrast, we observed a significant association between p16 overexpression and HPV16/18 genotypes. (mcmaster.ca)
  • This study aimed to evaluate p16 expression in breast cancer in comparison to normal breast tissue and determine the association between p16 expression and clinicopathological parameters in breast cancer. (advbiores.net)
  • It is a specific inhibitor of cdk4/cdk6, and a tumor suppressor involved in the pathogenesis of a variety of malignancies. (neobiotechnologies.com)
  • 2 The p16 protein is a cyclin dependent kinase inhibitor that suppresses cell proliferation 3 and is expressed in a wide range of tissues, including the breast, and in breast cancers. (bmj.com)
  • Mutations in cyclin-dependent kinase inhibitors controlling the G1 phase of the cell cycle are prevalent in various cancers. (koreamed.org)
  • Using these p16-3MR mice and in vivo bioluminescent imaging, the researchers observed a robust, but transient, increase in senescent cells at the site of cutaneous injury. (jax.org)
  • Likewise, p16/p21 double knockout mice, which have very few senescent cells, showed similar delays in wound closure. (jax.org)
  • Scar tissue (stained for collagen, in orange) is evident in healed wounds from transgenic p16-3MR mice lacking senescent cells (bottom panel, GCV-treated) compared to control mice (top panel, PBS-treated). (jax.org)
  • To understand how senescent cells promote repair, the Campisi team surveyed wound sites in GCV-treated p16-3MR mice and found fewer endothelial cells and fibroblasts, including myofibroblasts, which are contractile cells responsible for wound closure. (jax.org)
  • In addition, they discovered that senescent cells fluorescently isolated from p16-3MR wounds produced large amounts of PDGF-AA, a mitogen and chemoattractant for fibroblasts. (jax.org)
  • To investigate the clinical role of nm23 expression in identifying both high‐risk human papillomavirus (HR‐HPV) and high‐grade cervical lesions or carcinomas [cervical intraepithelial neoplasia 2 + (CIN2 + )], and to compare it with p16 overexpression, as this latter biomarker has already been reported widely in HR‐HPV infected cervical lesions. (mcmaster.ca)
  • We confirm the diagnostic value of p16 overexpression. (mcmaster.ca)
  • The relationship between p16 overexpression and poor prognosis of breast cancer has been reported in some studies. (advbiores.net)
  • Our results show that overexpression of p16 in SKOV3 cells leads to growth inhibition following atRA treatment. (temple.edu)
  • Herpes virus thymidine kinase (HSV-tk) is used in suicide gene therapy. (umich.edu)
  • Lyoma virus enhancer, HSV-tk enhancer and promoter, HSV thymidine kinase. (umich.edu)
  • Cdk4-mediated phosphorylation of Rb protein is inhibited by p16, a product of a possible tumor suppressor gene. (nih.gov)
  • However, if CKI's mutations don't stop the cell, the Cyclin D is transcribed. (wikipedia.org)
  • Furthermore, cfDNA sequencing resulted in increased identification of potentially actionable mutations compared with tissue-based NGS, including clinically relevant mutations in the BRAF , FGFR2 , and EGFR oncogenes, the last of which was associated with durable clinical benefit in a patient treated with the EGFR inhibitor erlotinib. (aacrjournals.org)
  • Our results indirectly support the theory that p16 expression is negatively regulated by the functional Rb protein. (nih.gov)
  • The p19ARF protein, which is encoded by the same locus as p16, also leads to cell cycle arrest by inhibiting the ability of MDM2 to inactivate TP53. (medscape.com)
  • Only 1 of the p16-negative specimens had a mutation of exon 2 of the CDKN2 gene. (nih.gov)
  • Immunohistochemical evaluation of nm23 and p16 in 143 cervical biopsy specimens including negative, low‐ and high‐grade lesions and squamous carcinomas (SC). (mcmaster.ca)
  • Expression of p15, p16, p21 and p27 did not vary in granulosa and theca cells by the follicle stage. (biomedcentral.com)
  • These preliminary findings suggest that the initiation of oocyte growth, which seems to lead follicle growth, is associated with diminished p16 expression in the mouse ovary. (biomedcentral.com)
  • Further studies are needed to investigate the factors that regulate the expression of p16 in the oocyte, which might also govern the initiation of primordial follicle growth. (biomedcentral.com)
  • DHA-enriched fish oil upregulates cyclin-dependent kinase inhibitor 2A (P16 INK ) expression and downregulates telomerase activity without modulating effects of PPARγ Pro12Ala polymorphism in type 2 diabetic patients: A randomized, double-blind, placebo-controlled clinical trial. (bvsalud.org)
  • In addition, between-group comparisons showed significant differences in the changes in telomerase activity (p = 0.003) and P16 mRNA expression (p = 0.028) and non-significant differences in TNF-α and IL-6 mRNA expression. (bvsalud.org)
  • The gene *DHA interaction could not affect changes in P16, IL-6 , or TNF-α mRNA expression or in telomerase activity in PBMC. (bvsalud.org)
  • Short- time DHA-enriched fish oil supplementation caused increased levels of P16 expression and a decline in telomerase activity compared with the control group without modulating the effects of Pro12Ala polymorphism on the PPARγ gene . (bvsalud.org)
  • p16 expression can be induced in a regulated fashion in the doubly transgenic mice by administering antibiotic doxycycline or tetracycline. (foxchase.org)
  • Our results indicate that p18 is temporarily upregulated while p16 is downregulated after BMP4 over-expression indicating a potential mechanism by which BMP4 can offset the effect of aging on the osteogenic potential and the bone regenerative potential of aged MDSCs. (pitt.edu)
  • Moreover, the relationship between p16 expression and age, tumor size, carcinoma subtype, tumor grade, and lymph node involvement was investigated in the tumor group. (advbiores.net)
  • p16 expression showed a significant difference between the tumor group and the two control groups with a significantly higher expression in the tumor group. (advbiores.net)
  • No significant relationship was detected between p16 expression and other clinicopathological factors. (advbiores.net)
  • p16 seems to have a rather significant expression in breast cancer in comparison to normal breast parenchyma. (advbiores.net)
  • However, among clinicopathological parameters, we found only a direct relationship between lymph node involvement and intensity of p16 expression. (advbiores.net)
  • Oncogenic Ras induces p19ARF and growth arrest in mouse embryo fibroblasts lacking p21Cip1 and p27Kip1 without activating cyclin D-dependent kinases. (ku.dk)
  • Despite the small p16 sequence database, our calculations of high conservation correctly predicted loss of cell cycle arrest function in 75% of tested codons, and low conservation correctly predicted wild-type function in 80-90% of codons. (nih.gov)
  • These cyclin-dependent kinase inhibitor protein emerges only in their specific cell cycle phase. (wikipedia.org)
  • Each Cyclin/CDK complex are specific to the part of the cell cycle phase. (wikipedia.org)
  • Each CDK and cyclin can be identified based on the location of the cell cycle. (wikipedia.org)
  • In the cyclin-dependent kinase (CDK) family or CDK, Cyclin, and CKIs, serine/threonine kinases play an integral role in regulating the eukaryotic cell cycle. (wikipedia.org)
  • PTEN encodes a protein kinase of the same name and functions as a tumor suppressor through regulation of cell proliferation. (medscape.com)
  • Preclinical studies demonstrated that LOXO-101 inhibited the proliferation of cancer cell lines harboring oncogenic TRK fusions in a dose-dependent manner and resulted in suppression of tumor growth in vivo , consistent with previous studies. (aacrjournals.org)
  • The pharmaceutical industry currently uses cyclin-dependent kinase (CDK) inhibitors to target cell proliferation for cancer chemotherapy. (foxchase.org)
  • The P16 Antibody Rabbit reagent is RUO (Research Use Only) to test human serum or cell culture lab samples. (genprofiling.com)
  • Activation of p21 or p16 therefore causes cell cycle arrest. (medscape.com)
  • The aim of the present study was to determine the significance of this tumor suppressor gene for ovarian tumorigenesis, investigating both numerical aberrations of chromosome 9 and p16 gene alterations in 28 cases of ovarian tumors, by the fluorescence in situ hybridization (FISH) technique. (iiarjournals.org)
  • Materials and Methods: To investigate both the presence of numerical abnormalities of chromosome 9 and p16 gene alterations in ovarian cancer, we studied 28 cases by the fluorescence in situ hybridization (FISH) technique using a DNA p16 probe and an a-satellite probe specific for chromosome 9. (iiarjournals.org)
  • Conclusion: Numerical aberrations of chromosome 9 and p16 gene deletion are common findings in ovarian cancer. (iiarjournals.org)
  • Data suggest that the p16 gene, located in the short arms of chromosome 9, may play a role in ovarian carcinogenesis. (iiarjournals.org)
  • There are few studies focusing on the molecular analysis of p16 gene in ovarian cancer ( 13 - 16 ). (iiarjournals.org)
  • CONCLUSION: Primary tumor volume plays a crucial role in predicting local tumor response, particularly in p16-positive OPSCC. (lu.se)
  • Results: From the 121 recruited women, 76 screened positive in at least one exam (LBCC or DS-p16/Ki-67) and had a diagnostic conclusion. (edu.br)
  • HPV-associated, p16-positive, oropharyngeal tumors (OPSCC) are more radiosensitive and have better outcome. (lu.se)
  • RESULTS: In the p16-positive cohort (n = 433), the volume exponent c was 1.44 (95%CI 1.06-1.91), compared to 0.90 (0.54-1.32) for p16-negative tumors (n = 90). (lu.se)
  • An additional dose of 6.8 Gy (interquartile range 4.8-9.1) may theoretically counteract the more radioresistant behavior of p16-negative tumors. (lu.se)
  • The estimated α/β-ratio for p16-positive oropharyngeal tumors aligns with previous HNSCC studies, whereas the impact of prolonged OTT was slightly less than previously reported. (lu.se)
  • The orally available, highly selective small-molecule TRK family inhibitor LOXO-101 is currently being tested in a phase I dose-escalation study in patients with advanced solid tumors. (aacrjournals.org)
  • Loss of function of the p16 gene has been reported to occur mainly by homozygous deletion, mutation or aberrant DNA methylation of the promoter of the region ( 5 - 8 ). (iiarjournals.org)
  • It moves into the cytoplasm and eventually activates a specific cyclin-dependent kinase (CDK). (wikipedia.org)
  • p16 status is an important prognostic indicator in HNSCC and the p16 positive/HPV16 negative group is likely a distinct subgroup lacking any HPV genotype. (neobiotechnologies.com)
  • Human IgG antibody Laboratories manufactures the p16 antibody rabbit reagents distributed by Genprice. (genprofiling.com)
  • Cyclin E forms complexes during this interval with CDK2. (biomedcentral.com)
  • The structure of CDK2-CyclinA and p27 is determined by crystallography, demonstrating that the inhibitor of p27 stretches at the top of the Cyclin-CDK complex. (wikipedia.org)
  • Here, we generated knockout mouse models for each of these three cyclin-dependent kinase inhibitors using engineered nucleases. (koreamed.org)
  • Objective: To access p16/Ki-67 double staining (DS) in cervical cells performance for detecting precursor lesions of cervical cancer, in comparison to immediate repetition of the liquid-based cervical cytology (LBCC) in women with screening cytology results of atypical squamous cells of undetermined significance (ASC-US) or low-grade squamous intraepithelial lesion (LSIL). (edu.br)
  • Women were addressed to the Cervical Referral Services (SRC) in each state and examined with colposcopy, LBCC and DS-p16/Ki-67. (edu.br)
  • In these studies, we investigated the role of p16 in mediating atRA induced growth arrest. (temple.edu)