Relevant bibliographies by topics / INK4b

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Academic literature on the topic 'INK4b'

Author: Grafiati
Published: 4 June 2021
Last updated: 17 February 2022

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Journal articles on the topic "INK4b"

1

Malumbres, Marcos, Ignacio Pérez De Castro, María I. Hernández, María Jiménez, Teresa Corral, and Angel Pellicer. "Cellular Response to Oncogenic Ras Involves Induction of the Cdk4 and Cdk6 Inhibitor p15INK4b." Molecular and Cellular Biology 20, no. 8 (April 15, 2000): 2915–25. http://dx.doi.org/10.1128/mcb.20.8.2915-2925.2000.

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ABSTRACT The cell cycle inhibitor p15 INK4b is frequently inactivated by homozygous deletion together with p16 INK4a and p19 ARF in some types of tumors. Although the tumor suppressor capability of p15 INK4b is still questioned, it has been found to be specifically inactivated by hypermethylation in hematopoietic malignancies in the absence of p16 INK4a alterations. Here we show that, in vitro, p15 INK4b is a strong inhibitor of cellular transformation by Ras. Surprisingly, p15 INK4b is induced in cultured cells by oncogenic Ras to an extent similar to that of p16 INK4a , and their expression is associated with premature G1 arrest and senescence. Ras-dependent induction of these two INK4 genes is mediated mainly by the Raf-Mek-Erk pathway. Studies with activated and dominant negative forms of Ras effectors indicate that the Raf-Mek-Erk pathway is essential for induction of both the p15 INK4b and p16 INK4a promoters, although other Ras effector pathways can collaborate, giving rise to a stronger response. Our results indicate that p15 INK4b , by itself, is able to stop cell transformation by Ras and other oncogenes such as Rgr (a new oncogene member of the Ral-GDS family, whose action is mediated through Ras). In fact, embryonic fibroblasts isolated from p15 INK4b knockout mice are susceptible to transformation by the Ras or Rgr oncogene whereas wild-type embryonic fibroblasts are not. Similarly, p15 INK4b -deficient mouse embryo fibroblasts are more sensitive than wild-type cells to transformation by a combination of the Rgr and E1A oncogenes. The cell cycle inhibitor p15 INK4b is therefore involved, at least in some cell types, in the tumor suppressor activity triggered after inappropriate oncogenic Ras activation in the cell.
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Klangby, Ulf, Ismail Okan, Kristinn P. Magnusson, Martin Wendland, Peter Lind, and Klas G. Wiman. "p16/INK4a and p15/INK4b Gene Methylation and Absence of p16/INK4a mRNA and Protein Expression in Burkitt's Lymphoma." Blood 91, no. 5 (March 1, 1998): 1680–87. http://dx.doi.org/10.1182/blood.v91.5.1680.

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Abstract The fact that the p16/INK4a and p15/INK4b genes are frequently inactivated in human malignancies and that p16/INK4a null mice spontaneously develop B-cell lymphomas prompted us to examine the status of both genes in Burkitt's Lymphoma (BL). We found a low frequency of p16/INK4a and p15/INK4b deletions and mutations in BL cell lines and biopsies. However, p16/INK4a exon 1 was methylated in 17 out of 19 BL lines (89.5%) and in 8 out of 19 BL biopsies (42%) analyzed. p15/INK4b Exon 1 was also methylated, although at a lower frequency. p16/INK4a mRNA was readily detected in BL lines carrying unmethylated p16/INK4a, but not in those carrying methylated p16/INK4a. No p16/INK4a protein was detected in any of the BL lines and biopsies examined. In contrast, only one out of seven lymphoblastoid cell lines (LCLs) examined was methylated in p16/INK4a exon 1, and three out of the six LCLs with unmethylated p16/INK4a expressed detectable levels of p16/INK4a protein. Thus, the frequent p16/INK4a methylation in BL lines correlates with downregulation of p16/INK4a expression, suggesting that exon 1 methylation is responsible for silencing the p16/INK4a gene in BL.
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Klangby, Ulf, Ismail Okan, Kristinn P. Magnusson, Martin Wendland, Peter Lind, and Klas G. Wiman. "p16/INK4a and p15/INK4b Gene Methylation and Absence of p16/INK4a mRNA and Protein Expression in Burkitt's Lymphoma." Blood 91, no. 5 (March 1, 1998): 1680–87. http://dx.doi.org/10.1182/blood.v91.5.1680.1680_1680_1687.

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The fact that the p16/INK4a and p15/INK4b genes are frequently inactivated in human malignancies and that p16/INK4a null mice spontaneously develop B-cell lymphomas prompted us to examine the status of both genes in Burkitt's Lymphoma (BL). We found a low frequency of p16/INK4a and p15/INK4b deletions and mutations in BL cell lines and biopsies. However, p16/INK4a exon 1 was methylated in 17 out of 19 BL lines (89.5%) and in 8 out of 19 BL biopsies (42%) analyzed. p15/INK4b Exon 1 was also methylated, although at a lower frequency. p16/INK4a mRNA was readily detected in BL lines carrying unmethylated p16/INK4a, but not in those carrying methylated p16/INK4a. No p16/INK4a protein was detected in any of the BL lines and biopsies examined. In contrast, only one out of seven lymphoblastoid cell lines (LCLs) examined was methylated in p16/INK4a exon 1, and three out of the six LCLs with unmethylated p16/INK4a expressed detectable levels of p16/INK4a protein. Thus, the frequent p16/INK4a methylation in BL lines correlates with downregulation of p16/INK4a expression, suggesting that exon 1 methylation is responsible for silencing the p16/INK4a gene in BL.
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Saunderson, Emily A., Kevin Rouault-Pierre, John G. Gribben, and Gabriella Ficz. "CRISPR/Cas9-Targeted De Novo DNA Methylation Is Maintained and Impacts the Colony Forming Potential of Human Hematopoietic CD34+ Cells." Blood 134, Supplement_1 (November 13, 2019): 2517. http://dx.doi.org/10.1182/blood-2019-130267.

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Introduction The epigenome is significantly perturbed in hematological malignancies with global DNA hypomethylation and localized hypermethylation of gene promoter CpG islands. Whether specific gene promoter hypermethylation can contribute to the clonal expansion of hematopoietic stem and progenitor cells (HSPCs) in humans by affecting HSPC biology, independently of genetic mutations, has not previously been investigated due to the lack of appropriate tools. We show for the first time that it is possible to target de novo DNA methylation using CRISPR/Cas9 in human CD34+ cells isolated from cord blood (CB). DNA methylation targeted to key cell cycle control gene promoters, INK4b (p15) and ARF (p14), is permanently maintained after dCas9 3A3L degradation and inherited as cells differentiate; inhibiting gene expression and affecting the colony forming potential of CD34+ cells. This demonstrates that specific DNA hypermethylation events can permanently change HSPC biology and impact differentiation, potentially contributing to pre-malignant processes. Methods Human CD34+ HSPCs were isolated from human CB and maintained in liquid culture for 24 hours before nucleofection with mRNA encoding an adapted form of CRISPR/Cas9 which has no nuclease activity (dCas9) and is fused to the catalytic domain of DNA methyltransferase 3A (DNMT3A) and 3L (3A3L). The nucleofection cocktail contained dCas9 3A3L or dCas9 3A3L-mut (lacks methyltransferase activity) and 1 to 3 guide RNAs to target DNA methylation to combinations of the INK4a-ARF-INK4b locus. Cells were then seeded into methylcellulose for a primary colony forming assay (CFU). Colonies were scored after 14 days and cells were either harvested and pooled or individual colonies were picked for single-colony molecular analyses. The DNA was extracted and methylation at the INK4a-ARF-INK4b promoters was quantified using targeted bisulfite sequencing; target gene expression was measured using qPCR. The remaining cells from the primary CFU were re-plated a second (secondary CFU) and third (tertiary CFU) time and colonies were again scored after 14 days. Results and Conclusions Targeting DNA methylation to the INK4a-ARF-INK4b locus or INK4b individually in human CD34+ cells resulted in maintenance of hypermethylation at ARF and/or INK4b gene promoters in individual BFU-E (burst-forming unit-erythroid) and CFU-GM (granulocyte, macrophage) colonies as measured by single-colony targeted bisulfite sequencing after the primary CFU; causing heritable repression of INK4b gene expression in the differentiated cells. Some CpGs were up to 90% methylated, indicating that DNA methylation added at these gene promoters is highly stable as cells differentiate. Hypermethylation of ARF and INK4b was found in some colonies even after the tertiary CFU, demonstrating long-term maintenance of promoter hypermethylation. Unexpectedly, no DNA hypermethylation was detected at INK4a in differentiated cells, but whether this is the case for all subpopulations of HSPCs (i.e. HSCs or lymphoid progenitors) is under investigation. Hypermethylation of INK4b and ARF increased the colony forming potential of CD34+ cells in primary, secondary and tertiary CFUs, compared to the control. Conversely, methylation targeted to INK4b alone did not significantly affect the number of colonies in the first CFU, and decreased the number of colonies in the secondary CFU. This suggests a complex interplay between key cell cycle regulators ARF and INK4b in CD34+ cells and during differentiation which can be disrupted by DNA hypermethylation and gene repression. These findings demonstrate the novel insights we can gain by using CRISPR/Cas9 tools to target DNA methylation and these investigations will reveal how gene promoter hypermethylation can impact HSPC function. Furthermore, studying this locus may uncover an important role for DNA hypermethylation in the development of myeloid malignancies, since INK4b is frequently hypermethylated, but rarely mutated, in myeloid dysplastic/proliferative neoplasms and acute myeloid leukemia. Disclosures Gribben: Janssen: Consultancy, Honoraria, Research Funding; Celgene: Consultancy, Honoraria, Research Funding; Abbvie: Consultancy, Honoraria, Research Funding; Acerta/Astra Zeneca: Consultancy, Honoraria, Research Funding.
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Kia, Sima Kheradmand, Marcin M. Gorski, Stavros Giannakopoulos, and C. Peter Verrijzer. "SWI/SNF Mediates Polycomb Eviction and Epigenetic Reprogramming of the INK4b-ARF-INK4a Locus." Molecular and Cellular Biology 28, no. 10 (March 10, 2008): 3457–64. http://dx.doi.org/10.1128/mcb.02019-07.

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ABSTRACT Stable silencing of the INK4b-ARF-INK4a tumor suppressor locus occurs in a variety of human cancers, including malignant rhabdoid tumors (MRTs). MRTs are extremely aggressive cancers caused by the loss of the hSNF5 subunit of the SWI/SNF chromatin-remodeling complex. We found previously that, in MRT cells, hSNF5 is required for p16 INK4a induction, mitotic checkpoint activation, and cellular senescence. Here, we investigated how the balance between Polycomb group (PcG) silencing and SWI/SNF activation affects epigenetic control of the INK4b-ARF-INK4a locus in MRT cells. hSNF5 reexpression in MRT cells caused SWI/SNF recruitment and activation of p15 INK4b and p16 INK4a , but not of p14 ARF . Gene activation by hSNF5 is strictly dependent on the SWI/SNF motor subunit BRG1. SWI/SNF mediates eviction of the PRC1 and PRC2 PcG silencers and extensive chromatin reprogramming. Concomitant with PcG complex removal, the mixed lineage leukemia 1 (MLL1) protein is recruited and active histone marks supplant repressive ones. Strikingly, loss of PcG complexes is accompanied by DNA methyltransferase DNMT3B dissociation and reduced DNA methylation. Thus, various chromatin states can be modulated by SWI/SNF action. Collectively, these findings emphasize the close interconnectivity and dynamics of diverse chromatin modifications in cancer and gene control.
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Rosu-Myles, Michael, and Linda Wolff. "p15Ink4b Maintains Normal Levels of Granulocyte-Macrophage Progenitors In Vivo." Blood 106, no. 11 (November 16, 2005): 2280. http://dx.doi.org/10.1182/blood.v106.11.2280.2280.

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Abstract Maintaining a balance between the proliferation and differentiation of hematopoietic stem and progenitor cells is crucial for normal maintenance of the hematopoietic system. The INK4 family of cyclin-dependent kinase inhibitors traditionally function in regulating cell proliferation by blocking G1/S phase transition during cell cycle. Loss of expression of one INK4 family member, p15INK4B, has been associated with acute myeloid leukemia (AML) and myelodysplasia and mice that lack p15Ink4b are more prone to developing retrovirus-induced AML. These data suggest an important role for p15INK4B in myeloid differentiation. Here we examined the hematopoietic progenitor pool in p15Ink4b deficient (Ink4b−/−) mice to determine its potential role in regulating hematopoietic precursors. In myeloid progenitor colony assays, bone marrow (BM) from Ink4b−/− mice were found to contain a 1.4 fold greater number of progenitors committed to the formation of granulocytes and macrophages (CFU-GM). This in vitro data was supported by flow cytometric analysis which determined that Ink4b−/− BM contained a 3-fold greater proportion of granulocyte-macrophage progenitors (GMP) (11+/−1.2% vs 34+/−9%) concomitant with a 2-fold decrease in common myeloid progenitors (CMP) (56+/−2 % vs 34+/−7 %). GMP isolated from Ink4b−/− BM also demonstrated a 3-fold greater propensity to form CFU-GM. Despite these differences, the proportion of cycling GMP or CMP in Ink4b−/− and wt mice were identical as determined by propidium iodide and Hoecsht dye DNA stains and in vivo BrdU incorporation. However, in response to specific cytokines, Ink4b−/− CMP showed an increased potential for GMP differentiation and a decreased capacity to form megakaryocyte-erythroid progenitors (MEP). Our work demonstrates that p15Ink4b functions in maintaining normal levels of CFU-GM and may regulate CMP differentiation in response to specific factors.
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Zhang, H., X. Li, L. Ge, J. Yang, J. Sun, and Q. Niu. "Methylation of CpG island of p14(ARK), p15(INK4b) and p16(INK4a) genes in coke oven workers." Human & Experimental Toxicology 34, no. 2 (May 16, 2014): 191–97. http://dx.doi.org/10.1177/0960327114533576.

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To detect the blood genomic DNA methylation in coke oven workers and find a possible early screening index for occupational lung cancer, 74 coke oven workers as the exposed group and 47 water pump workers as the controls were surveyed, and urine samples and peripheral blood mononuclear cells (PBMCs) were collected. Airborne benzo[a]pyrene (B[a]P) levels in workplace and urinary 1-hydroxypyrene (1-OH-Py) levels were determined by high-performance liquid chromatography. DNA damage of PBMCs and the p14(ARK), p15(INK4b) and p16(INK4a) gene CpG island methylation in the promoter region were detected by comet assay and methylation-specific polymerase chain reaction techniques, respectively. Results show that compared with the controls, concentration of airborne B[a]Ps was elevated in the coke plant, and urinary 1-OH-Py’s level and DNA olive tail moment in comet assay were significantly increased in the coke oven workers, and p14(ARK), p15(INK4b) and p16(INK4a) gene methylation rates were also significantly increased. With the working years and urinary 1-OH-Py’s level, the rates of p14(ARK) and p16(INK4a) gene methylation were significantly increased while that of p15(INK4b) gene methylation displayed no statistical change. We conclude that PBMCs’ p14(ARK) and p16(INK4a) gene methylation may be used for screening and warning lung cancer in coke oven workers.
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Tasaka, Taizo, James Berenson, Robert Vescio, Toshiyasu Hirama, Carl W. Miller, Masami Nagai, Jiro Takahara, and H. Phillip Koeffler. "Analysis of the p16 INK4A , p15 INK4B and p18 INK4C genes in multiple myeloma." British Journal of Haematology 96, no. 1 (January 1997): 98–102. http://dx.doi.org/10.1046/j.1365-2141.1997.8552482.x.

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Nazarenko, M. S., A. V. Markov, I. N. Lebedev, A. A. Sleptsov, J. A. Koroleva, A. V. Frolov, O. L. Barbarash, L. S. Barbarash, and V. P. Puzirev. "Methylation profile of INK4B-ARF-INK4A locus in atherosclerosis." Russian Journal of Genetics 49, no. 6 (June 2013): 681–84. http://dx.doi.org/10.1134/s1022795413060070.

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Markus, Jan, Matthew T. Garin, Naomi Galili, Azra Raza, Michael J. Thirman, Michelle M. LeBeau, Janet D. Rowley, and Linda Wolff. "Methylation-Independent Silencing of the Tumor Suppressor p15INK4B by CBFb-SMMHC in Acute Myeloid Leukemias with inv(16)." Blood 106, no. 11 (November 16, 2005): 1615. http://dx.doi.org/10.1182/blood.v106.11.1615.1615.

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Abstract The tumor suppressor INK4B(p15) gene is silenced by CpG island hypermethylation in a majority of acute myeloid leukemias (AML). This silencing can be reversed by the treatment with hypomethylating agents, and these agents are currently being tested for therapeutic intervention. So far, it was not investigated whether or not the INK4B is hypermethylated in all cytogenetic subtypes of AML. Our experiments, which compare levels of INK4B methylation in AML with inv(16), t(8:21) and t(15;17) reveal a strikingly low level of methylation in all leukemias with inv(16). This contrasts with significant levels of DNA methylation in a high proportion of the AML from the other two groups. Surprisingly, even though there is a lack of INK4B methylation in samples from patients with inv(16), expression of the gene is very low when compared to that of PBL from healthy individuals or HL60 cells. Subsequent experiments uncovered a novel mechanism to explain the low level of INK4B expression in the inv(16) AMLs. Overexpression of the aberrant chromosome 16-associated gene CBFb-MYH11 in U937 cells results in failure to induce INK4B in response to vitamin D3. Furthermore, CBFb-SMMHC, encoded by CBFb-MYH11 directly represses transcription from an INK4B promoter in a reporter assay. Electromobility shift assays in the AML-derived cell line ME-1 and U937 cells expressing the fusion gene demonstrate that the repression is due to a change in the composition of the complexes recognizing the binding sites for the transcription regulator CBF. In conclusion, we have found that methylation is not the only way to induce silencing of the tumor suppressor p15INK4B in AML. In inv(16)-containing AML, loss of gene expression is accomplished by the direct transcriptional repressor activity of CBFβ-SMMHC.
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Dissertations / Theses on the topic "INK4b"

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Quesnel, Bruno. "Gene p16 ink4a , p15 ink4b, et hemopathies malignes." Lille 2, 1997. http://www.theses.fr/1997LIL2T009.

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Carter, Tina. "A study of the INK4A/ARF and INK4B loci in childhood acute lymphoblastic leukaemia using quantitative real time polymerase chain reaction." University of Western Australia. School of Paediatrics and Child Health, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0077.

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[Truncated abstract] Childhood acute lymphoblastic leukaemia (ALL) accounts for the largest number of cases of childhood cancer (25-35%) and is the primary cause of cancer related morbidity. Today more than 76% of children with ALL are alive and disease free at 5 years. Approximately one in 900 individuals between the ages of 16 and 44 years is a survivor of childhood cancer. In contrast, those patients who relapse with childhood ALL currently have a 6-year event free survival of 20-30%. The short arm of chromosome 9p is mutated or deleted in many cancers including leukaemia. Aberrations of the INK4A/ARF and INK4B loci at the 9p21 band are linked to the development and progression of cancer. In murine cancer models there is evidence to suggest that mutations of Ink4a/Arf and p53 gene loci promote resistance to chemotherapeutic drugs known to trigger apoptosis. The initial aim of this project was to develop an accurate, reproducible method to detect deletions at the INK4A/ARF locus in patient bone marrow specimens. This technique was then applied to detect the incidence of deletions of this locus in childhood ALL specimens. The hypothesis developed was that deletion at the INK4A/ARF locus at diagnosis in childhood ALL is an independent prognostic marker and is involved in disease progression. A secondary aim of this study was to determine which deletions at the INK4A/ARF and INK4B loci are the most relevant in leukaemogenesis in childhood ALL. ... This study has shown that deletion of the INK4A/ARF locus is an independent prognostic indicator in childhood ALL. In addition, the frequency of deletion at the INK4A/ARF and INK4B loci is increased at relapse compared to diagnosis in childhood ALL. In the relapse study group, deletion of the p16INK4A gene at diagnosis was associated with a decreased median time to relapse compared to other genes analysed. Murine studies suggest that such deletions may result in an increased resistance to chemotherapy. If the findings from this study are confirmed in a larger cohort, it is expected that therapeutic interventions based on assessment of the p16INK4A gene in diagnostic childhood ALL specimens will be implemented to prevent relapse in standard risk patients and help to improve the outcome in high risk patients.
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Li, Junan. "Structural and functional studies on Tumor Suppressor INK4 Proteins P16(INK4A) and P18(INK4C) /." The Ohio State University, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488194825665461.

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Tanaka, Tomoyuki. "High incidence of allelic loss on chromosome 5 and inactivation of p15^{INK4B} and p16^{INK4A} tumor suppressor genes in oxystress-induced renal cell carcinoma of rats." Kyoto University, 1999. http://hdl.handle.net/2433/181736.

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Draney, Carrie. "Overexpression of HDAC1 Induces Functional β-cell Mass." BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/6573.

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Type 2 diabetes is a metabolic disorder that results in β-cell dysfunction and ultimate destruction, and leads to impaired glucose homeostasis. High rates of proliferation and differentiation of pancreatic β-cells occurs mostly during neonatal development. However, research shows these mechanisms remain intact as β-cell proliferation has been observed during pregnancy and obesity. We have shown that overexpression of the β-cell transcription factor Nkx6.1 is sufficient to induce β-cell proliferation. Exploration of the transcriptional targets of Nkx6.1 has identified histone deacetylase 1 (HDAC1) as a down-stream target of Nkx6.1. Here we demonstrate that HDAC1 overexpression is sufficient to induce β-cell proliferation, enhance β-cell survival upon exposure to apoptotic stimuli and maintains glucose stimulated insulin secretion (GSIS). Our data suggests overexpression of HDAC1 leads to p15/INK4b suppression, a cell cycle inhibitor, potentially explaining the mechanism behind these observed effects. These data demonstrate that HDAC1 overexpression is sufficient to induce β-cell proliferation and enhance cell survival while maintaining glucose stimulated insulin secretion.
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Dodge, Jonathan Eldon. "Selective variegated methylation of the p15/INK4B CpG island is a high frequency event in acute myeloid leukemia (AML)." Diss., The University of Arizona, 2000. http://hdl.handle.net/10150/284143.

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We attempted to define target genes that were inactivated in acute myeloid leukemia (AML) by DNA methylation. We hypothesized that hypermethylation of 51 CpG islands is associated with transcriptional silencing of the corresponding gene and participates in either the emergence of drug resistance or the conversion of normal cells to cancer cells. To test this hypothesis the DNA methylation status of the 5' CpG islands of dCK containing 49 CpGs, p15 containing 80 CpGs, and p16 containing 53 CpGs was determined by sodium bisulfite sequencing of normal human peripheral blood lymphocytes (PBL) and bone marrow (NBM), human leukemia cell lines, and cytosine-arabinoside (ara-C)-resistant adult acute myeloid leukemia (AML) patients. In PBL and NBM dCK, p15, and p16 were all unmethylated. dCK was unmethylated in the paired ara-C-sensitive (/S) ara-C-resistant (/R) leukemia cell lines HL60/S & /R and K562/S & /R, and in the 8 AML patients analyzed. p16 was unmethylated in KG-l and KG-1a and both had detectable p16 mRNA and protein. None of the 8 AML patients had aberrant methylation of p16. For p15, a variegated pattern of aberrant methylation was found in KG-1, and complete methylation of p15 was found in KG-1a. The variegated pattern of p15 methylation seen in KG-1 and the complete methylation seen in KG-1a were both associated with no detectable p15 mRNA or protein. p15 was aberrantly methylated in 6 of the 8 AML patients, 5 had a variegated pattern of methylation, and 1 showed complete methylation. We next introduced ectopic p15 and p16 into the p15 and p16 negative human T-cell lymphocytic leukemia cell line Jurkat. The p15 positive clones grew at a slower rate than the parent cell or p16 positive clones as measured by growth in liquid culture and MTS assay. cDNA microarray expression analysis differentiated p15 and p16 positive subclones from the parent cell line but not from each other. This suggests that despite the selective methylation of p15 but not p16 in AML, p15 and p16 are functionally similar.
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Nilsson, Lisa. "The cell cycle regulators p18Ink4c and p19Ink4d : in vivo studies of their roles in tumorigenesis and development." Doctoral thesis, Umeå University, Molecular Biology (Faculty of Science and Technology), 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1357.

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Progression through the G1, S, G2 and M phases of the cell cycle is controlled by cyclin-dependent kinases (Cdks) and cyclins. These proteins form active Cdk:cyclin complexes that phosphorylate specific substrates. The Cdk:cyclin complexes of the G1/S transition regulate the progression of cells into the S phase by phosphorylating the retinoblastoma protein (Rb). This prevents Rb from sequestering E2F, a transcription factor that induces expression of genes required for DNA synthesis. This process is in part regulated by a family of Cdk inhibitors (CKIs) called the Ink4 family (Inhibitors of Cdk4). The Ink4 family of CKIs consists of four members; p16Ink4a, p15Ink4b, p18Ink4c and p19Ink4d, and they bind specifically to Cdk4 and Cdk6, thereby negatively regulating their kinase activities and cell cycle progression. Because of its cell cycle inhibitory role, p16Ink4a is frequently mutated or deleted in human cancer, whereas the other Ink4 genes are only occasionally altered in cancer. The overall aim of this thesis was to study the roles of p18Ink4c and p19Ink4d using in vivo models of cancer and embryonic development. In paper I, we analyzed the tumor spectrum in mice lacking p53, Ink4c and Ink4d. p53 is a tumor suppressor and one of the most frequently mutated genes in human cancer. Mice carrying mutated p53 alleles are highly tumor-prone but develop predominantly lymphomas. However, the combined loss of p53 and Ink4c (but not Ink4d) caused a shift in the tumor spectrum to increased incidences of hemangiomas and hemangiosarcomas, as well as appearance of medulloblastomas, a tumor of the cerebellum. These data, revealed in the absence of p53, suggest a cell-type specific tumor suppressing role for p18Ink4c. In paper II, loss of Ink4c was evaluated in another tumor-prone mouse model; the Eµ-Myc mouse. This is a transgenic mouse overexpressing c-Myc in B cells causing clonal B cell lymphomas. Surprisingly, precancerous B cells and lymphomas from Eµ-Myc mice exhibited elevated levels of p18Ink4c mRNA and protein despite high rates of proliferation. Moreover, loss of Ink4c in this model did not affect the rate of cell proliferation or the onset of tumor development. We conclude from these studies that Ink4c is not an important tumor suppressor of Myc-induced lymphomas. To gain insight into the role of Ink4 genes in early vertebrate development, the African clawed frog, Xenopus laevis, was analyzed for the presence of Ink4 homologs. Paper III describes the cloning and characterization of a gene homologous to Ink4d, Xl-Ink4d. This CKI is expressed throughout frog embryo development, making Xl-Ink4d the only CKI present during the cleavage stages of X. laevis. Antisense morpholino oligonucleotides directed against Xl-Ink4d were used to knock down the protein level of Xl-Ink4d during development. This resulted in defects in head tissues and reduced expression of Twist, a gene important for neural crest cell migration. We therefore propose that Xl-Ink4d is important for proper neural crest differentiation in the frog.

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Thirukkumaran, P. "Regulation of INK4 gene expression in breast cancer." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0003/MQ35003.pdf.

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Voss, Martin Henner. "p16-INK4a controls the morphology program associated with cellular senescence." [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=976851105.

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Jones, Rebecca May. "Regulation and function of the INK4a/ARF tumour suppressor locus." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444810/.

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The CDKN2a locus encodes two important tumour suppressors, pl61NK4a and ARF. The two genes share a common exon which is translated in different reading frames. pl6,NK4a binds to CDK4 and CDK6, preventing them from forming active complexes with D cyclins. As a result, pRb does not undergo the phosphorylation necessary for the transition from the G1 to S phase of the cell cycle. ARF inhibits the ubiquitination of p53 by MDM2, thereby causing the accumulation of p53. There is a growing awareness that the CDKN2a locus plays a central role in the cellular defences against transformation, and in the cellular response to stress. For example, pl6INK4a is involved in senescence, a permanent cell cycle arrest triggered in primary human fibroblasts in response to many stresses, including the overexpression of oncogenes. However, little is known about the regulation of pl6INK4a under these circumstances, and work in this thesis investigates this issue using overexpression of Myc as a model. The thesis also describes the characterisation of human diploid fibroblasts (Milan cells) from a patient homozygous for the R24P mutation of pl6INK4a. As this mutation is in exon la, ARF is unaffected. The mutant pl6INK4a cannot bind to CDK4, but retains some capacity to bind to CDK6. Milan cells have also been used in combination with shRNA targeting ARF to investigate the relative roles of pl6INK4a and ARF in the prevention of transformation. A panel of Milan cells were produced expressing telomerase, with combinations of Myc, Ras and shRNA targeting ARF, and the ability of the cells to grow in soft agar was assessed. A similar panel of Milan expressing p53 shRNA was also built up. These cells were used to investigate whether ablation of ARF can substitute for the loss of p53 function often associated with transformation, and to help identify which aspects of the p53 pathway are activated in the defence against transformation.
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Books on the topic "INK4b"

1

Fourie, Ockert Johannes. Characterization of a novel INK4A/ARF transcript. Ottawa: National Library of Canada, 2002.

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Urbanowicz, Artur. Inkub. Vesper, 2019.

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Hayes, Michelle. Investigation and characterisation of cell lines containing a deletion in the INK4a Locus under normal and pro-apoptotic conditions. 2003.

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Book chapters on the topic "INK4b"

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Kamijo, Takehiko. "INK4A." In Encyclopedia of Cancer, 1865–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3062.

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Kamijo, Takehiko. "INK4A." In Encyclopedia of Cancer, 1–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_3062-5.

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Kamijo, Takehiko. "INK4A." In Encyclopedia of Cancer, 2277–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_3062.

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Enders, Greg H. "Ink4a Locus: Beyond Cell Cycle." In Cancer Genome and Tumor Microenvironment, 217–29. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0711-0_10.

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Carnero, A., and G. J. Hannon. "The INK4 Family of CDK Inhibitors." In Current Topics in Microbiology and Immunology, 43–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-71941-7_3.

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Pomerantz, Jason, Nicole Schreiber-Agus, Nanette Liegeois, Alice Tam, Kenneth P. Olive, Ronald A. DePinho, and Lynda Chin. "The Role for ink4a in Melanoma Pathogenesis." In The Biology of Tumors, 1–14. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-1352-4_1.

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del Gutierrez Arroyo, Ana, and Gordon Peters. "The INK4A/Arf Network — Cell Cycle Checkpoint or Emergency Brake?" In Genome Instability in Cancer Development, 227–47. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3764-3_8.

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Bartsch, Detlef, M. Kersting, T. Schilling, A. Ramaswamy, B. Gerdes, D. Bastian, M. Schuermann, and M. Rothmund. "p16 INK4a -Alterationen in Gastrinomen und nicht-funktionellen neuroendokrinen Inselzellkarzinomen." In Deutsche Gesellschaft für Chirurgie, 543–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60133-0_107.

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Gerdes, B., P. Barth, M. Kersting, J. Wittenberg, A. Wild, and D. K. Bartsch. "Alterationen der Tumorsuppressorgene p16 INK4a, TP53 und DPC4 sind hilfreich in der Diskriminierung maligner von benignen zystischen Pankreastumoren." In Deutsche Gesellschaft für Chirurgie, 145–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56698-1_37.

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Hesketh, Robin. "INK4A/MTS1/CDK41/CDKN2, INK4B/MTS2, INK4C, INK4D." In The Oncogene & Tumour Suppressor Gene Factsbook, 499–505. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012344548-3/50091-1.

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Conference papers on the topic "INK4b"

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Camacho, Cristel V., Brian McEllin, Pavlina Todorova, Bipasha Mukherjee, Michael D. Story, Robert M. Bachoo, and Sandeep Burma. "Abstract 2360: Complex DNA damage cooperates with Ink4a/Ink4b/Arf loss to generate high grade gliomas in transgenic mouse models." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2360.

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Zhu, Sinan, P. Taneja, R. Kendig, F. Kai, D. Maglic, and K. Inoue. "Abstract 2958: Cyclin D1 regulates the ARF and INK4a promoters." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2958.

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Lu, Yi. "Abstract 3864: Blocking hypoxia-induced tumor cell migration by p16/INK4A." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3864.

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Wagner, S., N. Würdemann, C. Langer, JP Klussmann, and C. Wittekindt. "HPV-Inzidenz und p16INK4a Expression beim Kopf-Hals-Karzinom." In 100 JAHRE DGHNO-KHC: WO KOMMEN WIR HER? WO STEHEN WIR? WO GEHEN WIR HIN? Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727870.

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Seishima, Ryo, Takeyuki Wada, Hirotoshi Hasegawa, Yoshiyuki Ishii, Koji Okabayashi, Masashi Tsuruta, Yuko Kitagawa, Hideyuki Saya, and Osamu Nagano. "Abstract 65:Ink4a/Arflocus drives gastric tumorigenesis through induction of parietal cell loss." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-65.

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Li, Zhongyou, Olga Mejia, and Carlos Caulin. "Abstract 479: p53 mutations and Ink4a/Arf deletion cooperate to induce metastatic skin carcinomas." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-479.

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Davis, Stephani, and Hatem E. Sabaawy. "Abstract 1581: Tumor suppressor functions of the zebrafish ink4ab: a novel cyclin-dependent kinase inhibitor." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1581.

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Hill, Kristen S., Xue Wang, Youngchul Kim, Jane L. Messina, and Minjung Kim. "Abstract 4164: Synergism between NEDD9 overexpression and loss of PTEN and INK4A/ARF in melanoma tumorigenesis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4164.

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Linke, SP, TM Bremer, F. Wärnberg, W. Zhou, L. Goldstein, K. Jirström, and R.-M. Amini. "P4-18-01: Prognostic Role of Tumor and Stromal p16/INK4A in Ductal Carcinoma In Situ (DCIS)." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p4-18-01.

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Schofield, Heather, Filip Bednar, Meredith Collins, Wei Yan, Yaqing Zhang, Nikhil Shyam, Jaime Eberle, et al. "Abstract LB-061: Bmi1 is required for the initiation of pancreatic cancer through an Ink4a-independent mechanism." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-lb-061.

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Reports on the topic "INK4b"

1

Swafford, D. S., J. Tesfaigzi, and S. A. Belinsky. Expression of the p16{sup INK4a} tumor suppressor gene in rodent lung tumors. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381388.

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