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https://www.readbyqxmd.com/read/27905995/cdkn2b-methylation-is-associated-with-carotid-artery-calcification-in-ischemic-stroke-patients
#1
Shuyu Zhou, Yumeng Zhang, Li Wang, Zhizhong Zhang, Biyang Cai, Keting Liu, Hao Zhang, Minhui Dai, Lingli Sun, Xiaomeng Xu, Huan Cai, Xinfeng Liu, Guangming Lu, Gelin Xu
BACKGROUND: Cyclin-dependent kinase inhibitor 2A/2B (CDKN2A/2B) near chromosome 9p21 have been associated with both atherosclerosis and artery calcification, but the underlying mechanisms remained largely unknown. Considering that CDKN2A/2B is a frequently reported site for DNA methylation, this study aimed to evaluate whether carotid artery calcification (CarAC) is related to methylation levels of CDKN2A/2B in patients with ischemic stroke. METHODS: DNA methylation levels of CDKN2A/2B were measured in 322 ischemic stroke patients using peripheral blood leukocytes...
December 1, 2016: Journal of Translational Medicine
https://www.readbyqxmd.com/read/27904447/long-term-survival-in-glioblastoma-methyl-guanine-methyl-transferase-mgmt-promoter-methylation-as-independent-favourable-prognostic-factor
#2
Uros Smrdel, Mara Popovic, Matjaz Zwitter, Emanuela Bostjancic, Andrej Zupan, Viljem Kovac, Damjan Glavac, Drago Bokal, Janja Jerebic
BACKGROUND: In spite of significant improvement after multi-modality treatment, prognosis of most patients with glioblastoma remains poor. Standard clinical prognostic factors (age, gender, extent of surgery and performance status) do not clearly predict long-term survival. The aim of this case-control study was to evaluate immuno-histochemical and genetic characteristics of the tumour as additional prognostic factors in glioblastoma. PATIENTS AND METHODS: Long-term survivor group were 40 patients with glioblastoma with survival longer than 30 months...
December 1, 2016: Radiology and Oncology
https://www.readbyqxmd.com/read/27903974/lncrnas-are-altered-in-lung-squamous-cell-carcinoma-and-lung-adenocarcinoma
#3
Bing Liu, Yifei Chen, Jiong Yang
Long non-coding RNAs (lncRNAs) have been implicated in pathogenesis of various cancers, including lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD). We used cBioPortal to analyze lncRNA alteration frequencies and their ability to predict overall survival (OS) using 504 LUSC and 522 LUAD samples from The Cancer Genome Atlas (TCGA) database. In LUSC, 624 lncRNAs had alteration rates > 1% and 64 > 10%. In LUAD 625 lncRNAs had alteration rates > 1% and 36 > 10%. Among those, 620 lncRNAs had alteration frequencies > 1% in both LUSC and LUAD, while 22 were LUSC-specific and 23 were LUAD-specific...
November 26, 2016: Oncotarget
https://www.readbyqxmd.com/read/27899773/-a-novel-treatment-strategy-for-pancreatic-cancer-based-on-gene-profiles
#4
Hideyuki Hayashi, Hiroshi Nishihara
Pancreatic cancer has one of the highest rates of mortality among malignancies and the development of promising future therapies is strongly required. Recently, the utility of gene aberrations as biomarkers for determining therapeutic strategies has been demonstrated in several types of cancer. The detection of druggable mutations that aid in the selection of effective molecular targeting drugs is feasible in clinical settings for certain cancers. On the other hand, personalized therapy for pancreatic cancer guided by genomic biomarkers has not yet been realized and suitable molecular targets for the disease have been unclear until now...
November 2016: Gan to Kagaku Ryoho. Cancer & Chemotherapy
https://www.readbyqxmd.com/read/27899186/familial-pancreatic-cancer
#5
REVIEW
Gloria M Petersen
Familial pancreatic cancer (FPC) includes those kindreds that contain at least two first-degree relatives with pancreatic ductal adenocarcinoma. At least 12 known hereditary syndromes or genes are associated with increased risk of developing pancreatic cancer, the foremost being BRCA2 and CDKN2A. Research into the identification of mutations in known cancer predisposition genes and through next-generation sequencing has revealed extensive heterogeneity. The development of genetic panel testing has enabled genetic risk assessment and predisposition testing to be routinely offered...
October 2016: Seminars in Oncology
https://www.readbyqxmd.com/read/27893710/muc1-c-activates-bmi1-in-human-cancer-cells
#6
M Hiraki, T Maeda, A Bouillez, M Alam, A Tagde, K Hinohara, Y Suzuki, T Markert, M Miyo, K Komura, R Ahmad, H Rajabi, D Kufe
B-cell-specific Moloney murine leukemia virus integration site 1 (BMI1) is a component of the polycomb repressive complex 1 (PRC1) complex that is overexpressed in breast and other cancers, and promotes self-renewal of cancer stem-like cells. The oncogenic mucin 1 (MUC1) C-terminal (MUC1-C) subunit is similarly overexpressed in human carcinoma cells and has been linked to their self-renewal. There is no known relationship between MUC1-C and BMI1 in cancer. The present studies demonstrate that MUC1-C drives BMI1 transcription by a MYC-dependent mechanism in breast and other cancer cells...
November 28, 2016: Oncogene
https://www.readbyqxmd.com/read/27893424/accumulated-promoter-methylation-as-a-potential-biomarker-for-esophageal-cancer
#7
Xianzhen Peng, Hengchuan Xue, Lingshuang Lü, Peiyi Shi, Jianping Wang, Jianming Wang
We performed a two-stage molecular epidemiological study to explore DNA methylation profiles for potential biomarkers of esophageal squamous cell carcinoma (ESCC) in a Chinese population. Infinium Methylation 450K BeadChip was used to identify genes with differentially methylated CpG sites. Sixteen candidate genes were validated by sequencing 1160 CpG sites in their promoter regions using the Illumina MiSeq platform. When excluding sites with negative changes, 10 genes (BNIP3, BRCA1, CCND1, CDKN2A, HTATIP2, ITGAV, NFKB1, PIK3R1, PRDM16 and PTX3) showed significantly different methylation levels among cancer lesions, remote normal-appearing tissues, and healthy controls...
November 22, 2016: Oncotarget
https://www.readbyqxmd.com/read/27891214/one-step-immortalization-of-primary-human-airway-epithelial-cells-capable-of-oncogenic-transformation
#8
Jordan L Smith, Liam C Lee, Abigail Read, Qiuning Li, Bing Yu, Chih-Shia Lee, Ji Luo
BACKGROUND: The ability to transform normal human cells into cancer cells with the introduction of defined genetic alterations is a valuable method for understanding the mechanisms of oncogenesis. Easy establishment of immortalized but non-transformed human cells from various tissues would facilitate these genetic analyses. RESULTS: We report here a simple, one-step immortalization method that involves retroviral vector mediated co-expression of the human telomerase protein and a shRNA targeting the CDKN2A gene locus...
2016: Cell & Bioscience
https://www.readbyqxmd.com/read/27890785/genomic-characterization-of-dysplastic-nevi-unveils-implications-for-diagnosis-of-melanoma
#9
Rachel D Melamed, Iraz T Aydin, Geena Susan Rajan, Robert Phelps, David N Silvers, Kevin J Emmett, Georg Brunner, Raul Rabadan, Julide Tok Celebi
A well-defined risk factor and precursor for cutaneous melanoma is the dysplastic nevus. These benign tumors represent clonal hyperproliferation of melanocytes that are in a senescent-like state, but with occasional malignant transformation events. To portray the mutational repertoire of dysplastic nevi in patients with the dysplastic nevus syndrome, and to determine the discriminatory profiles of melanocytic nevi (including dysplastic nevi) from melanoma, we sequenced exomes of melanocytic nevi including dysplastic nevi (n = 19), followed by a targeted gene panel (785 genes) characterization of melanocytic nevi (n = 46) and primary melanomas (n = 42)...
November 24, 2016: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/27889930/receptor-tyrosine-kinase-amplification-is-predictive-of-distant-metastasis-in-patients-with-oral-squamous-cell-carcinoma
#10
Yu Oikawa, Kei-Ichi Morita, Kou Kayamori, Kousuke Tanimoto, Kei Sakamoto, Hiroto Katoh, Shumpei Ishikawa, Johji Inazawa, Hiroyuki Harada
This study aimed to clarify the genomic factors associated with the diagnosis and prognosis of oral squamous cell carcinoma via next-generation sequencing. We evaluated data from 220 cases of oral squamous cell carcinoma. Genomic DNA was eluted using formalin-fixed, paraffin-embedded samples, and targeted resequencing of 50 cancer-related genes was performed. In total, 311 somatic mutations were detected in 220 patients, consisting of 68 synonymous mutations and 243 non-synonymous mutations. Genes carrying mutations included TP53, CDKN2A, and PIK3CA in 79 (35...
November 27, 2016: Cancer Science
https://www.readbyqxmd.com/read/27883322/molecular-biology-and-genetic-mechanisms-in-the-progression-of-the-malignant-skin-melanoma
#11
Sofija Pejkova, Gjorgje Dzokic, Smilja Tudzarova-Gjorgova, Sasho Panov
Malignant skin melanoma is a tumor deriving from transformed skin melanocytes as a result of complex interactions between genetic and environmental factors. This melanoma has a potential to metastasize early and very often it is resistant to the existing modalities of the systemic therapy. As in any other neoplasms, certain types of melanoma may skip certain stages of progression. The progression from one stage to another is accompanied by specific biological changes. Several key changes in the melanoma tumorogenesis influence the regulation of the cell proliferation and vitality, including the RAS-RAF-ERK, PI3K-AKT, and p16INK4/CDK4/RB pathways...
November 1, 2016: Prilozi (Makedonska Akademija Na Naukite i Umetnostite. Oddelenie za Medicinski Nauki)
https://www.readbyqxmd.com/read/27872202/genome-wide-overexpression-screen-identifies-genes-able-to-bypass-p16-mediated-senescence-in-melanoma
#12
Won Jae Lee, Dubravka Škalamera, Mareike Dahmer-Heath, Konstanin Shakhbazov, Max V Ranall, Carly Fox, Duncan Lambie, Alexander J Stevenson, Paul Yaswen, Thomas J Gonda, Brian Gabrielli
Malignant melanomas often arise from nevi, which result from initial oncogene-induced hyperproliferation of melanocytes that are maintained in a CDKN2A/p16-mediated senescent state. Thus, genes that can bypass this senescence barrier are likely to contribute to melanoma development. We have performed a gain-of-function screen of 17,030 lentivirally expressed human open reading frames (ORFs) in a melanoma cell line containing an inducible p16 construct to identify such genes. Genes known to bypass p16-induced senescence arrest, including the human papilloma virus 18 E7 gene (HPV18E7), and genes such as the p16-binding CDK6 with expected functions, as well as panel of novel genes, were identified, including high-mobility group box (HMGB) proteins...
November 21, 2016: Journal of Biomolecular Screening
https://www.readbyqxmd.com/read/27865459/molecular-pathogenesis-of-pancreatic-cancer
#13
T J Grant, K Hua, A Singh
Pancreatic cancers arise predominantly from ductal epithelial cells of the exocrine pancreas and are of the ductal adenocarcinoma histological subtype (PDAC). PDAC is an aggressive disease associated with a poor clinical prognosis, weakly effective therapeutic options, and a lack of early detection methods. Furthermore, the genetic and phenotypic heterogeneity of PDAC complicates efforts to identify universally efficacious therapies. PDACs commonly harbor activating mutations in the KRAS oncogene, which is a potent driver of tumor initiation and maintenance...
2016: Progress in Molecular Biology and Translational Science
https://www.readbyqxmd.com/read/27865273/genetics-of-pancreatic-cancer-and-its-implications-on-therapy
#14
REVIEW
Talar Tatarian, Jordan M Winter
Over the past decade, emerging technologies have provided new insights into the genomic landscape of pancreatic ductal adenocarcinoma (PDA). In addition to the commonly recognized genetic drivers of pancreatic carcinogenesis (KRAS, CDKN2A, TP53, SMAD4), new genes and pathways have been implicated. However, these efforts have not identified any new high-frequency actionable mutations, limiting the success of mutation-targeted therapy in PDA. This article provides a report on the current landscape of pancreas cancer genetics and targeted therapeutics...
December 2016: Surgical Clinics of North America
https://www.readbyqxmd.com/read/27863190/human-papillomavirus-drives-tumor-development-throughout-the-head-and-neck-improved-prognosis-is-associated-with-an-immune-response-largely-restricted-to-the-oropharynx
#15
Ankur Chakravarthy, Stephen Henderson, Stephen M Thirdborough, Christian H Ottensmeier, Xiaoping Su, Matt Lechner, Andrew Feber, Gareth J Thomas, Tim R Fenton
Purpose In squamous cell carcinomas of the head and neck (HNSCC), the increasing incidence of oropharyngeal squamous cell carcinomas (OPSCCs) is attributable to human papillomavirus (HPV) infection. Despite commonly presenting at late stage, HPV-driven OPSCCs are associated with improved prognosis compared with HPV-negative disease. HPV DNA is also detectable in nonoropharyngeal (non-OPSCC), but its pathogenic role and clinical significance are unclear. The objectives of this study were to determine whether HPV plays a causal role in non-OPSCC and to investigate whether HPV confers a survival benefit in these tumors...
December 2016: Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology
https://www.readbyqxmd.com/read/27844328/molecular-profiling-of-thymoma-and-thymic-carcinoma-genetic-differences-and-potential-novel-therapeutic-targets
#16
Franz Enkner, Bettina Pichlhöfer, Alexandru Teodor Zaharie, Milica Krunic, Tina Maria Holper, Stefan Janik, Bernhard Moser, Karin Schlangen, Barbara Neudert, Karin Walter, Brigitte Migschitz, Leonhard Müllauer
Thymoma and thymic carcinoma are thymic epithelial tumors (TETs). We performed a molecular profiling to investigate the pathogenesis of TETs and identify novel targets for therapy. We analyzed 37 thymomas (18 type A, 19 type B3) and 35 thymic carcinomas. The sequencing of 50 genes detected nonsynonymous mutations in 16 carcinomas affecting ALK, ATM, CDKN2A, ERBB4, FGFR3, KIT, NRAS and TP53. Only two B3 thymomas had a mutation in noncoding regions of the SMARCB1 and STK11 gene respectively. Three type A thymomas harbored a nonsynonymous HRAS mutation...
November 14, 2016: Pathology Oncology Research: POR
https://www.readbyqxmd.com/read/27834349/differentiated-exophytic-vulvar-intraepithelial-lesions-are-genetically-distinct-from-keratinizing-squamous-cell-carcinomas-and-contain-mutations-in-pik3ca
#17
Jaclyn C Watkins, Brooke E Howitt, Neil S Horowitz, Lauren L Ritterhouse, Fei Dong, Laura E MacConaill, Elizabeth Garcia, Neal I Lindeman, Larissa J Lee, Ross S Berkowitz, Marisa R Nucci, Christopher P Crum
Human papillomavirus-negative keratinizing vulvar cancers typically harbor TP53 mutations as do their precursors, differentiated vulvar intraepithelial neoplasia. However, atypical verruciform proliferations are also associated with these malignancies and their pathogenesis is poorly understood. This study compared 11 atypical verruciform lesions, including atypical verruciform hyperplasia, vulvar acanthosis with altered differentiation, and verruciform lichen simplex chronicus, with 14 human papillomavirus-negative keratinizing squamous cell carcinomas...
November 11, 2016: Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc
https://www.readbyqxmd.com/read/27804060/uptake-of-genetic-counseling-genetic-testing-and-surveillance-in-hereditary-malignant-melanoma-cdkn2a-in-norway
#18
Trine Levin, Lovise Mæhle
Germline mutations in the CDKN2A gene are associated with an increased risk of malignant melanoma and pancreatic cancer. In order to find out if the behavior pattern in families with a CDKN2A mutation is similar to what we previously have described in families with a BRCA1 mutation, we have studied the uptake of genetic services in probands and their relatives. We describe whether they attend genetic counseling when invited, whether they want a mutation test after being counseled and whether they adhere to recommendations for surveillance...
November 1, 2016: Familial Cancer
https://www.readbyqxmd.com/read/27801591/detection-of-proteome-changes-in-human-colon-cancer-induced-by-cell-surface-binding-of-growth-inhibitory-human-galectin-4-using-quantitative-silac-based-proteomics
#19
Malwina Michalak, Uwe Warnken, Sabine André, Martina Schnölzer, Hans-Joachim Gabius, Juergen Kopitz
Endogenous lectins have the capacity to translate glycan-encoded information on the cell surface into effects on cell growth. As test case to examine changes in protein presence associated with tumor growth inhibition, we applied SILAC-based proteomics on human colon carcinoma cells treated with galectin-4 (Gal-4). The five tested lines LS 180, Vaco 432, Colo 205, CX 1 and HCT 116 responded with differentiation and reduced proliferation to Gal-4 binding. In proteomic analysis (mass spectral data deposited with PRIDE - PXD003489), 2654 proteins were quantified: 190 down- and 115 up-regulated (>2-fold)...
November 1, 2016: Journal of Proteome Research
https://www.readbyqxmd.com/read/27793210/investigation-of-ezh2-pathways-for-novel-epigenetic-treatment-strategies-in-oropharyngeal-cancer
#20
Sherif Idris, Cameron Lindsay, Morris Kostiuk, Colin Andrews, David W J Côté, Daniel A O'Connell, Jeffrey Harris, Hadi Seikaly, Vincent L Biron
BACKGROUND: In recent decades, the incidence of oropharyngeal squamous cell carcinoma (OPSCC) has been rising worldwide as a result of increasing oncogenic human papillomavirus (HPV) infections in the oropharynx. EZH2 is an epigenetic regulatory protein associated with tumor aggressiveness and negative survival outcomes in several human cancers. We aimed to determine the role of EZH2 as a potential therapeutic epigenetic target in HPV-positive and negative OPSCC. METHODS: The expression of EZH2 was measured by immunohistochemistry (IHC) and droplet digital PCR (ddPCR) in 2 HPV-positive and 2 HPV-negative cell lines...
October 28, 2016: Journal of Otolaryngology—Head & Neck Surgery
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