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Genomic and Functional Approaches to Understanding Cancer Aneuploidy.
Taylor AM, Shih J, Ha G, Gao GF, Zhang X, Berger AC, Schumacher SE, Wang C, Hu H, Liu J, Lazar AJ, Cancer Genome Atlas Research Network, Cherniack AD, Beroukhim R, Meyerson M
(2018) Cancer Cell 33: 676-689.e3
MeSH Terms: Aneuploidy, Carcinoma, Squamous Cell, Cell Cycle, Cell Proliferation, Chromosome Aberrations, Chromosome Deletion, Chromosomes, Human, Pair 3, Databases, Genetic, Genomics, Humans, Mutation Rate, Tumor Suppressor Protein p53
Show Abstract · Added October 30, 2019
Aneuploidy, whole chromosome or chromosome arm imbalance, is a near-universal characteristic of human cancers. In 10,522 cancer genomes from The Cancer Genome Atlas, aneuploidy was correlated with TP53 mutation, somatic mutation rate, and expression of proliferation genes. Aneuploidy was anti-correlated with expression of immune signaling genes, due to decreased leukocyte infiltrates in high-aneuploidy samples. Chromosome arm-level alterations show cancer-specific patterns, including loss of chromosome arm 3p in squamous cancers. We applied genome engineering to delete 3p in lung cells, causing decreased proliferation rescued in part by chromosome 3 duplication. This study defines genomic and phenotypic correlates of cancer aneuploidy and provides an experimental approach to study chromosome arm aneuploidy.
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
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Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas.
Campbell JD, Yau C, Bowlby R, Liu Y, Brennan K, Fan H, Taylor AM, Wang C, Walter V, Akbani R, Byers LA, Creighton CJ, Coarfa C, Shih J, Cherniack AD, Gevaert O, Prunello M, Shen H, Anur P, Chen J, Cheng H, Hayes DN, Bullman S, Pedamallu CS, Ojesina AI, Sadeghi S, Mungall KL, Robertson AG, Benz C, Schultz A, Kanchi RS, Gay CM, Hegde A, Diao L, Wang J, Ma W, Sumazin P, Chiu HS, Chen TW, Gunaratne P, Donehower L, Rader JS, Zuna R, Al-Ahmadie H, Lazar AJ, Flores ER, Tsai KY, Zhou JH, Rustgi AK, Drill E, Shen R, Wong CK, Cancer Genome Atlas Research Network, Stuart JM, Laird PW, Hoadley KA, Weinstein JN, Peto M, Pickering CR, Chen Z, Van Waes C
(2018) Cell Rep 23: 194-212.e6
MeSH Terms: Carcinoma, Squamous Cell, Cell Line, Tumor, DNA Methylation, Epithelial-Mesenchymal Transition, Gene Expression Regulation, Neoplastic, Genomics, Humans, Metabolic Networks and Pathways, Polymorphism, Genetic
Show Abstract · Added October 30, 2019
This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smoking and/or human papillomavirus (HPV). SCCs harbor 3q, 5p, and other recurrent chromosomal copy-number alterations (CNAs), DNA mutations, and/or aberrant methylation of genes and microRNAs, which are correlated with the expression of multi-gene programs linked to squamous cell stemness, epithelial-to-mesenchymal differentiation, growth, genomic integrity, oxidative damage, death, and inflammation. Low-CNA SCCs tended to be HPV(+) and display hypermethylation with repression of TET1 demethylase and FANCF, previously linked to predisposition to SCC, or harbor mutations affecting CASP8, RAS-MAPK pathways, chromatin modifiers, and immunoregulatory molecules. We uncovered hypomethylation of the alternative promoter that drives expression of the ΔNp63 oncogene and embedded miR944. Co-expression of immune checkpoint, T-regulatory, and Myeloid suppressor cells signatures may explain reduced efficacy of immune therapy. These findings support possibilities for molecular classification and therapeutic approaches.
Published by Elsevier Inc.
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Impaired functional vitamin B6 status is associated with increased risk of lung cancer.
Theofylaktopoulou D, Midttun Ø, Ueland PM, Meyer K, Fanidi A, Zheng W, Shu XO, Xiang YB, Prentice R, Pettinger M, Thomson CA, Giles GG, Hodge A, Cai Q, Blot WJ, Wu J, Johansson M, Hultdin J, Grankvist K, Stevens VL, McCullough MM, Weinstein SJ, Albanes D, Ziegler R, Freedman ND, Langhammer A, Hveem K, Naess M, Sesso HD, Gaziano JM, Buring JE, Lee IM, Severi G, Zhang X, Stampfer MJ, Han J, Smith-Warner SA, Zeleniuch-Jacquotte A, Le Marchand L, Yuan JM, Wang R, Butler LM, Koh WP, Gao YT, Rothman N, Ericson U, Sonestedt E, Visvanathan K, Jones MR, Relton C, Brennan P, Johansson M, Ulvik A
(2018) Int J Cancer 142: 2425-2434
MeSH Terms: Aged, Biomarkers, Carcinoma, Squamous Cell, Case-Control Studies, Cohort Studies, Female, Humans, Lung Neoplasms, Male, Middle Aged, Odds Ratio, Risk Factors, Vitamin B 6
Show Abstract · Added April 3, 2018
Circulating vitamin B6 levels have been found to be inversely associated with lung cancer. Most studies have focused on the B6 form pyridoxal 5'-phosphate (PLP), a direct biomarker influenced by inflammation and other factors. Using a functional B6 marker allows further investigation of the potential role of vitamin B6 status in the pathogenesis of lung cancer. We prospectively evaluated the association of the functional marker of vitamin B6 status, the 3-hydroxykynurenine:xanthurenic acid (HK:XA) ratio, with risk of lung cancer in a nested case-control study consisting of 5,364 matched case-control pairs from the Lung Cancer Cohort Consortium (LC3). We used conditional logistic regression to evaluate the association between HK:XA and lung cancer, and random effect models to combine results from different cohorts and regions. High levels of HK:XA, indicating impaired functional B6 status, were associated with an increased risk of lung cancer, the odds ratio comparing the fourth and the first quartiles (OR ) was 1.25 (95% confidence interval, 1.10-1.41). Stratified analyses indicated that this association was primarily driven by cases diagnosed with squamous cell carcinoma. Notably, the risk associated with HK:XA was approximately 50% higher in groups with a high relative frequency of squamous cell carcinoma, i.e., men, former and current smokers. This risk of squamous cell carcinoma was present in both men and women regardless of smoking status.
© 2017 UICC.
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13 MeSH Terms
Kinetics of the Human Papillomavirus Type 16 E6 Antibody Response Prior to Oropharyngeal Cancer.
Kreimer AR, Johansson M, Yanik EL, Katki HA, Check DP, Lang Kuhs KA, Willhauck-Fleckenstein M, Holzinger D, Hildesheim A, Pfeiffer R, Williams C, Freedman ND, Huang WY, Purdue MP, Michel A, Pawlita M, Brennan P, Waterboer T
(2017) J Natl Cancer Inst 109:
MeSH Terms: Aged, Antibodies, Viral, Carcinoma, Squamous Cell, Case-Control Studies, Cohort Studies, Female, Human papillomavirus 16, Humans, Incidence, Kinetics, Male, Middle Aged, Oncogene Proteins, Viral, Oropharyngeal Neoplasms, Papillomavirus Infections, Repressor Proteins, Risk Factors, Sensitivity and Specificity, United States
Show Abstract · Added August 15, 2017
Background - In a European cohort, it was previously reported that 35% of oropharyngeal cancer (OPC) patients were human papillomavirus type-16 (HPV16) seropositive up to 10 years before diagnosis vs 0.6% of cancer-free controls. Here, we describe the kinetics of HPV16-E6 antibodies prior to OPC diagnosis.
Methods - We used annual serial prediagnostic blood samples from the PLCO Cancer Screening Trial. Antibodies to HPV were initially assessed in prediagnostic blood drawn at study enrollment from 198 incident head and neck cancer patients (median years to cancer diagnosis = 6.6) and 924 matched control subjects using multiplex serology, and subsequently in serial samples (median = 5/individual). Available tumor samples were identified and tested for HPV16 RNA to define HPV-driven OPC.
Results - HPV16-E6 antibodies were present at baseline in 42.3% of 52 OPC patients and 0.5% of 924 control subjects. HPV16-E6 antibody levels were highly elevated and stable across serial blood samples for 21 OPC patients who were seropositive at baseline, as well as for one OPC patient who seroconverted closer to diagnosis. All five subjects with HPV16-driven OPC tumors were HPV16-E6-seropositive, and the four subjects with HPV16-negative OPC tumors were seronegative. The estimated 10-year cumulative risk of OPC was 6.2% (95% confidence interval [CI] = 1.8% to 21.5%) for HPV16-E6-seropositive men, 1.3% (95% CI = 0.1% to 15.3%) for HPV16-E6-seropositive women, and 0.04% (95% CI = 0.03% to 0.06%) among HPV16-E6-seronegative individuals.
Conclusions - Forty-two percent of subjects diagnosed with OPC between 1994 and 2009 in a US cohort were HPV16-E6 seropositive, with stable antibody levels during annual follow-up for up to 13 years prior to diagnosis. Tumor analysis indicated that the sensitivity and specificity of HPV16-E6 antibodies were exceptionally high in predicting HPV-driven OPC.
Published by Oxford University Press 2017. This work is written by US Government employees and is in the public domain in the US.
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19 MeSH Terms
Integrated genomic and molecular characterization of cervical cancer.
Cancer Genome Atlas Research Network, Albert Einstein College of Medicine, Analytical Biological Services, Barretos Cancer Hospital, Baylor College of Medicine, Beckman Research Institute of City of Hope, Buck Institute for Research on Aging, Canada's Michael Smith Genome Sciences Centre, Harvard Medical School, Helen F. Graham Cancer Center &Research Institute at Christiana Care Health Services, HudsonAlpha Institute for Biotechnology, ILSbio, LLC, Indiana University School of Medicine, Institute of Human Virology, Institute for Systems Biology, International Genomics Consortium, Leidos Biomedical, Massachusetts General Hospital, McDonnell Genome Institute at Washington University, Medical College of Wisconsin, Medical University of South Carolina, Memorial Sloan Kettering Cancer Center, Montefiore Medical Center, NantOmics, National Cancer Institute, National Hospital, Abuja, Nigeria, National Human Genome Research Institute, National Institute of Environmental Health Sciences, National Institute on Deafness &Other Communication Disorders, Ontario Tumour Bank, London Health Sciences Centre, Ontario Tumour Bank, Ontario Institute for Cancer Research, Ontario Tumour Bank, The Ottawa Hospital, Oregon Health &Science University, Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, SRA International, St Joseph's Candler Health System, Eli &Edythe L. Broad Institute of Massachusetts Institute of Technology &Harvard University, Research Institute at Nationwide Children's Hospital, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, University of Bergen, University of Texas MD Anderson Cancer Center, University of Abuja Teaching Hospital, University of Alabama at Birmingham, University of California, Irvine, University of California Santa Cruz, University of Kansas Medical Center, University of Lausanne, University of New Mexico Health Sciences Center, University of North Carolina at Chapel Hill, University of Oklahoma Health Sciences Center, University of Pittsburgh, University of São Paulo, Ribeir ão Preto Medical School, University of Southern California, University of Washington, University of Wisconsin School of Medicine &Public Health, Van Andel Research Institute, Washington University in St Louis
(2017) Nature 543: 378-384
MeSH Terms: APOBEC-1 Deaminase, Adenocarcinoma, B7-H1 Antigen, Carcinoma, Squamous Cell, Caspase 8, Female, Genomics, HLA-A Antigens, Human papillomavirus 16, Humans, Keratins, Mitogen-Activated Protein Kinase Kinases, Molecular Targeted Therapy, Mutation, Nuclear Proteins, PTEN Phosphohydrolase, Phosphatidylinositol 3-Kinases, Programmed Cell Death 1 Ligand 2 Protein, Protein-Serine-Threonine Kinases, Proteomics, Proto-Oncogene Proteins p21(ras), RNA, Long Noncoding, Receptor, ErbB-3, Receptor, Transforming Growth Factor-beta Type II, Receptors, Transforming Growth Factor beta, Signal Transduction, Transcription Factors, Uterine Cervical Neoplasms, Virus Integration
Show Abstract · Added October 30, 2019
Cervical cancer remains one of the leading causes of cancer-related deaths worldwide. Here we report the extensive molecular characterization of 228 primary cervical cancers, one of the largest comprehensive genomic studies of cervical cancer to date. We observed notable APOBEC mutagenesis patterns and identified SHKBP1, ERBB3, CASP8, HLA-A and TGFBR2 as novel significantly mutated genes in cervical cancer. We also discovered amplifications in immune targets CD274 (also known as PD-L1) and PDCD1LG2 (also known as PD-L2), and the BCAR4 long non-coding RNA, which has been associated with response to lapatinib. Integration of human papilloma virus (HPV) was observed in all HPV18-related samples and 76% of HPV16-related samples, and was associated with structural aberrations and increased target-gene expression. We identified a unique set of endometrial-like cervical cancers, comprised predominantly of HPV-negative tumours with relatively high frequencies of KRAS, ARID1A and PTEN mutations. Integrative clustering of 178 samples identified keratin-low squamous, keratin-high squamous and adenocarcinoma-rich subgroups. These molecular analyses reveal new potential therapeutic targets for cervical cancers.
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Integrated genomic characterization of oesophageal carcinoma.
Cancer Genome Atlas Research Network, Analysis Working Group: Asan University, BC Cancer Agency, Brigham and Women’s Hospital, Broad Institute, Brown University, Case Western Reserve University, Dana-Farber Cancer Institute, Duke University, Greater Poland Cancer Centre, Harvard Medical School, Institute for Systems Biology, KU Leuven, Mayo Clinic, Memorial Sloan Kettering Cancer Center, National Cancer Institute, Nationwide Children’s Hospital, Stanford University, University of Alabama, University of Michigan, University of North Carolina, University of Pittsburgh, University of Rochester, University of Southern California, University of Texas MD Anderson Cancer Center, University of Washington, Van Andel Research Institute, Vanderbilt University, Washington University, Genome Sequencing Center: Broad Institute, Washington University in St. Louis, Genome Characterization Centers: BC Cancer Agency, Broad Institute, Harvard Medical School, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, University of North Carolina, University of Southern California Epigenome Center, University of Texas MD Anderson Cancer Center, Van Andel Research Institute, Genome Data Analysis Centers: Broad Institute, Brown University:, Harvard Medical School, Institute for Systems Biology, Memorial Sloan Kettering Cancer Center, University of California Santa Cruz, University of Texas MD Anderson Cancer Center, Biospecimen Core Resource: International Genomics Consortium, Research Institute at Nationwide Children’s Hospital, Tissue Source Sites: Analytic Biologic Services, Asan Medical Center, Asterand Bioscience, Barretos Cancer Hospital, BioreclamationIVT, Botkin Municipal Clinic, Chonnam National University Medical School, Christiana Care Health System, Cureline, Duke University, Emory University, Erasmus University, Indiana University School of Medicine, Institute of Oncology of Moldova, International Genomics Consortium, Invidumed, Israelitisches Krankenhaus Hamburg, Keimyung University School of Medicine, Memorial Sloan Kettering Cancer Center, National Cancer Center Goyang, Ontario Tumour Bank, Peter MacCallum Cancer Centre, Pusan National University Medical School, Ribeirão Preto Medical School, St. Joseph’s Hospital &Medical Center, St. Petersburg Academic University, Tayside Tissue Bank, University of Dundee, University of Kansas Medical Center, University of Michigan, University of North Carolina at Chapel Hill, University of Pittsburgh School of Medicine, University of Texas MD Anderson Cancer Center, Disease Working Group: Duke University, Memorial Sloan Kettering Cancer Center, National Cancer Institute, University of Texas MD Anderson Cancer Center, Yonsei University College of Medicine, Data Coordination Center: CSRA Inc., Project Team: National Institutes of Health
(2017) Nature 541: 169-175
MeSH Terms: Adenocarcinoma, Carcinoma, Squamous Cell, Esophageal Neoplasms, Esophageal Squamous Cell Carcinoma, Genome, Human, Genomics, Humans, Molecular Targeted Therapy, Mutation, Stomach Neoplasms
Show Abstract · Added October 30, 2019
Oesophageal cancers are prominent worldwide; however, there are few targeted therapies and survival rates for these cancers remain dismal. Here we performed a comprehensive molecular analysis of 164 carcinomas of the oesophagus derived from Western and Eastern populations. Beyond known histopathological and epidemiologic distinctions, molecular features differentiated oesophageal squamous cell carcinomas from oesophageal adenocarcinomas. Oesophageal squamous cell carcinomas resembled squamous carcinomas of other organs more than they did oesophageal adenocarcinomas. Our analyses identified three molecular subclasses of oesophageal squamous cell carcinomas, but none showed evidence for an aetiological role of human papillomavirus. Squamous cell carcinomas showed frequent genomic amplifications of CCND1 and SOX2 and/or TP63, whereas ERBB2, VEGFA and GATA4 and GATA6 were more commonly amplified in adenocarcinomas. Oesophageal adenocarcinomas strongly resembled the chromosomally unstable variant of gastric adenocarcinoma, suggesting that these cancers could be considered a single disease entity. However, some molecular features, including DNA hypermethylation, occurred disproportionally in oesophageal adenocarcinomas. These data provide a framework to facilitate more rational categorization of these tumours and a foundation for new therapies.
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LIM-Only Protein 4 (LMO4) and LIM Domain Binding Protein 1 (LDB1) Promote Growth and Metastasis of Human Head and Neck Cancer (LMO4 and LDB1 in Head and Neck Cancer).
Simonik EA, Cai Y, Kimmelshue KN, Brantley-Sieders DM, Loomans HA, Andl CD, Westlake GM, Youngblood VM, Chen J, Yarbrough WG, Brown BT, Nagarajan L, Brandt SJ
(2016) PLoS One 11: e0164804
MeSH Terms: Adaptor Proteins, Signal Transducing, Animals, Carcinoma, Squamous Cell, Cell Line, Tumor, Cell Movement, Cell Proliferation, DNA-Binding Proteins, Gene Expression Regulation, Neoplastic, Humans, LIM Domain Proteins, Mice, Mouth Neoplasms, Neoplasm Metastasis, Neoplasm Transplantation, Tissue Culture Techniques, Transcription Factors
Show Abstract · Added March 29, 2017
Squamous cell carcinoma of the head and neck (HNSCC) accounts for more than 300,000 deaths worldwide per year as a consequence of tumor cell invasion of adjacent structures or metastasis. LIM-only protein 4 (LMO4) and LIM-domain binding protein 1 (LDB1), two directly interacting transcriptional adaptors that have important roles in normal epithelial cell differentiation, have been associated with increased metastasis, decreased differentiation, and shortened survival in carcinoma of the breast. Here, we implicate two LDB1-binding proteins, single-stranded binding protein 2 (SSBP2) and 3 (SSBP3), in controlling LMO4 and LDB1 protein abundance in HNSCC and in regulating specific tumor cell functions in this disease. First, we found that the relative abundance of LMO4, LDB1, and the two SSBPs correlated very significantly in a panel of human HNSCC cell lines. Second, expression of these proteins in tumor primaries and lymph nodes involved by metastasis were concordant in 3 of 3 sets of tissue. Third, using a Matrigel invasion and organotypic reconstruct assay, CRISPR/Cas9-mediated deletion of LDB1 in the VU-SCC-1729 cell line, which is highly invasive of basement membrane and cellular monolayers, reduced tumor cell invasiveness and migration, as well as proliferation on tissue culture plastic. Finally, inactivation of the LDB1 gene in these cells decreased growth and vascularization of xenografted human tumor cells in vivo. These data show that LMO4, LDB1, and SSBP2 and/or SSBP3 regulate metastasis, proliferation, and angiogenesis in HNSCC and provide the first evidence that SSBPs control LMO4 and LDB1 protein abundance in a cancer context.
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16 MeSH Terms
Hedgehog and TGFβ signaling converge on Gli2 to control bony invasion and bone destruction in oral squamous cell carcinoma.
Cannonier SA, Gonzales CB, Ely K, Guelcher SA, Sterling JA
(2016) Oncotarget 7: 76062-76075
MeSH Terms: Animals, Bone and Bones, Carcinoma, Squamous Cell, Cell Line, Tumor, Disease Models, Animal, Gene Expression, Hedgehog Proteins, Heterografts, Humans, Mice, Mouth Neoplasms, Neoplasm Invasiveness, Nuclear Proteins, Parathyroid Hormone-Related Protein, Signal Transduction, Transforming Growth Factor beta, Zinc Finger Protein Gli2
Show Abstract · Added April 26, 2017
Oral Squamous Cell Carcinoma (OSCC) is the sixth most common cancer worldwide. OSCC invasion into the lymph nodes and mandible correlates with increased rates of recurrence and lower overall survival. Tumors that infiltrate mandibular bone proliferate rapidly and induce bone destruction. While survival rates have increased 12% over the last 20 years, this improvement is attributed to general advances in prevention, earlier detection, and updated treatments. Additionally, despite decades of research, the molecular mechanisms of OSCC invasion into the mandible are not well understood. Parathyroid Hormone-related Protein (PTHrP), has been shown to be essential for mandibular invasion in OSCC animal models, and our previous studies demonstrate that the transcription factor Gli2 increases PTHrP expression in tumor metastasis to bone. In OSCC, we investigated regulators of Gli2, including Hedgehog, TGFβ, and Wnt signaling to elucidate how PTHrP expression is controlled. Here we show that canonical Hedgehog and TGFβ signaling cooperate to increase PTHrP expression and mandibular invasion in a Gli2-dependent manner. Additionally, in an orthotopic model of mandibular invasion, inhibition of Gli2 using shRNA resulted in a significant decrease of both PTHrP expression and bony invasion. Collectively, our findings demonstrate that multiple signaling pathways converge on Gli2 to mediate PTHrP expression and bony invasion, highlighting Gli2 as a therapeutic target to prevent bony invasion in OSCC.
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17 MeSH Terms
Laminin-111 peptide C16 regulates invadopodia activity of malignant cells through β1 integrin, Src and ERK 1/2.
Siqueira AS, Pinto MP, Cruz MC, Smuczek B, Cruz KS, Barbuto JA, Hoshino D, Weaver AM, Freitas VM, Jaeger RG
(2016) Oncotarget 7: 47904-47917
MeSH Terms: Carcinoma, Squamous Cell, Cell Line, Tumor, Fibrosarcoma, Head and Neck Neoplasms, Humans, Integrin beta1, Laminin, MAP Kinase Signaling System, Mouth Neoplasms, Peptide Fragments, Podosomes, Squamous Cell Carcinoma of Head and Neck, Transfection, src-Family Kinases
Show Abstract · Added April 26, 2017
Laminin peptides influence tumor behavior. In this study, we addressed whether laminin peptide C16 (KAFDITYVRLKF, γ1 chain) would increase invadopodia activity of cells from squamous cell carcinoma (CAL27) and fibrosarcoma (HT1080). We found that C16 stimulates invadopodia activity over time in both cell lines. Rhodamine-conjugated C16 decorates the edge of cells, suggesting a possible binding to membrane receptors. Flow cytometry showed that C16 increases activated β1 integrin, and β1 integrin miRNA-mediated depletion diminishes C16-induced invadopodia activity in both cell lines. C16 stimulates Src and ERK 1/2 phosphorylation, and ERK 1/2 inhibition decreases peptide-induced invadopodia activity. C16 also increases cortactin phosphorylation in both cells lines. Based on our findings, we propose that C16 regulates invadopodia activity over time of squamous carcinoma and fibrosarcoma cells, probably through β1 integrin, Src and ERK 1/2 signaling pathways.
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14 MeSH Terms
Distinct patterns of somatic genome alterations in lung adenocarcinomas and squamous cell carcinomas.
Campbell JD, Alexandrov A, Kim J, Wala J, Berger AH, Pedamallu CS, Shukla SA, Guo G, Brooks AN, Murray BA, Imielinski M, Hu X, Ling S, Akbani R, Rosenberg M, Cibulskis C, Ramachandran A, Collisson EA, Kwiatkowski DJ, Lawrence MS, Weinstein JN, Verhaak RG, Wu CJ, Hammerman PS, Cherniack AD, Getz G, Cancer Genome Atlas Research Network, Artyomov MN, Schreiber R, Govindan R, Meyerson M
(2016) Nat Genet 48: 607-16
MeSH Terms: Adenocarcinoma, Antigens, Neoplasm, Carcinoma, Squamous Cell, DNA Copy Number Variations, Genome, Human, Humans, Lung Neoplasms, Recurrence
Show Abstract · Added August 8, 2016
To compare lung adenocarcinoma (ADC) and lung squamous cell carcinoma (SqCC) and to identify new drivers of lung carcinogenesis, we examined the exome sequences and copy number profiles of 660 lung ADC and 484 lung SqCC tumor-normal pairs. Recurrent alterations in lung SqCCs were more similar to those of other squamous carcinomas than to alterations in lung ADCs. New significantly mutated genes included PPP3CA, DOT1L, and FTSJD1 in lung ADC, RASA1 in lung SqCC, and KLF5, EP300, and CREBBP in both tumor types. New amplification peaks encompassed MIR21 in lung ADC, MIR205 in lung SqCC, and MAPK1 in both. Lung ADCs lacking receptor tyrosine kinase-Ras-Raf pathway alterations had mutations in SOS1, VAV1, RASA1, and ARHGAP35. Regarding neoantigens, 47% of the lung ADC and 53% of the lung SqCC tumors had at least five predicted neoepitopes. Although targeted therapies for lung ADC and SqCC are largely distinct, immunotherapies may aid in treatment for both subtypes.
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8 MeSH Terms