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Gene expression in triple-negative breast cancer in relation to survival.
Wang S, Beeghly-Fadiel A, Cai Q, Cai H, Guo X, Shi L, Wu J, Ye F, Qiu Q, Zheng Y, Zheng W, Bao PP, Shu XO
(2018) Breast Cancer Res Treat 171: 199-207
MeSH Terms: Adult, Aged, Biomarkers, Tumor, Female, Gene Expression, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Middle Aged, Neoplasm Grading, Neoplasm Staging, Population Surveillance, Prognosis, Registries, Survival Analysis, Triple Negative Breast Neoplasms
Show Abstract · Added December 6, 2018
PURPOSE - The identification of biomarkers related to the prognosis of triple-negative breast cancer (TNBC) is critically important for improved understanding of the biology that drives TNBC progression.
METHODS - We evaluated gene expression in total RNA isolated from formalin-fixed paraffin-embedded tumor samples using the NanoString nCounter assay for 469 TNBC cases from the Shanghai Breast Cancer Survival Study. We used Cox regression to quantify Hazard Ratios (HR) and corresponding confidence intervals (CI) for overall survival (OS) and disease-free survival (DFS) in models that included adjustment for breast cancer intrinsic subtype. Of 302 genes in our discovery analysis, 22 were further evaluated in relation to OS among 134 TNBC cases from the Nashville Breast Health Study and the Southern Community Cohort Study; 16 genes were further evaluated in relation to DFS in 335 TNBC cases from four gene expression omnibus datasets. Fixed-effect meta-analysis was used to combine results across data sources.
RESULTS - Twofold higher expression of EOMES (HR 0.90, 95% CI 0.83-0.97), RASGRP1 (HR 0.89, 95% CI 0.82-0.97), and SOD2 (HR 0.80, 95% CI 0.66-0.96) was associated with better OS. Twofold higher expression of EOMES (HR 0.89, 95% CI 0.81-0.97) and RASGRP1 (HR 0.87, 95% CI 0.81-0.95) was also associated with better DFS. On the contrary, a doubling of FA2H (HR 1.14, 95% CI 1.06-1.22) and GSPT1 (HR 1.33, 95% CI 1.14-1.55) expression was associated with shorter DFS.
CONCLUSIONS - We identified five genes (EOMES, FA2H, GSPT1, RASGRP1, and SOD2) that may serve as potential prognostic biomarkers and/or therapeutic targets for TNBC.
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16 MeSH Terms
The Cancer Genome Atlas Comprehensive Molecular Characterization of Renal Cell Carcinoma.
Ricketts CJ, De Cubas AA, Fan H, Smith CC, Lang M, Reznik E, Bowlby R, Gibb EA, Akbani R, Beroukhim R, Bottaro DP, Choueiri TK, Gibbs RA, Godwin AK, Haake S, Hakimi AA, Henske EP, Hsieh JJ, Ho TH, Kanchi RS, Krishnan B, Kwiatkowski DJ, Lui W, Merino MJ, Mills GB, Myers J, Nickerson ML, Reuter VE, Schmidt LS, Shelley CS, Shen H, Shuch B, Signoretti S, Srinivasan R, Tamboli P, Thomas G, Vincent BG, Vocke CD, Wheeler DA, Yang L, Kim WY, Robertson AG, Cancer Genome Atlas Research Network, Spellman PT, Rathmell WK, Linehan WM
(2018) Cell Rep 23: 313-326.e5
MeSH Terms: Biomarkers, Tumor, Carcinoma, Renal Cell, Cyclin-Dependent Kinase Inhibitor p16, Genome, Human, Humans, Kidney Neoplasms, Metabolic Networks and Pathways, Nuclear Proteins, PTEN Phosphohydrolase, Phenotype, Survival Analysis, Transcription Factors, Tumor Suppressor Proteins, Ubiquitin Thiolesterase
Show Abstract · Added October 30, 2019
Renal cell carcinoma (RCC) is not a single disease, but several histologically defined cancers with different genetic drivers, clinical courses, and therapeutic responses. The current study evaluated 843 RCC from the three major histologic subtypes, including 488 clear cell RCC, 274 papillary RCC, and 81 chromophobe RCC. Comprehensive genomic and phenotypic analysis of the RCC subtypes reveals distinctive features of each subtype that provide the foundation for the development of subtype-specific therapeutic and management strategies for patients affected with these cancers. Somatic alteration of BAP1, PBRM1, and PTEN and altered metabolic pathways correlated with subtype-specific decreased survival, while CDKN2A alteration, increased DNA hypermethylation, and increases in the immune-related Th2 gene expression signature correlated with decreased survival within all major histologic subtypes. CIMP-RCC demonstrated an increased immune signature, and a uniform and distinct metabolic expression pattern identified a subset of metabolically divergent (MD) ChRCC that associated with extremely poor survival.
Published by Elsevier Inc.
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Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas.
Schaub FX, Dhankani V, Berger AC, Trivedi M, Richardson AB, Shaw R, Zhao W, Zhang X, Ventura A, Liu Y, Ayer DE, Hurlin PJ, Cherniack AD, Eisenman RN, Bernard B, Grandori C, Cancer Genome Atlas Network
(2018) Cell Syst 6: 282-300.e2
MeSH Terms: Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Basic Helix-Loop-Helix Transcription Factors, Biomarkers, Tumor, Carcinogenesis, Chromatin, Computational Biology, Genes, myc, Genomics, Humans, Neoplasms, Oncogenes, Proteomics, Proto-Oncogene Proteins c-myc, Repressor Proteins, Signal Transduction, Transcription Factors
Show Abstract · Added October 30, 2019
Although the MYC oncogene has been implicated in cancer, a systematic assessment of alterations of MYC, related transcription factors, and co-regulatory proteins, forming the proximal MYC network (PMN), across human cancers is lacking. Using computational approaches, we define genomic and proteomic features associated with MYC and the PMN across the 33 cancers of The Cancer Genome Atlas. Pan-cancer, 28% of all samples had at least one of the MYC paralogs amplified. In contrast, the MYC antagonists MGA and MNT were the most frequently mutated or deleted members, proposing a role as tumor suppressors. MYC alterations were mutually exclusive with PIK3CA, PTEN, APC, or BRAF alterations, suggesting that MYC is a distinct oncogenic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such as immune response and growth factor signaling; chromatin, translation, and DNA replication/repair were conserved pan-cancer. This analysis reveals insights into MYC biology and is a reference for biomarkers and therapeutics for cancers with alterations of MYC or the PMN.
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
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Differential cyclooxygenase expression levels and survival associations in type I and type II ovarian tumors.
Beeghly-Fadiel A, Wilson AJ, Keene S, El Ramahi M, Xu S, Marnett LJ, Fadare O, Crispens MA, Khabele D
(2018) J Ovarian Res 11: 17
MeSH Terms: Aged, Biomarkers, Tumor, Cyclooxygenase 1, Cyclooxygenase 2, Female, Gene Expression Regulation, Neoplastic, Humans, Immunohistochemistry, Kaplan-Meier Estimate, Middle Aged, Neoplasm Grading, Neoplasm Staging, Ovarian Neoplasms, Prognosis, Proportional Hazards Models, Prostaglandin-Endoperoxide Synthases
Show Abstract · Added March 21, 2018
BACKGROUND - High cyclooxygenase (COX)-2 expression in ovarian tumors has been associated with poor prognosis, but the role of COX-1 expression and its relation to survival is less clear. Here, we evaluated COX expression and associations with survival outcomes between type I (clear cell, mucinous, low grade endometrioid and low grade serous) and type II (high grade serous and high grade endometrioid) ovarian tumors.
METHODS - We developed and validated a new COX-1 antibody, and conducted immunohistochemical (IHC) staining for COX-1 and COX-2 on a tissue microarray (TMA) of 190 primary ovarian tumors. In addition to standard IHC scoring and H-scores to combine the percentage of positive cells and staining intensity, we also measured COX-1 and COX-2 mRNA expression by QPCR. High expression was defined as greater than or equal to median values. Clinical characteristics and disease outcomes were ascertained from medical records. Associations with disease-free survival (DFS) and overall survival (OS) were quantified by hazard ratios (HRs) and confidence intervals (CIs) from proportional hazards regression.
RESULTS - Type I tumors had high COX-2 expression, while type II tumors had high COX-1 expression. In multivariable adjusted regression models, higher COX-1 mRNA expression was associated with shorter DFS (HR: 6.37, 95% CI: 1.84-22.01) and OS (HR: 2.26, 95% CI: 1.04-4.91), while higher H-scores for COX-2 expression were associated with shorter DFS (HR: 1.92, 95% CI: 1.06-3.49). Stratified analysis indicated that COX-2 was significantly associated with DFS among cases with Type II tumors (HR: 1.93, 95% CI: 1.06-3.53).
CONCLUSIONS - These findings suggest that ovarian tumor type contributes to differences in COX expression levels and associations with survival.
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16 MeSH Terms
Established, emerging and elusive molecular targets in the treatment of lung cancer.
Gallant JN, Lovly CM
(2018) J Pathol 244: 565-577
MeSH Terms: Animals, Antineoplastic Agents, Biomarkers, Tumor, Clinical Decision-Making, Genetic Predisposition to Disease, Genomics, Humans, Lung Neoplasms, Molecular Targeted Therapy, Pathology, Molecular, Phenotype, Precision Medicine, Predictive Value of Tests, Prognosis
Show Abstract · Added September 10, 2020
Although histological subtype still underlies tumour classification and treatment, the recognition that lung cancer is, largely, a genetic disease has prompted a push to reconfigure cancer taxonomies according to molecular criteria. In this review, we discuss established (e.g. EGFR, ALK, ROS1, and programmed cell death 1/programmed death-ligand 1), emerging (e.g. MET, RET, and NTRK) and elusive (e.g. TP53, KRAS, and MYC) molecular targets in the treatment of lung cancer. We synthesize a large and rapidly growing body of literature regarding the discovery and therapeutic inhibition of these targets in lung cancer. Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Copyright © 2018 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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Biomarkers for assessing the effectiveness of immunotherapy in breast cancer.
Nixon MJ, Balko JM
(2018) Biomark Med 12: 97-100
MeSH Terms: B7-H1 Antigen, Biomarkers, Tumor, Breast Neoplasms, CTLA-4 Antigen, Female, Humans, Immunotherapy, Ipilimumab, Triple Negative Breast Neoplasms
Added March 14, 2018
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The Impact of Smoking and TP53 Mutations in Lung Adenocarcinoma Patients with Targetable Mutations-The Lung Cancer Mutation Consortium (LCMC2).
Aisner DL, Sholl LM, Berry LD, Rossi MR, Chen H, Fujimoto J, Moreira AL, Ramalingam SS, Villaruz LC, Otterson GA, Haura E, Politi K, Glisson B, Cetnar J, Garon EB, Schiller J, Waqar SN, Sequist LV, Brahmer J, Shyr Y, Kugler K, Wistuba II, Johnson BE, Minna JD, Kris MG, Bunn PA, Kwiatkowski DJ, LCMC2 investigators
(2018) Clin Cancer Res 24: 1038-1047
MeSH Terms: Adenocarcinoma of Lung, Adult, Aged, Aged, 80 and over, Antineoplastic Agents, Biomarkers, Tumor, Carcinogenesis, DNA Mutational Analysis, Female, High-Throughput Nucleotide Sequencing, Humans, Lung Neoplasms, Male, Middle Aged, Molecular Targeted Therapy, Mutation, Prognosis, Prospective Studies, Smoking, Survival Analysis, Treatment Outcome, Tumor Suppressor Protein p53, Young Adult
Show Abstract · Added April 3, 2018
Multiplex genomic profiling is standard of care for patients with advanced lung adenocarcinomas. The Lung Cancer Mutation Consortium (LCMC) is a multi-institutional effort to identify and treat oncogenic driver events in patients with lung adenocarcinomas. Sixteen U.S. institutions enrolled 1,367 patients with lung cancer in LCMC2; 904 were deemed eligible and had at least one of 14 cancer-related genes profiled using validated methods including genotyping, massively parallel sequencing, and IHC. The use of targeted therapies in patients with or p.V600E mutations, , or rearrangements, or amplification was associated with a survival increment of 1.5 years compared with those with such mutations not receiving targeted therapy, and 1.0 year compared with those lacking a targetable driver. Importantly, 60 patients with a history of smoking derived similar survival benefit from targeted therapy for alterations in //, when compared with 75 never smokers with the same alterations. In addition, coexisting mutations were associated with shorter survival among patients with , or alterations. Patients with adenocarcinoma of the lung and an oncogenic driver mutation treated with effective targeted therapy have a longer survival, regardless of prior smoking history. Molecular testing should be performed on all individuals with lung adenocarcinomas irrespective of clinical characteristics. Routine use of massively parallel sequencing enables detection of both targetable driver alterations and tumor suppressor gene and other alterations that have potential significance for therapy selection and as predictive markers for the efficacy of treatment. .
©2017 American Association for Cancer Research.
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The receptor tyrosine kinase EphA2 promotes glutamine metabolism in tumors by activating the transcriptional coactivators YAP and TAZ.
Edwards DN, Ngwa VM, Wang S, Shiuan E, Brantley-Sieders DM, Kim LC, Reynolds AB, Chen J
(2017) Sci Signal 10:
MeSH Terms: Adaptor Proteins, Signal Transducing, Amino Acid Transport System ASC, Animals, Biomarkers, Tumor, Breast Neoplasms, DNA-Binding Proteins, Disease Models, Animal, Ephrin-A2, Female, Glutaminase, Glutamine, Humans, Intracellular Signaling Peptides and Proteins, Mice, Mice, Knockout, Minor Histocompatibility Antigens, Muscle Proteins, Phosphoproteins, Transcription Factors, Tumor Cells, Cultured
Show Abstract · Added April 2, 2019
Malignant tumors reprogram cellular metabolism to support cancer cell proliferation and survival. Although most cancers depend on a high rate of aerobic glycolysis, many cancer cells also display addiction to glutamine. Glutamine transporters and glutaminase activity are critical for glutamine metabolism in tumor cells. We found that the receptor tyrosine kinase EphA2 activated the TEAD family transcriptional coactivators YAP and TAZ (YAP/TAZ), likely in a ligand-independent manner, to promote glutamine metabolism in cells and mouse models of HER2-positive breast cancer. Overexpression of EphA2 induced the nuclear accumulation of YAP and TAZ and increased the expression of YAP/TAZ target genes. Inhibition of the GTPase Rho or the kinase ROCK abolished EphA2-dependent YAP/TAZ nuclear localization. Silencing or substantially reduced the amount of intracellular glutamate through decreased expression of and , respectively, genes that encode proteins that promote glutamine uptake and metabolism. The regulatory DNA elements of both and contain TEAD binding sites and were bound by TEAD4 in an EphA2-dependent manner. In patient breast cancer tissues, expression positively correlated with that of and , as well as that of and Although high expression of predicted enhanced metastatic potential and poor patient survival, it also rendered HER2-positive breast cancer cells more sensitive to glutaminase inhibition. The findings define a previously unknown mechanism of EphA2-mediated glutaminolysis through YAP/TAZ activation in HER2-positive breast cancer and identify potential therapeutic targets in patients.
Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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Admixture mapping of uterine fibroid size and number in African American women.
Bray MJ, Edwards TL, Wellons MF, Jones SH, Hartmann KE, Velez Edwards DR
(2017) Fertil Steril 108: 1034-1042.e26
MeSH Terms: Adult, African Americans, Biological Specimen Banks, Biomarkers, Tumor, Cross-Sectional Studies, Databases, Factual, Electronic Health Records, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Heredity, Humans, Leiomyoma, Leiomyomatosis, Linear Models, Logistic Models, Middle Aged, Odds Ratio, Phenotype, Polymorphism, Single Nucleotide, Risk Factors, Tumor Burden, United States, Uterine Neoplasms
Show Abstract · Added February 21, 2019
OBJECTIVE - To evaluate the relationship between genetic ancestry and uterine fibroid characteristics.
DESIGN - Cross-sectional study.
SETTING - Not applicable.
PATIENT(S) - A total of 609 African American participants with image- or surgery-confirmed fibroids in a biorepository at Vanderbilt University electronic health record biorepository and the Coronary Artery Risk Development in Young Adults studies were included.
INTERVENTION(S) - None.
MAIN OUTCOME MEASURE(S) - Outcome measures include fibroid number (single vs. multiple), volume of largest fibroid, and largest fibroid dimension of all fibroid measurements.
RESULT(S) - Global ancestry meta-analyses revealed a significant inverse association between percentage of European ancestry and risk of multiple fibroids (odds ratio: 0.78; 95% confidence interval 0.66, 0.93; P=6.05 × 10). Local ancestry meta-analyses revealed five suggestive (P<4.80 × 10) admixture mapping peaks in 2q14.3-2q21.1, 3p14.2-3p14.1, 7q32.2-7q33, 10q21.1, 14q24.2-14q24.3, for number of fibroids and one suggestive admixture mapping peak (P<1.97 × 10) in 10q24.1-10q24.32 for volume of largest fibroid. Single variant association meta-analyses of the strongest associated region from admixture mapping of fibroid number (10q21.1) revealed a strong association at single nucleotide polymorphism variant rs12219990 (odds ratio: 0.41; 95% confidence interval 0.28, 0.60; P=3.82 × 10) that was significant after correction for multiple testing.
CONCLUSION(S) - Increasing African ancestry is associated with multiple fibroids but not with fibroid size. Local ancestry analyses identified several novel genomic regions not previously associated with fibroid number and increasing volume. Future studies are needed to explore the genetic impact that ancestry plays into the development of fibroid characteristics.
Copyright © 2017 American Society for Reproductive Medicine. Published by Elsevier Inc. All rights reserved.
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A prospective study of immune and inflammation markers and risk of lung cancer among female never smokers in Shanghai.
Shiels MS, Shu XO, Chaturvedi AK, Gao YT, Xiang YB, Cai Q, Hu W, Shelton G, Ji BT, Pinto LA, Kemp TJ, Rothman N, Zheng W, Hildesheim A, Lan Q
(2017) Carcinogenesis 38: 1004-1010
MeSH Terms: Acute-Phase Proteins, Adult, Aged, Biomarkers, Biomarkers, Tumor, Case-Control Studies, Chemokine CX3CL1, Chemokines, China, Cytokines, Female, Humans, Inflammation, Lung Neoplasms, Middle Aged, Prospective Studies, Receptors, Interleukin-6, Risk Assessment, Smoking
Show Abstract · Added April 3, 2018
There is a paucity of data on risk factors for lung cancer among never smokers. Here, we have carried out the first large study of circulating inflammation markers and lung cancer risk among female never smokers in Shanghai. A study of 248 lung cancer cases in female never smokers and 263 controls was nested within the Shanghai Women's Health Study (n = 75221), matched by dates of birth and blood collection (mean follow-up time = 7.5 years). Prediagnostic plasma levels of 65 inflammation markers were measured using a Luminex bead-based assay. Odds ratios (ORs) were estimated with multivariable logistic regression. Nine of 61 evaluable markers were statistically significantly associated with lung cancer risk among never smoking Chinese women (P-trend across categories <0.05). Soluble interleukin-6 receptor [sIL-6R; highest versus lowest category OR = 2.37; 95% confidence interval (CI) 1.40-4.02) and chemokine (C-C motif) ligand 2/monocyte chemotactic protein 1; (OR = 1.62; 95% CI 0.94-2.80) were associated with an increased risk of lung cancer, whereas interleukin (IL)-21 (OR = 0.53; 95%CI 0.31-0.93), chemokine (C-X3-C motif) ligand 1/fractalkine (OR = 0.54; 95% CI 0.30-0.96), soluble vascular endothelial growth factor receptor 2 (sVEGFR2, OR = 0.45; 95% CI 0.26-0.76), sVEGFR3 (OR = 0.53; 95% CI 0.32-0.90), soluble tumor necrosis factor receptor I (OR = 0.49; 95% CI 0.29-0.83), IL-10 (OR = 0.60; 95% CI 0.34-1.05) and C-reactive protein (OR = 0.63; 95% CI 0.37-1.06) were associated with a decreased risk. sIL-6R remained significantly associated with lung cancer risk >7.5 years prior to diagnosis. Markers involved in various aspects of the immune response were associated with subsequent lung cancer risk, implicating inflammation in the etiology of lung cancer among female never smokers.
Published by Oxford University Press 2017.
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