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Tobacco is the primary etiologic agent in worsened lung squamous cell carcinoma (LUSC) outcomes. Meanwhile, it has been shown that etiologic agents alter enhancer RNAs (eRNAs) expression. Therefore, we aimed to identify the effects of tobacco and electronic cigarette (e-cigarette) use on eRNA expression in relation to LUSC outcomes. We extracted eRNA counts from RNA-sequencing data of tumor/adjacent normal tissue and before/after e-cigarette tissue from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO), respectively. Tobacco-mediated LUSC eRNAs were correlated to patient survival, clinical variables, and immune-associated elements. eRNA expression was also correlated to mutation rates through the Repeated Evaluation of Variables Conditional Entropy and Redundance (REVEALER) algorithm and methylated sites through methylationArrayAnalysis. Differential expression analysis was then completed for the e-cigarette data to compare with key tobacco-mediated eRNAs. We identified 684 downregulated eRNAs and 819 upregulated eRNAs associated with tobacco-mediated LUSC, specifically, with the cancer pathological stage. We also observed a decrease in immune cell abundance in tobacco-mediated LUSC. Yet, we found an increased association of eRNA expression with immune cell abundance in tobacco-mediated LUSC. We identified 16 key eRNAs with significant correlations to 8 clinical variables, implicating these eRNAs in LUSC malignancy. Furthermore, we observed that these 16 eRNAs were highly associated with chromosomal alterations and reduced CpG site methylation. Finally, we observed large eRNA expression upregulation with e-cigarette use, which corresponded to the upregulation of the 16 key eRNAs. Our findings provide a novel mechanism by which tobacco and e-cigarette smoke influences eRNA interactions to promote LUSC pathogenesis and provide insight regarding disease progression at a molecular level.
Joseph C. Tsai; Omar A. Saad; Shruti Magesh; Jingyue Xu; Abby C. Lee; Wei Tse Li; Jaideep Chakladar; Mark M. Fuster; Eric Y. Chang; Jessica Wang-Rodriguez; Weg M. Ongkeko. Tobacco Smoke and Electronic Cigarette Vapor Alter Enhancer RNA Expression That Can Regulate the Pathogenesis of Lung Squamous Cell Carcinoma. Cancers 2021, 13, 4225 .
AMA StyleJoseph C. Tsai, Omar A. Saad, Shruti Magesh, Jingyue Xu, Abby C. Lee, Wei Tse Li, Jaideep Chakladar, Mark M. Fuster, Eric Y. Chang, Jessica Wang-Rodriguez, Weg M. Ongkeko. Tobacco Smoke and Electronic Cigarette Vapor Alter Enhancer RNA Expression That Can Regulate the Pathogenesis of Lung Squamous Cell Carcinoma. Cancers. 2021; 13 (16):4225.
Chicago/Turabian StyleJoseph C. Tsai; Omar A. Saad; Shruti Magesh; Jingyue Xu; Abby C. Lee; Wei Tse Li; Jaideep Chakladar; Mark M. Fuster; Eric Y. Chang; Jessica Wang-Rodriguez; Weg M. Ongkeko. 2021. "Tobacco Smoke and Electronic Cigarette Vapor Alter Enhancer RNA Expression That Can Regulate the Pathogenesis of Lung Squamous Cell Carcinoma." Cancers 13, no. 16: 4225.
The intra-tumor microbiome has recently been linked to epithelial–mesenchymal transition (EMT) in a number of cancers. However, the relationship between EMT and microbes in bladder cancer has not been explored. In this study, we profiled the abundance of individual microbe species in the tumor samples of over 400 muscle invasive bladder carcinoma (MIBC) patients. We then correlated microbe abundance to the expression of EMT-associated genes and genes in the extracellular matrix (ECM), which are key players in EMT. We discovered that a variety of microbes, including E. coli, butyrate-producing bacterium SM4/1, and a species of Oscillatoria, were associated with expression of classical EMT-associated genes, including E-cadherin, vimentin, SNAI2, SNAI3, and TWIST1. We also found significant correlations between microbial abundance and the expression of genes in the ECM, specifically collagens and elastin. Lastly, we found that a large number of microbes exhibiting significant correlations to EMT are also associated with clinical prognosis and outcomes. We further determined that the microbes we profiled were likely not environmental contaminants. In conclusion, we discovered that the intra-tumoral microbiome could potentially play a significant role in the regulation of EMT in MIBC.
Wei Li; Anjali Iyangar; Rohan Reddy; Jaideep Chakladar; Valmik Bhargava; Kyoko Sakamoto; Weg Ongkeko; Mahadevan Rajasekaran. The Bladder Microbiome Is Associated with Epithelial–Mesenchymal Transition in Muscle Invasive Urothelial Bladder Carcinoma. Cancers 2021, 13, 3649 .
AMA StyleWei Li, Anjali Iyangar, Rohan Reddy, Jaideep Chakladar, Valmik Bhargava, Kyoko Sakamoto, Weg Ongkeko, Mahadevan Rajasekaran. The Bladder Microbiome Is Associated with Epithelial–Mesenchymal Transition in Muscle Invasive Urothelial Bladder Carcinoma. Cancers. 2021; 13 (15):3649.
Chicago/Turabian StyleWei Li; Anjali Iyangar; Rohan Reddy; Jaideep Chakladar; Valmik Bhargava; Kyoko Sakamoto; Weg Ongkeko; Mahadevan Rajasekaran. 2021. "The Bladder Microbiome Is Associated with Epithelial–Mesenchymal Transition in Muscle Invasive Urothelial Bladder Carcinoma." Cancers 13, no. 15: 3649.
The implications of the microbiome on Coronavirus disease 2019 (COVID-19) prognosis has not been thoroughly studied. In this study we aimed to characterize the lung and blood microbiome and their implication on COVID-19 prognosis through analysis of peripheral blood mononuclear cell (PBMC) samples, lung biopsy samples, and bronchoalveolar lavage fluid (BALF) samples. In all three tissue types, we found panels of microbes differentially abundant between COVID-19 and normal samples correlated to immune dysregulation and upregulation of inflammatory pathways, including key cytokine pathways such as interleukin (IL)-2, 3, 5-10 and 23 signaling pathways and downregulation of anti-inflammatory pathways including IL-4 signaling. In the PBMC samples, six microbes were correlated with worse COVID-19 severity, and one microbe was correlated with improved COVID-19 severity. Collectively, our findings contribute to the understanding of the human microbiome and suggest interplay between our identified microbes and key inflammatory pathways which may be leveraged in the development of immune therapies for treating COVID-19 patients.
Kypros Dereschuk; Lauren Apostol; Ishan Ranjan; Jaideep Chakladar; Wei Li; Mahadevan Rajasekaran; Eric Chang; Weg Ongkeko. Identification of Lung and Blood Microbiota Implicated in COVID-19 Prognosis. Cells 2021, 10, 1452 .
AMA StyleKypros Dereschuk, Lauren Apostol, Ishan Ranjan, Jaideep Chakladar, Wei Li, Mahadevan Rajasekaran, Eric Chang, Weg Ongkeko. Identification of Lung and Blood Microbiota Implicated in COVID-19 Prognosis. Cells. 2021; 10 (6):1452.
Chicago/Turabian StyleKypros Dereschuk; Lauren Apostol; Ishan Ranjan; Jaideep Chakladar; Wei Li; Mahadevan Rajasekaran; Eric Chang; Weg Ongkeko. 2021. "Identification of Lung and Blood Microbiota Implicated in COVID-19 Prognosis." Cells 10, no. 6: 1452.
Patients with underlying cardiovascular conditions are particularly vulnerable to severe COVID-19. In this project, we aimed to characterize similarities in dysregulated immune pathways between COVID-19 patients and patients with cardiomyopathy, venous thromboembolism (VTE), or coronary artery disease (CAD). We hypothesized that these similarly dysregulated pathways may be critical to how cardiovascular diseases (CVDs) exacerbate COVID-19. To evaluate immune dysregulation in different diseases, we used four separate datasets, including RNA-sequencing data from human left ventricular cardiac muscle samples of patients with dilated or ischemic cardiomyopathy and healthy controls; RNA-sequencing data of whole blood samples from patients with single or recurrent event VTE and healthy controls; RNA-sequencing data of human peripheral blood mononuclear cells (PBMCs) from patients with and without obstructive CAD; and RNA-sequencing data of platelets from COVID-19 subjects and healthy controls. We found similar immune dysregulation profiles between patients with CVDs and COVID-19 patients. Interestingly, cardiomyopathy patients display the most similar immune landscape to COVID-19 patients. Additionally, COVID-19 patients experience greater upregulation of cytokine- and inflammasome-related genes than patients with CVDs. In all, patients with CVDs have a significant overlap of cytokine- and inflammasome-related gene expression profiles with that of COVID-19 patients, possibly explaining their greater vulnerability to severe COVID-19.
Abby Lee; Grant Castaneda; Wei Li; Chengyu Chen; Neil Shende; Jaideep Chakladar; Pam Taub; Eric Chang; Weg Ongkeko. COVID-19 Severity Potentially Modulated by Cardiovascular-Disease-Associated Immune Dysregulation. Viruses 2021, 13, 1018 .
AMA StyleAbby Lee, Grant Castaneda, Wei Li, Chengyu Chen, Neil Shende, Jaideep Chakladar, Pam Taub, Eric Chang, Weg Ongkeko. COVID-19 Severity Potentially Modulated by Cardiovascular-Disease-Associated Immune Dysregulation. Viruses. 2021; 13 (6):1018.
Chicago/Turabian StyleAbby Lee; Grant Castaneda; Wei Li; Chengyu Chen; Neil Shende; Jaideep Chakladar; Pam Taub; Eric Chang; Weg Ongkeko. 2021. "COVID-19 Severity Potentially Modulated by Cardiovascular-Disease-Associated Immune Dysregulation." Viruses 13, no. 6: 1018.
Osteoarthritis (OA) is the most common joint disorder in the United States, and the gut microbiome has recently emerged as a potential etiologic factor in OA development. Recent studies have shown that a microbiome is present at joint synovia. Therefore, we aimed to characterize the intra-articular microbiome within osteoarthritic synovia and to illustrate its role in OA disease progression. RNA-sequencing data from OA patient synovial tissue was aligned to a library of microbial reference genomes to identify microbial reads indicative of microbial abundance. Microbial abundance data of OA and normal samples was compared to identify differentially abundant microbes. We computationally explored the correlation of differentially abundant microbes to immunological gene signatures, immune signaling pathways, and immune cell infiltration. We found that microbes correlated to OA are related to dysregulation of two main functional pathways: increased inflammation-induced extracellular matrix remodeling and decreased cell signaling pathways crucial for joint and immune function. We also confirmed that the differentially abundant and biologically relevant microbes we had identified were not contaminants. Collectively, our findings contribute to the understanding of the human microbiome, well-known OA risk factors, and the role microbes play in OA pathogenesis. In conclusion, we present previously undiscovered microbes implicated in the OA disease progression that may be useful for future treatment purposes.
Joseph C. Tsai; Grant Casteneda; Abby Lee; Kypros Dereschuk; Wei Tse Li; Jaideep Chakladar; Alecio F. Lombardi; Weg M. Ongkeko; Eric Y. Chang. Identification and Characterization of the Intra-Articular Microbiome in the Osteoarthritic Knee. International Journal of Molecular Sciences 2020, 21, 8618 .
AMA StyleJoseph C. Tsai, Grant Casteneda, Abby Lee, Kypros Dereschuk, Wei Tse Li, Jaideep Chakladar, Alecio F. Lombardi, Weg M. Ongkeko, Eric Y. Chang. Identification and Characterization of the Intra-Articular Microbiome in the Osteoarthritic Knee. International Journal of Molecular Sciences. 2020; 21 (22):8618.
Chicago/Turabian StyleJoseph C. Tsai; Grant Casteneda; Abby Lee; Kypros Dereschuk; Wei Tse Li; Jaideep Chakladar; Alecio F. Lombardi; Weg M. Ongkeko; Eric Y. Chang. 2020. "Identification and Characterization of the Intra-Articular Microbiome in the Osteoarthritic Knee." International Journal of Molecular Sciences 21, no. 22: 8618.
An intra-pancreatic microbiota was recently discovered in several prominent studies. Since pancreatic adenocarcinoma (PAAD) is one of the most lethal cancers worldwide, and the intratumor microbiome was found to be a significant contributor to carcinogenesis in other cancers, this study aims to characterize the PAAD microbiome and elucidate how it may be associated with PAAD prognosis. We further explored the association between the intra-pancreatic microbiome and smoking and gender, which are both risk factors for PAAD. RNA-sequencing data from The Cancer Genome Atlas (TCGA) were used to infer microbial abundance, which was correlated to clinical variables and to cancer and immune-associated gene expression, to determine how microbes may contribute to cancer progression. We discovered that the presence of several bacteria species within PAAD tumors is linked to metastasis and immune suppression. This is the first large-scale study to report microbiome-immune correlations in human pancreatic cancer samples. Furthermore, we found that the increased prevalence and poorer prognosis of PAAD in males and smokers are linked to the presence of potentially cancer-promoting or immune-inhibiting microbes. Further study into the roles of these microbes in PAAD is imperative for understanding how a pro-tumor microenvironment may be treated to limit cancer progression.
Jaideep Chakladar; Selena Z. Kuo; Grant Castaneda; Wei Tse Li; Aditi Gnanasekar; Michael Andrew Yu; Eric Y. Chang; Xiao Qi Wang; Weg M. Ongkeko. The Pancreatic Microbiome Is Associated with Carcinogenesis and Worse Prognosis in Males and Smokers. Cancers 2020, 12, 2672 .
AMA StyleJaideep Chakladar, Selena Z. Kuo, Grant Castaneda, Wei Tse Li, Aditi Gnanasekar, Michael Andrew Yu, Eric Y. Chang, Xiao Qi Wang, Weg M. Ongkeko. The Pancreatic Microbiome Is Associated with Carcinogenesis and Worse Prognosis in Males and Smokers. Cancers. 2020; 12 (9):2672.
Chicago/Turabian StyleJaideep Chakladar; Selena Z. Kuo; Grant Castaneda; Wei Tse Li; Aditi Gnanasekar; Michael Andrew Yu; Eric Y. Chang; Xiao Qi Wang; Weg M. Ongkeko. 2020. "The Pancreatic Microbiome Is Associated with Carcinogenesis and Worse Prognosis in Males and Smokers." Cancers 12, no. 9: 2672.
As of 28 August 2020, there have been 5.88 million Coronavirus Disease 2019 (COVID19) cases and 181,000 COVID-19 related deaths in the United States alone. Given the lack of an effective pharmaceutical treatment for COVID-19, the high contagiousness of the disease and its varied clinical outcomes, identifying patients at risk of progressing to severe disease is crucial for the allocation of valuable healthcare resources during this pandemic. Current research has shown that there is a higher prevalence of cardiovascular comorbidities amongst patients with severe COVID-19 or COVID-19-related deaths, but the link between cardiovascular disease and poorer prognosis is poorly understood. We believe that pre-existing immune dysregulation that accompanies cardiovascular disease predisposes patients to a harmful inflammatory immune response, leading to their higher risk of severe disease. Thus, in this project, we aim to characterize immune dysregulation in patients with cardiomyopathy, venous thromboembolism and COVID-19 patients by looking at immune-associated gene dysregulation, immune infiltration and dysregulated immunological pathways and gene signatures.
Grant E Castaneda; Abby C Lee; Wei Tse Li; Chengyu Chen; Jaideep Chakladar; Eric Y. Chang; Weg M. Ongkeko. Comparative analysis of immune-associated genes in COVID-19, cardiomyopathy and venous thromboembolism. 2020, 1 .
AMA StyleGrant E Castaneda, Abby C Lee, Wei Tse Li, Chengyu Chen, Jaideep Chakladar, Eric Y. Chang, Weg M. Ongkeko. Comparative analysis of immune-associated genes in COVID-19, cardiomyopathy and venous thromboembolism. . 2020; ():1.
Chicago/Turabian StyleGrant E Castaneda; Abby C Lee; Wei Tse Li; Chengyu Chen; Jaideep Chakladar; Eric Y. Chang; Weg M. Ongkeko. 2020. "Comparative analysis of immune-associated genes in COVID-19, cardiomyopathy and venous thromboembolism." , no. : 1.
The COVID-19 pandemic caused by the SARS-CoV-2 virus, overlaps with the ongoing epidemics of cigarette smoking and electronic cigarette (e-cig) vaping. However, there is scarce data relating COVID-19 risks and outcome with cigarette or e-cig use. In this study, we mined three independent RNA expression datasets from smokers and vapers to understand the potential relationship between vaping/smoking and the dysregulation of key genes and pathways related to COVID-19. We found that smoking, but not vaping, upregulates ACE2, the cellular receptor that SARS-CoV-2 requires for infection. Both smoking and use of nicotine and flavor-containing e-cigs led to upregulation of pro-inflammatory cytokines and inflammasome-related genes. Specifically, chemokines including CCL20 and CXCL8 are upregulated in smokers, and CCL5 and CCR1 are upregulated in flavor/nicotine-containing e-cig users. We also found genes implicated in inflammasomes, such as CXCL1, CXCL2, NOD2, and ASC, to be upregulated in smokers and these e-cig users. Vaping flavor and nicotine-less e-cigs, however, did not lead to significant cytokine dysregulation and inflammasome activation. Release of inflammasome products, such as IL-1B, and cytokine storms are hallmarks of COVID-19 infection, especially in severe cases. Therefore, our findings demonstrated that smoking or vaping may critically exacerbate COVID-19-related inflammation or increase susceptibility to COVID-19.
Abby Lee; Jaideep Chakladar; Wei Li; Chengyu Chen; Eric Chang; Jessica Wang-Rodriguez; Weg Ongkeko. Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation. International Journal of Molecular Sciences 2020, 21, 5513 .
AMA StyleAbby Lee, Jaideep Chakladar, Wei Li, Chengyu Chen, Eric Chang, Jessica Wang-Rodriguez, Weg Ongkeko. Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation. International Journal of Molecular Sciences. 2020; 21 (15):5513.
Chicago/Turabian StyleAbby Lee; Jaideep Chakladar; Wei Li; Chengyu Chen; Eric Chang; Jessica Wang-Rodriguez; Weg Ongkeko. 2020. "Tobacco, but Not Nicotine and Flavor-Less Electronic Cigarettes, Induces ACE2 and Immune Dysregulation." International Journal of Molecular Sciences 21, no. 15: 5513.
Hepatocellular carcinoma (HCC) is one of the deadliest cancers in the world. Previous studies have identified the importance of alcohol and hepatitis B (HBV) infection on HCC carcinogenesis, indicating synergy in the methods by which these etiologies advance cancer. However, the specific molecular mechanism behind alcohol and HBV-mediated carcinogenesis remains unknown. Because the microbiome is emerging as a potentially important regulator of cancer development, this study aims to classify the effects of HBV and alcohol on the intratumoral liver microbiome. RNA-sequencing data from The Cancer Genome Atlas (TCGA) were used to infer microbial abundance. This abundance was then correlated to clinical variables and to cancer and immune-associated gene expression, in order to determine how microbial abundance may contribute to differing cancer progression between etiologies. We discovered that the liver microbiome is likely oncogenic after exposure to alcohol or HBV, although these etiological factors could decrease the abundance of a few oncogenic microbes, which would lead to a tumor suppressive effect. In HBV-induced tumors, this tumor suppressive effect was inferred based on the downregulation of microbes that induce cancer and stem cell pathways. Alcohol-induced tumors were observed to have distinct microbial profiles from HBV-induced tumors, and different microbes are clinically relevant in each cohort, suggesting that the effects of the liver microbiome may be different in response to different etiological factors. Collectively, our data suggest that HBV and alcohol operate within a normally oncogenic microbiome to promote tumor development, but are also able to downregulate certain oncogenic microbes. Insight into why these microbes are downregulated following exposure to HBV or alcohol, and why the majority of oncogenic microbes are not downregulated, may be critical for understanding whether a pro-tumor liver microbiome could be suppressed or reversed to limit cancer progression.
Jaideep Chakladar; Lindsay M. Wong; Selena Z. Kuo; Wei Tse Li; Michael Andrew Yu; Eric Y. Chang; Xiao Qi Wang; Weg M. Ongkeko. The Liver Microbiome Is Implicated in Cancer Prognosis and Modulated by Alcohol and Hepatitis B. Cancers 2020, 12, 1642 .
AMA StyleJaideep Chakladar, Lindsay M. Wong, Selena Z. Kuo, Wei Tse Li, Michael Andrew Yu, Eric Y. Chang, Xiao Qi Wang, Weg M. Ongkeko. The Liver Microbiome Is Implicated in Cancer Prognosis and Modulated by Alcohol and Hepatitis B. Cancers. 2020; 12 (6):1642.
Chicago/Turabian StyleJaideep Chakladar; Lindsay M. Wong; Selena Z. Kuo; Wei Tse Li; Michael Andrew Yu; Eric Y. Chang; Xiao Qi Wang; Weg M. Ongkeko. 2020. "The Liver Microbiome Is Implicated in Cancer Prognosis and Modulated by Alcohol and Hepatitis B." Cancers 12, no. 6: 1642.
The COVID-19 pandemic is marked by a wide range of clinical disease courses, ranging from asymptomatic to deadly. There have been many studies seeking to explore the correlations between COVID-19 clinical outcomes and various clinical variables, including age, sex, race, underlying medical problems, and social habits. In particular, the relationship between smoking and COVID-19 outcome is controversial, with multiple conflicting reports in the current literature. In this study, we aim to analyze how smoking may affect the SARS-CoV-2 infection rate. We analyzed sequencing data from lung and oral epithelial samples obtained from The Cancer Genome Atlas (TCGA). We found that the receptor and transmembrane protease necessary for SARS-CoV-2 entry into host cells, ACE2 and TMPRSS2, respectively, were upregulated in smoking samples from both lung and oral epithelial tissue. We then explored the mechanistic hypothesis that smoking may upregulate ACE2 expression through the upregulation of the androgen pathway. ACE2 and TMPRSS2 upregulation were both correlated to androgen pathway enrichment and the specific upregulation of central pathway regulatory genes. These data provide a potential model for the increased susceptibility of smoking patients to COVID-19 and encourage further exploration into the androgen and tobacco upregulation of ACE2 to understand the potential clinical ramifications.
Jaideep Chakladar; Neil Shende; Wei Tse Li; Mahadevan Rajasekaran; Eric Y. Chang; Weg M. Ongkeko. Smoking-Mediated Upregulation of the Androgen Pathway Leads to Increased SARS-CoV-2 Susceptibility. International Journal of Molecular Sciences 2020, 21, 3627 .
AMA StyleJaideep Chakladar, Neil Shende, Wei Tse Li, Mahadevan Rajasekaran, Eric Y. Chang, Weg M. Ongkeko. Smoking-Mediated Upregulation of the Androgen Pathway Leads to Increased SARS-CoV-2 Susceptibility. International Journal of Molecular Sciences. 2020; 21 (10):3627.
Chicago/Turabian StyleJaideep Chakladar; Neil Shende; Wei Tse Li; Mahadevan Rajasekaran; Eric Y. Chang; Weg M. Ongkeko. 2020. "Smoking-Mediated Upregulation of the Androgen Pathway Leads to Increased SARS-CoV-2 Susceptibility." International Journal of Molecular Sciences 21, no. 10: 3627.
Papillary thyroid carcinoma (PTC) variants exhibit different prognosis, but critical characteristics of PTC variants that contribute to differences in pathogenesis are not well-known. This study aims to characterize dysregulated immune-associated and cancer-associated genes in three PTC subtypes to explore how the interplay between cancer and immune processes causes differential prognosis. RNA-sequencing data from The Cancer Genome Atlas (TCGA) were used to identify dysregulated genes in each variant. The dysregulation profiles of the subtypes were compared using functional pathways clustering and correlations to relevant clinical variables, genomic alterations, and microRNA regulation. We discovered that the dysregulation profiles of classical PTC (CPTC) and the tall cell variant (TCPTC) are similar and are distinct from that of the follicular variant (FVPTC). However, unique cancer or immune-associated genes are associated with clinical variables for each subtype. Cancer-related genes MUC1, FN1, and S100-family members were the most clinically relevant in CPTC, while APLN and IL16, both immune-related, were clinically relevant in FVPTC. RAET-family members, also immune-related, were clinically relevant in TCPTC. Collectively, our data suggest that dysregulation of both cancer and immune associated genes defines the gene expression landscapes of PTC variants, but different cancer or immune related genes may drive the phenotype of each variant.
Jaideep Chakladar; Wei Tse Li; Michael Bouvet; Eric Y. Chang; Jessica Wang-Rodriguez; Weg M. Ongkeko. Papillary Thyroid Carcinoma Variants are Characterized by Co-dysregulation of Immune and Cancer Associated Genes. Cancers 2019, 11, 1179 .
AMA StyleJaideep Chakladar, Wei Tse Li, Michael Bouvet, Eric Y. Chang, Jessica Wang-Rodriguez, Weg M. Ongkeko. Papillary Thyroid Carcinoma Variants are Characterized by Co-dysregulation of Immune and Cancer Associated Genes. Cancers. 2019; 11 (8):1179.
Chicago/Turabian StyleJaideep Chakladar; Wei Tse Li; Michael Bouvet; Eric Y. Chang; Jessica Wang-Rodriguez; Weg M. Ongkeko. 2019. "Papillary Thyroid Carcinoma Variants are Characterized by Co-dysregulation of Immune and Cancer Associated Genes." Cancers 11, no. 8: 1179.