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1,057 results on '"Rom, William N."'

1. Asbestosis

Author

Henderson, Ian, primary, Sterman, Daniel H., additional, Smith, Robert L., additional, and Rom, William N., additional

Published
2022
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4. Integrated metabolomics and proteomics highlight altered nicotinamide and polyamine pathways in lung adenocarcinoma

Author

Fahrmann, Johannes F, Grapov, Dmitry, Wanichthanarak, Kwanjeera, DeFelice, Brian C, Salemi, Michelle R, Rom, William N, Gandara, David R, Phinney, Brett S, Fiehn, Oliver, Pass, Harvey, and Miyamoto, Suzanne

Subjects
Lung, Cancer, Lung Cancer, Biotechnology, Lung Adenocarcinoma, Metabolomics, Proteomics, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Lung cancer is the leading cause of cancer mortality in the United States with non-small cell lung cancer (NSCLC) adenocarcinoma being the most common histological type. Early perturbations in cellular metabolism are a hallmark of cancer, but the extent of these changes in early stage lung adenocarcinoma remains largely unknown. In the current study, an integrated metabolomics and proteomics approach was utilized to characterize the biochemical and molecular alterations between malignant and matched control tissue from 27 subjects diagnosed with early stage lung adenocarcinoma. Differential analysis identified 71 metabolites and 1102 proteins that delineated tumor from control tissue. Integrated results indicated four major metabolic changes in early stage adenocarcinoma: (1) increased glycosylation and glutaminolysis; (2) elevated Nrf2 activation; (3) increase in nicotinic and nicotinamide salvaging pathways; and (4) elevated polyamine biosynthesis linked to differential regulation of the SAM/nicotinamide methyl-donor pathway. Genomic data from publicly available databases were included to strengthen proteomic findings. Our findings provide insight into the biochemical and molecular biological reprogramming that may accompanies early stage lung tumorigenesis and highlight potential therapeutic targets.

Published
2017

5. Risk Factors Associated With Quantitative Evidence of Lung Emphysema and Fibrosis in an HIV-Infected Cohort

Author

Leader, Joseph K, Crothers, Kristina, Huang, Laurence, King, Mark A, Morris, Alison, Thompson, Bruce W, Flores, Sonia C, Drummond, Michael B, Rom, William N, and Diaz, Philip T

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Chronic Obstructive Pulmonary Disease, Clinical Research, Prevention, Infectious Diseases, Emphysema, Lung, HIV/AIDS, Aetiology, 2.1 Biological and endogenous factors, Infection, Respiratory, Good Health and Well Being, Adult, Anti-HIV Agents, CD4 Lymphocyte Count, Cohort Studies, Cross-Sectional Studies, Female, HIV Infections, Humans, Male, Middle Aged, Pulmonary Emphysema, Pulmonary Fibrosis, Risk Factors, Tomography, X-Ray Computed, emphysema, pulmonary fibrosis, lung, computed tomography, HIV, Clinical Sciences, Public Health and Health Services, Virology, Clinical sciences, Epidemiology, Public health
Abstract

IntroductionThe disease spectrum for HIV-infected individuals has shifted toward comorbid non-AIDS conditions including chronic lung disease, but quantitative image analysis of lung disease has not been performed.ObjectivesTo quantify the prevalence of structural changes of the lung indicating emphysema or fibrosis on radiographic examination.MethodsA cross-sectional analysis of 510 HIV-infected participants in the multicenter Lung-HIV study was performed. Data collected included demographics, biological markers of HIV, pulmonary function testing, and chest computed tomographic examinations. Emphysema and fibrosis-like changes were quantified on computed tomographic images based on threshold approaches.ResultsIn our cohort, 69% was on antiretroviral therapy, 13% had a current CD4 cell count less than 200 cells per microliter, 39% had an HIV viral load greater than 500 copies per milliliter, and 25% had at least a trace level of emphysema (defined as >2.5% of voxels

Published
2016

6. Serum phosphatidylethanolamine levels distinguish benign from malignant solitary pulmonary nodules and represent a potential diagnostic biomarker for lung cancer

Author

Fahrmann, Johannes F, Grapov, Dmitry, DeFelice, Brian C, Taylor, Sandra, Kim, Kyoungmi, Kelly, Karen, Wikoff, William R, Pass, Harvey, Rom, William N, Fiehn, Oliver, and Miyamoto, Suzanne

Subjects
Clinical Research, Prevention, Lung, Biomedical Imaging, Cancer, Lung Cancer, Clinical Trials and Supportive Activities, 4.2 Evaluation of markers and technologies, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Aged, Biomarkers, Tumor, Diagnosis, Differential, Female, Humans, Lung Neoplasms, Male, Metabolome, Metabolomics, Middle Aged, Neoplasm Staging, Phosphatidylethanolamines, ROC Curve, Solitary Pulmonary Nodule, Lung cancer, metabolomics, phospholipids, biomarkers, solitary pulmonary nodules, Oncology & Carcinogenesis
Abstract

BackgroundRecent computed tomography (CT) screening trials showed that it is effective for early detection of lung cancer, but were plagued by high false positive rates. Additional blood biomarker tests designed to complement CT screening and reduce false positive rates are highly desirable.ObjectiveIdentify blood-based metabolite biomarkers for diagnosing lung cancer.MehtodsSerum samples from subjects participating in a CT screening trial were analyzed using untargeted GC-TOFMS and HILIC-qTOFMS-based metabolomics. Samples were acquired prior to diagnosis (pre-diagnostic, n= 17), at-diagnosis (n= 25) and post-diagnosis (n= 19) of lung cancer and from subjects with benign nodules (n= 29).ResultsUnivariate analysis identified 40, 102 and 30 features which were significantly different between subjects with malignant (pre-, at- and post-diagnosis) solitary pulmonary nodules (SPNs) and benign SPNs, respectively. Ten metabolites were consistently different between subjects presenting malignant (pre- and at-diagnosis) or benign SPNs. Three of these 10 metabolites were phosphatidylethanolamines (PE) suggesting alterations in lipid metabolism. Accuracies of 77%, 83% and 78% in the pre-diagnosis group and 69%, 71% and 67% in the at-diagnosis group were determined for PE(34:2), PE(36:2) and PE(38:4), respectively.ConclusionsThis study demonstrates evidence of early metabolic alterations that can possibly distinguish malignant from benign SPNs. Further studies in larger pools of samples are warranted.

Published
2016

7. Enrichment of the lung microbiome with oral taxa is associated with lung inflammation of a Th17 phenotype

Author

Segal, Leopoldo N, Clemente, Jose C, Tsay, Jun-Chieh J, Koralov, Sergei B, Keller, Brian C, Wu, Benjamin G, Li, Yonghua, Shen, Nan, Ghedin, Elodie, Morris, Alison, Diaz, Phillip, Huang, Laurence, Wikoff, William R, Ubeda, Carles, Artacho, Alejandro, Rom, William N, Sterman, Daniel H, Collman, Ronald G, Blaser, Martin J, and Weiden, Michael D

Subjects
Microbiology, Biological Sciences, Lung, Clinical Research, Genetics, Aetiology, 2.1 Biological and endogenous factors, Respiratory, Inflammatory and immune system, Bronchoalveolar Lavage Fluid, Humans, Microbiota, Pneumonia, Respiratory Aspiration, Th17 Cells, Medical Microbiology
Abstract

Microaspiration is a common phenomenon in healthy subjects, but its frequency is increased in chronic inflammatory airway diseases, and its role in inflammatory and immune phenotypes is unclear. We have previously demonstrated that acellular bronchoalveolar lavage samples from half of the healthy people examined are enriched with oral taxa (here called pneumotypeSPT) and this finding is associated with increased numbers of lymphocytes and neutrophils in bronchoalveolar lavage. Here, we have characterized the inflammatory phenotype using a multi-omic approach. By evaluating both upper airway and acellular bronchoalveolar lavage samples from 49 subjects from three cohorts without known pulmonary disease, we observed that pneumotypeSPT was associated with a distinct metabolic profile, enhanced expression of inflammatory cytokines, a pro-inflammatory phenotype characterized by elevated Th-17 lymphocytes and, conversely, a blunted alveolar macrophage TLR4 response. The cellular immune responses observed in the lower airways of humans with pneumotypeSPT indicate a role for the aspiration-derived microbiota in regulating the basal inflammatory status at the pulmonary mucosal surface.

Published
2016

8. Differential N‑Glycosylation Patterns in Lung Adenocarcinoma Tissue

Author

Ruhaak, L Renee, Taylor, Sandra L, Stroble, Carol, Nguyen, Uyen Thao, Parker, Evan A, Song, Ting, Lebrilla, Carlito B, Rom, William N, Pass, Harvey, Kim, Kyoungmi, Kelly, Karen, and Miyamoto, Suzanne

Subjects
Biochemistry and Cell Biology, Biological Sciences, Cancer, Rare Diseases, Lung, Lung Cancer, Adenocarcinoma, Adenocarcinoma of Lung, Aged, Aged, 80 and over, Carbohydrate Sequence, Female, Fucose, Galactose, Gene Expression Regulation, Neoplastic, Glycomics, Glycosylation, Glycosyltransferases, Humans, Lung Neoplasms, Male, Mannose, Middle Aged, Molecular Sequence Data, Neoplasm Proteins, Polysaccharides, Protein Processing, Post-Translational, N-Glycosylation, NSCLC, tissue, nLC-MS profiling, gene expression, nLC−MS profiling, Chemical Sciences, Biochemistry & Molecular Biology, Biological sciences, Chemical sciences
Abstract

To decrease the mortality of lung cancer, better screening and diagnostic tools as well as treatment options are needed. Protein glycosylation is one of the major post-translational modifications that is altered in cancer, but it is not exactly clear which glycan structures are affected. A better understanding of the glycan structures that are differentially regulated in lung tumor tissue is highly desirable and will allow us to gain greater insight into the underlying biological mechanisms of aberrant glycosylation in lung cancer. Here, we assess differential glycosylation patterns of lung tumor tissue and nonmalignant tissue at the level of individual glycan structures using nLC-chip-TOF-MS. Using tissue samples from 42 lung adenocarcinoma patients, 29 differentially expressed (FDR < 0.05) glycan structures were identified. The levels of several oligomannose type glycans were upregulated in tumor tissue. Furthermore, levels of fully galactosylated glycans, some of which were of the hybrid type and mostly without fucose, were decreased in cancerous tissue, whereas levels of non- or low-galactosylated glycans mostly with fucose were increased. To further assess the regulation of the altered glycosylation, the glycomics data was compared to publicly available gene expression data from lung adenocarcinoma tissue compared to nonmalignant lung tissue. The results are consistent with the possibility that the observed N-glycan changes have their origin in differentially expressed glycosyltransferases. These results will be used as a starting point for the further development of clinical glycan applications in the fields of imaging, drug targeting, and biomarkers for lung cancer.

Published
2015

10. Metabolomic markers of altered nucleotide metabolism in early stage adenocarcinoma.

Author

Wikoff, William R, Grapov, Dmitry, Fahrmann, Johannes F, DeFelice, Brian, Rom, William N, Pass, Harvey I, Kim, Kyoungmi, Nguyen, UyenThao, Taylor, Sandra L, Gandara, David R, Kelly, Karen, Fiehn, Oliver, and Miyamoto, Suzanne

Subjects
Humans, Adenocarcinoma, Lung Neoplasms, Nucleotides, Neoplasm Staging, Early Diagnosis, Aged, Aged, 80 and over, Middle Aged, Female, Male, Gas Chromatography-Mass Spectrometry, Metabolic Networks and Pathways, Metabolomics, Metabolome, Biomarkers, Tumor, Adenocarcinoma of Lung, Rare Diseases, Cancer, Prevention, Lung Cancer, Lung, Clinical Sciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Adenocarcinoma, a type of non-small cell lung cancer, is the most frequently diagnosed lung cancer and the leading cause of lung cancer mortality in the United States. It is well documented that biochemical changes occur early in the transition from normal to cancer cells, but the extent to which these alterations affect tumorigenesis in adenocarcinoma remains largely unknown. Herein, we describe the application of mass spectrometry and multivariate statistical analysis in one of the largest biomarker research studies to date aimed at distinguishing metabolic differences between malignant and nonmalignant lung tissue. Gas chromatography time-of-flight mass spectrometry was used to measure 462 metabolites in 39 malignant and nonmalignant lung tissue pairs from current or former smokers with early stage (stage IA-IB) adenocarcinoma. Statistical mixed effects models, orthogonal partial least squares discriminant analysis and network integration, were used to identify key cancer-associated metabolic perturbations in adenocarcinoma compared with nonmalignant tissue. Cancer-associated biochemical alterations were characterized by (i) decreased glucose levels, consistent with the Warburg effect, (ii) changes in cellular redox status highlighted by elevations in cysteine and antioxidants, alpha- and gamma-tocopherol, (iii) elevations in nucleotide metabolites 5,6-dihydrouracil and xanthine suggestive of increased dihydropyrimidine dehydrogenase and xanthine oxidoreductase activity, (iv) increased 5'-deoxy-5'-methylthioadenosine levels indicative of reduced purine salvage and increased de novo purine synthesis, and (v) coordinated elevations in glutamate and UDP-N-acetylglucosamine suggesting increased protein glycosylation. The present study revealed distinct metabolic perturbations associated with early stage lung adenocarcinoma, which may provide candidate molecular targets for personalizing therapeutic interventions and treatment efficacy monitoring.

Published
2015

14. Experimental Human Exposure to Air Pollutants Is Essential to Understand Adverse Health Effects

Author

Rom, William N, Boushey, Homer, and Caplan, Arthur

Subjects
Lung, Patient Safety, Clinical Research, Asthma, Climate-Related Exposures and Conditions, 2.2 Factors relating to the physical environment, Aetiology, Respiratory, Generic health relevance, Good Health and Well Being, Air Pollutants, Animals, Dose-Response Relationship, Drug, Ethics Committees, Research, Evidence-Based Medicine, Humans, Informed Consent, Inhalation Exposure, Lung Diseases, Research Subjects, Risk Assessment, Risk Factors, Therapeutic Human Experimentation, chamber studies, ozone, particulate matter, Cardiorespiratory Medicine and Haematology, Respiratory System
Abstract

Air pollution has been found to cause significant global mortality, with 6.8 million excess deaths attributed to air pollution each year, and similarly large numbers of exacerbations of asthma, chronic obstructive pulmonary disease, and cardiovascular diseases. Epidemiological research has identified associations, and experimental human exposure has provided critical information on dose-response relationships of adverse effects caused by controlled human exposure to individual pollutants. Human exposures further enable examination of the relationship of adverse effects such as symptoms and pulmonary function changes to presumed mechanisms of disease revealed through analysis of bronchoalveolar lavage fluid obtained from the lower respiratory tract. In this Perspective, we analyze the ethics of human exposure, the importance of the information gained, and the risks of such exposure. We find that these studies appear to have been done with proper approval of institutional review boards, were done with informed consent from the participants, and have rarely been associated with serious adverse events.

Published
2013

17. Figure S1 from Metabolomic Markers of Altered Nucleotide Metabolism in Early Stage Adenocarcinoma

Author

Wikoff, William R., primary, Grapov, Dmitry, primary, Fahrmann, Johannes F., primary, DeFelice, Brian, primary, Rom, William N., primary, Pass, Harvey I., primary, Kim, Kyoungmi, primary, Nguyen, UyenThao, primary, Taylor, Sandra L., primary, Gandara, David R., primary, Kelly, Karen, primary, Fiehn, Oliver, primary, and Miyamoto, Suzanne, primary

Published
2023
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18. Supplemental Table S4 from Metabolomic Markers of Altered Nucleotide Metabolism in Early Stage Adenocarcinoma

Author

Wikoff, William R., primary, Grapov, Dmitry, primary, Fahrmann, Johannes F., primary, DeFelice, Brian, primary, Rom, William N., primary, Pass, Harvey I., primary, Kim, Kyoungmi, primary, Nguyen, UyenThao, primary, Taylor, Sandra L., primary, Gandara, David R., primary, Kelly, Karen, primary, Fiehn, Oliver, primary, and Miyamoto, Suzanne, primary

Published
2023
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20. Supplementary File Table All (excel) from Lower Airway Dysbiosis Affects Lung Cancer Progression

Author

Tsay, Jun-Chieh J., primary, Wu, Benjamin G., primary, Sulaiman, Imran, primary, Gershner, Katherine, primary, Schluger, Rosemary, primary, Li, Yonghua, primary, Yie, Ting-An, primary, Meyn, Peter, primary, Olsen, Evan, primary, Perez, Luisannay, primary, Franca, Brendan, primary, Carpenito, Joseph, primary, Iizumi, Tadasu, primary, El-Ashmawy, Mariam, primary, Badri, Michelle, primary, Morton, James T., primary, Shen, Nan, primary, He, Linchen, primary, Michaud, Gaetane, primary, Rafeq, Samaan, primary, Bessich, Jamie L., primary, Smith, Robert L., primary, Sauthoff, Harald, primary, Felner, Kevin, primary, Pillai, Ray, primary, Zavitsanou, Anastasia-Maria, primary, Koralov, Sergei B., primary, Mezzano, Valeria, primary, Loomis, Cynthia A., primary, Moreira, Andre L., primary, Moore, William, primary, Tsirigos, Aristotelis, primary, Heguy, Adriana, primary, Rom, William N., primary, Sterman, Daniel H., primary, Pass, Harvey I., primary, Clemente, Jose C., primary, Li, Huilin, primary, Bonneau, Richard, primary, Wong, Kwok-Kin, primary, Papagiannakopoulos, Thales, primary, and Segal, Leopoldo N., primary

Published
2023
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21. Supplementary Table from Lower Airway Dysbiosis Affects Lung Cancer Progression

Author

Tsay, Jun-Chieh J., primary, Wu, Benjamin G., primary, Sulaiman, Imran, primary, Gershner, Katherine, primary, Schluger, Rosemary, primary, Li, Yonghua, primary, Yie, Ting-An, primary, Meyn, Peter, primary, Olsen, Evan, primary, Perez, Luisannay, primary, Franca, Brendan, primary, Carpenito, Joseph, primary, Iizumi, Tadasu, primary, El-Ashmawy, Mariam, primary, Badri, Michelle, primary, Morton, James T., primary, Shen, Nan, primary, He, Linchen, primary, Michaud, Gaetane, primary, Rafeq, Samaan, primary, Bessich, Jamie L., primary, Smith, Robert L., primary, Sauthoff, Harald, primary, Felner, Kevin, primary, Pillai, Ray, primary, Zavitsanou, Anastasia-Maria, primary, Koralov, Sergei B., primary, Mezzano, Valeria, primary, Loomis, Cynthia A., primary, Moreira, Andre L., primary, Moore, William, primary, Tsirigos, Aristotelis, primary, Heguy, Adriana, primary, Rom, William N., primary, Sterman, Daniel H., primary, Pass, Harvey I., primary, Clemente, Jose C., primary, Li, Huilin, primary, Bonneau, Richard, primary, Wong, Kwok-Kin, primary, Papagiannakopoulos, Thales, primary, and Segal, Leopoldo N., primary

Published
2023
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22. Supplementary Figure All from Lower Airway Dysbiosis Affects Lung Cancer Progression

Author

Tsay, Jun-Chieh J., primary, Wu, Benjamin G., primary, Sulaiman, Imran, primary, Gershner, Katherine, primary, Schluger, Rosemary, primary, Li, Yonghua, primary, Yie, Ting-An, primary, Meyn, Peter, primary, Olsen, Evan, primary, Perez, Luisannay, primary, Franca, Brendan, primary, Carpenito, Joseph, primary, Iizumi, Tadasu, primary, El-Ashmawy, Mariam, primary, Badri, Michelle, primary, Morton, James T., primary, Shen, Nan, primary, He, Linchen, primary, Michaud, Gaetane, primary, Rafeq, Samaan, primary, Bessich, Jamie L., primary, Smith, Robert L., primary, Sauthoff, Harald, primary, Felner, Kevin, primary, Pillai, Ray, primary, Zavitsanou, Anastasia-Maria, primary, Koralov, Sergei B., primary, Mezzano, Valeria, primary, Loomis, Cynthia A., primary, Moreira, Andre L., primary, Moore, William, primary, Tsirigos, Aristotelis, primary, Heguy, Adriana, primary, Rom, William N., primary, Sterman, Daniel H., primary, Pass, Harvey I., primary, Clemente, Jose C., primary, Li, Huilin, primary, Bonneau, Richard, primary, Wong, Kwok-Kin, primary, Papagiannakopoulos, Thales, primary, and Segal, Leopoldo N., primary

Published
2023
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23. Data from Lower Airway Dysbiosis Affects Lung Cancer Progression

Author

Tsay, Jun-Chieh J., primary, Wu, Benjamin G., primary, Sulaiman, Imran, primary, Gershner, Katherine, primary, Schluger, Rosemary, primary, Li, Yonghua, primary, Yie, Ting-An, primary, Meyn, Peter, primary, Olsen, Evan, primary, Perez, Luisannay, primary, Franca, Brendan, primary, Carpenito, Joseph, primary, Iizumi, Tadasu, primary, El-Ashmawy, Mariam, primary, Badri, Michelle, primary, Morton, James T., primary, Shen, Nan, primary, He, Linchen, primary, Michaud, Gaetane, primary, Rafeq, Samaan, primary, Bessich, Jamie L., primary, Smith, Robert L., primary, Sauthoff, Harald, primary, Felner, Kevin, primary, Pillai, Ray, primary, Zavitsanou, Anastasia-Maria, primary, Koralov, Sergei B., primary, Mezzano, Valeria, primary, Loomis, Cynthia A., primary, Moreira, Andre L., primary, Moore, William, primary, Tsirigos, Aristotelis, primary, Heguy, Adriana, primary, Rom, William N., primary, Sterman, Daniel H., primary, Pass, Harvey I., primary, Clemente, Jose C., primary, Li, Huilin, primary, Bonneau, Richard, primary, Wong, Kwok-Kin, primary, Papagiannakopoulos, Thales, primary, and Segal, Leopoldo N., primary

Published
2023
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24. Supplemental Material from Metabolomic Markers of Altered Nucleotide Metabolism in Early Stage Adenocarcinoma

Author

Wikoff, William R., primary, Grapov, Dmitry, primary, Fahrmann, Johannes F., primary, DeFelice, Brian, primary, Rom, William N., primary, Pass, Harvey I., primary, Kim, Kyoungmi, primary, Nguyen, UyenThao, primary, Taylor, Sandra L., primary, Gandara, David R., primary, Kelly, Karen, primary, Fiehn, Oliver, primary, and Miyamoto, Suzanne, primary

Published
2023
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26. Supplementary Table S4 from A Panel of Novel Detection and Prognostic Methylated DNA Markers in Primary Non–Small Cell Lung Cancer and Serum DNA

Author

Ooki, Akira, primary, Maleki, Zahra, primary, Tsay, Jun-Chieh J., primary, Goparaju, Chandra, primary, Brait, Mariana, primary, Turaga, Nitesh, primary, Nam, Hae-Seong, primary, Rom, William N., primary, Pass, Harvey I., primary, Sidransky, David, primary, Guerrero-Preston, Rafael, primary, and Hoque, Mohammad Obaidul, primary

Published
2023
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27. Data from A Gene Expression Classifier from Whole Blood Distinguishes Benign from Malignant Lung Nodules Detected by Low-Dose CT

Author

Kossenkov, Andrew V., primary, Qureshi, Rehman, primary, Dawany, Noor B., primary, Wickramasinghe, Jayamanna, primary, Liu, Qin, primary, Majumdar, R. Sonali, primary, Chang, Celia, primary, Widura, Sandy, primary, Kumar, Trisha, primary, Horng, Wen-Hwai, primary, Konnisto, Eric, primary, Criner, Gerard, primary, Tsay, Jun-Chieh J., primary, Pass, Harvey, primary, Yendamuri, Sai, primary, Vachani, Anil, primary, Bauer, Thomas, primary, Nam, Brian, primary, Rom, William N., primary, Showe, Michael K., primary, and Showe, Louise C., primary

Published
2023
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28. Supplementary information from A Panel of Novel Detection and Prognostic Methylated DNA Markers in Primary Non–Small Cell Lung Cancer and Serum DNA

Author

Ooki, Akira, primary, Maleki, Zahra, primary, Tsay, Jun-Chieh J., primary, Goparaju, Chandra, primary, Brait, Mariana, primary, Turaga, Nitesh, primary, Nam, Hae-Seong, primary, Rom, William N., primary, Pass, Harvey I., primary, Sidransky, David, primary, Guerrero-Preston, Rafael, primary, and Hoque, Mohammad Obaidul, primary

Published
2023
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29. Supplementary File S1 from A Gene Expression Classifier from Whole Blood Distinguishes Benign from Malignant Lung Nodules Detected by Low-Dose CT

Author

Kossenkov, Andrew V., primary, Qureshi, Rehman, primary, Dawany, Noor B., primary, Wickramasinghe, Jayamanna, primary, Liu, Qin, primary, Majumdar, R. Sonali, primary, Chang, Celia, primary, Widura, Sandy, primary, Kumar, Trisha, primary, Horng, Wen-Hwai, primary, Konnisto, Eric, primary, Criner, Gerard, primary, Tsay, Jun-Chieh J., primary, Pass, Harvey, primary, Yendamuri, Sai, primary, Vachani, Anil, primary, Bauer, Thomas, primary, Nam, Brian, primary, Rom, William N., primary, Showe, Michael K., primary, and Showe, Louise C., primary

Published
2023
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30. Figure S3 from A Gene Expression Classifier from Whole Blood Distinguishes Benign from Malignant Lung Nodules Detected by Low-Dose CT

Author

Kossenkov, Andrew V., primary, Qureshi, Rehman, primary, Dawany, Noor B., primary, Wickramasinghe, Jayamanna, primary, Liu, Qin, primary, Majumdar, R. Sonali, primary, Chang, Celia, primary, Widura, Sandy, primary, Kumar, Trisha, primary, Horng, Wen-Hwai, primary, Konnisto, Eric, primary, Criner, Gerard, primary, Tsay, Jun-Chieh J., primary, Pass, Harvey, primary, Yendamuri, Sai, primary, Vachani, Anil, primary, Bauer, Thomas, primary, Nam, Brian, primary, Rom, William N., primary, Showe, Michael K., primary, and Showe, Louise C., primary

Published
2023
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31. Table S3 from A Gene Expression Classifier from Whole Blood Distinguishes Benign from Malignant Lung Nodules Detected by Low-Dose CT

Author

Kossenkov, Andrew V., primary, Qureshi, Rehman, primary, Dawany, Noor B., primary, Wickramasinghe, Jayamanna, primary, Liu, Qin, primary, Majumdar, R. Sonali, primary, Chang, Celia, primary, Widura, Sandy, primary, Kumar, Trisha, primary, Horng, Wen-Hwai, primary, Konnisto, Eric, primary, Criner, Gerard, primary, Tsay, Jun-Chieh J., primary, Pass, Harvey, primary, Yendamuri, Sai, primary, Vachani, Anil, primary, Bauer, Thomas, primary, Nam, Brian, primary, Rom, William N., primary, Showe, Michael K., primary, and Showe, Louise C., primary

Published
2023
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33. Data from Optical Detection of Buccal Epithelial Nanoarchitectural Alterations in Patients Harboring Lung Cancer: Implications for Screening

Author

Roy, Hemant K., primary, Subramanian, Hariharan, primary, Damania, Dhwanil, primary, Hensing, Thomas A., primary, Rom, William N., primary, Pass, Harvey I., primary, Ray, Daniel, primary, Rogers, Jeremy D., primary, Bogojevic, Andrej, primary, Shah, Maitri, primary, Kuzniar, Tomasz, primary, Pradhan, Prabhakar, primary, and Backman, Vadim, primary

Published
2023
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34. Data from Gene Expression Profiles in Peripheral Blood Mononuclear Cells Can Distinguish Patients with Non–Small Cell Lung Cancer from Patients with Nonmalignant Lung Disease

Author

Showe, Michael K., primary, Vachani, Anil, primary, Kossenkov, Andrew V., primary, Yousef, Malik, primary, Nichols, Calen, primary, Nikonova, Elena V., primary, Chang, Celia, primary, Kucharczuk, John, primary, Tran, Bao, primary, Wakeam, Elliot, primary, Yie, Ting An, primary, Speicher, David, primary, Rom, William N., primary, Albelda, Steven, primary, and Showe, Louise C., primary

Published
2023
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35. Supplementary Figure 1 from Optical Detection of Buccal Epithelial Nanoarchitectural Alterations in Patients Harboring Lung Cancer: Implications for Screening

Author

Roy, Hemant K., primary, Subramanian, Hariharan, primary, Damania, Dhwanil, primary, Hensing, Thomas A., primary, Rom, William N., primary, Pass, Harvey I., primary, Ray, Daniel, primary, Rogers, Jeremy D., primary, Bogojevic, Andrej, primary, Shah, Maitri, primary, Kuzniar, Tomasz, primary, Pradhan, Prabhakar, primary, and Backman, Vadim, primary

Published
2023
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36. Supplementary Methods, Figure Legend from Optical Detection of Buccal Epithelial Nanoarchitectural Alterations in Patients Harboring Lung Cancer: Implications for Screening

Author

Roy, Hemant K., primary, Subramanian, Hariharan, primary, Damania, Dhwanil, primary, Hensing, Thomas A., primary, Rom, William N., primary, Pass, Harvey I., primary, Ray, Daniel, primary, Rogers, Jeremy D., primary, Bogojevic, Andrej, primary, Shah, Maitri, primary, Kuzniar, Tomasz, primary, Pradhan, Prabhakar, primary, and Backman, Vadim, primary

Published
2023
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41. Contributors

Author

Adjei, Alex A., primary, Ahn, Mjung-Ju, additional, Amos, Chris I., additional, Antonicelli, Alberto, additional, Asamura, Hisao, additional, Atwood, Todd, additional, Baas, Paul, additional, Bailey-Wilson, Joan E., additional, Ball, David, additional, Barlesi, Fabrice, additional, Bazan, Jose G., additional, Belderbos, José, additional, Bezjak, Andrea, additional, Billingham, Lucinda J., additional, Boffetta, Paolo, additional, Bonifazi, Martina, additional, Brahmer, Julie R., additional, Brambilla, Elisabeth, additional, Brims, Fraser, additional, Brunelli, Alessandro, additional, Bryant, Ayesha, additional, Campbell, Nicholas, additional, Carter, Brett W., additional, Cerfolio, Robert, additional, Cho, Byoung Chul, additional, Cho, William C.S., additional, Choy, Hak, additional, Chu, Chia-Yu, additional, Colburn, Glenda, additional, Colt, Henri, additional, Rosell Costa, Rafael, additional, Darling, Gail E., additional, Davis, Mellar, additional, de Groot, Patricia M., additional, de Koning, Harry J., additional, De Leyn, Paul, additional, De Ruysscher, Dirk, additional, Demiral, Ayşe Nur, additional, Derks, Jules, additional, Detterbeck, Frank C., additional, Devarakonda, Siddhartha, additional, Dingemans, Anne-Marie C., additional, Donington, Jessica S., additional, Dresler, Carolyn M., additional, Dubinett, Steven M., additional, Dy, Grace K., additional, Erasmus, Jeremy J., additional, Fairchild, Alysa, additional, Fennell, Dean A., additional, Fernando, Hiran C., additional, Filosso, Pier Luigi, additional, Flores, Raja, additional, Fong, Kwun, additional, Fox, Jesme, additional, Gandara, David R., additional, Gandhi, Leena, additional, Gaspar, Laurie, additional, Gasparini, Stefano, additional, Gazdar, Adi F., additional, Giaccone, Giuseppe, additional, Girard, Nicolas, additional, Goldstraw, Peter, additional, Gore, Elizabeth M., additional, Goss, Glenwood, additional, Govindan, Ramaswamy, additional, Greenberg, Alissa K., additional, Grunenwald, 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Published
2018
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44. Fibrogenesis

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Munger, John S., Rom, William N., Cagle, Philip T., editor, Zander, Dani S., editor, Popper, Helmut H., editor, Jagirdar, Jaishree, editor, Haque, Abida K., editor, and Barrios, Roberto, editor

Published
2008
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