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2. Integrative multi-omics profiling in human decedents receiving pig heart xenografts

Author

Schmauch, Eloi, Piening, Brian, Mohebnasab, Maedeh, Xia, Bo, Zhu, Chenchen, Stern, Jeffrey, Zhang, Weimin, Dowdell, Alexa K., Kim, Jacqueline I., Andrijevic, David, Khalil, Karen, Jaffe, Ian S., Loza, Bao-Li, Gragert, Loren, Camellato, Brendan R., Oliveira, Michelli F., O’Brien, Darragh P., Chen, Han M., Weldon, Elaina, Gao, Hui, Gandla, Divya, Chang, Andrew, Bhatt, Riyana, Gao, Sarah, Lin, Xiangping, Reddy, Kriyana P., Kagermazova, Larisa, Habara, Alawi H., Widawsky, Sophie, Liang, Feng-Xia, Sall, Joseph, Loupy, Alexandre, Heguy, Adriana, Taylor, Sarah E. B., Zhu, Yinan, Michael, Basil, Jiang, Lihua, Jian, Ruiqi, Chong, Anita S., Fairchild, Robert L., Linna-Kuosmanen, Suvi, Kaikkonen, Minna U., Tatapudi, Vasishta, Lorber, Marc, Ayares, David, Mangiola, Massimo, Narula, Navneet, Moazami, Nader, Pass, Harvey, Herati, Ramin S., Griesemer, Adam, Kellis, Manolis, Snyder, Michael P., Montgomery, Robert A., Boeke, Jef D., and Keating, Brendan J.

Published
2024
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4. Surgical results of the Lung Cancer Mutation Consortium 3 trial: A phase II multicenter single-arm study to investigate the efficacy and safety of atezolizumab as neoadjuvant therapy in patients with stages IB-select IIIB resectable non-small cell lung cancer.

Author

Rusch, Valerie, Nicholas, Alan, Patterson, G, Waqar, Salama, Toloza, Eric, Haura, Eric, Raz, Dan, Reckamp, Karen, Merritt, Robert, Owen, Dwight, Finley, David, McNamee, Ciaran, Blasberg, Justin, Garon, Edward, Mitchell, John, Doebele, Robert, Baciewicz, Frank, Pass, Harvey, Schulze, Katja, Johnson, Ann, Bunn, Paul, Johnson, Bruce, Kris, Mark, Kwiatkowski, David, Wistuba, Ignacio, Chaft, Jamie, Carbone, David, Lee, Jay, and Nagasaka, Misako

Subjects
immunotherapy, lung cancer, neoadjuvant therapy, Aged, Female, Humans, Carcinoma, Non-Small-Cell Lung, ErbB Receptors, Immune Checkpoint Inhibitors, Lung Neoplasms, Mutation, Neoadjuvant Therapy, Receptor Protein-Tyrosine Kinases, Male, Middle Aged
Abstract

OBJECTIVE: Multimodality treatment for resectable non-small cell lung cancer has long remained at a therapeutic plateau. Immune checkpoint inhibitors are highly effective in advanced non-small cell lung cancer and promising preoperatively in small clinical trials for resectable non-small cell lung cancer. This large multicenter trial tested the safety and efficacy of neoadjuvant atezolizumab and surgery. METHODS: Patients with stage IB to select IIIB resectable non-small cell lung cancer and Eastern Cooperative Oncology Group performance status 0/1 were eligible. Patients received atezolizumab 1200 mg intravenously every 3 weeks for 2 cycles or less followed by resection. The primary end point was major pathological response in patients without EGFR/ALK+ alterations. Pre- and post-treatment computed tomography, positron emission tomography, pulmonary function tests, and biospecimens were obtained. Adverse events were recorded by Common Terminology Criteria for Adverse Events v.4.0. RESULTS: From April 2017 to February 2020, 181 patients were entered in the study. Baseline characteristics were mean age, 65.1 years; female, 93 of 181 (51%); nonsquamous histology, 112 of 181 (62%); and clinical stages IIB to IIIB, 147 of 181 (81%). In patients without EGFR/ALK alterations who underwent surgery, the major pathological response rate was 20% (29/143; 95% confidence interval, 14-28) and the pathological complete response rate was 6% (8/143; 95% confidence interval, 2-11). There were no grade 4/5 treatment-related adverse events preoperatively. Of 159 patients (87.8%) undergoing surgery, 145 (91%) had pathologic complete resection. There were 5 (3%) intraoperative complications, no intraoperative deaths, and 2 postoperative deaths within 90 days, 1 treatment related. Median disease-free and overall survival have not been reached. CONCLUSIONS: Neoadjuvant atezolizumab in resectable stage IB to IIIB non-small cell lung cancer was well tolerated, yielded a 20% major pathological response rate, and allowed safe, complete surgical resection. These results strongly support the further development of immune checkpoint inhibitors as preoperative therapy in locally advanced non-small cell lung cancer.

Published
2023

6. Mapping the landscape of histomorphological cancer phenotypes using self-supervised learning on unlabeled, unannotated pathology slides

Author

Quiros, Adalberto Claudio, Coudray, Nicolas, Yeaton, Anna, Yang, Xinyu, Liu, Bojing, Le, Hortense, Chiriboga, Luis, Karimkhan, Afreen, Narula, Navneet, Moore, David A., Park, Christopher Y., Pass, Harvey, Moreira, Andre L., Quesne, John Le, Tsirigos, Aristotelis, and Yuan, Ke

Subjects
Computer Science - Computer Vision and Pattern Recognition, Computer Science - Machine Learning
Abstract

Definitive cancer diagnosis and management depend upon the extraction of information from microscopy images by pathologists. These images contain complex information requiring time-consuming expert human interpretation that is prone to human bias. Supervised deep learning approaches have proven powerful for classification tasks, but they are inherently limited by the cost and quality of annotations used for training these models. To address this limitation of supervised methods, we developed Histomorphological Phenotype Learning (HPL), a fully blue{self-}supervised methodology that requires no expert labels or annotations and operates via the automatic discovery of discriminatory image features in small image tiles. Tiles are grouped into morphologically similar clusters which constitute a library of histomorphological phenotypes, revealing trajectories from benign to malignant tissue via inflammatory and reactive phenotypes. These clusters have distinct features which can be identified using orthogonal methods, linking histologic, molecular and clinical phenotypes. Applied to lung cancer tissues, we show that they align closely with patient survival, with histopathologically recognised tumor types and growth patterns, and with transcriptomic measures of immunophenotype. We then demonstrate that these properties are maintained in a multi-cancer study. These results show the clusters represent recurrent host responses and modes of tumor growth emerging under natural selection. Code, pre-trained models, learned embeddings, and documentation are available to the community at https://github.com/AdalbertoCq/Histomorphological-Phenotype-Learning

Published
2022

9. The International Association for the Study of Lung Cancer Pleural Mesothelioma Staging Project: Proposal for Revision of the TNM Stage Groupings in the Forthcoming (Ninth) Edition of the TNM Classification for Pleural Mesothelioma

Author

Nowak, Anna K., Giroux, Dorothy J., Eisele, Megan, Rosenthal, Adam, Bille, Andrea, Gill, Ritu R., Kindler, Hedy L., Pass, Harvey I., Rice, David, Ripley, R Taylor, Wolf, Andrea, Friedberg, Joseph, Nishimura, Katherine, and Rusch, Valerie W.

Published
2024
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10. The International Association for the Study of Lung Cancer Mesothelioma Staging Project: Proposals for Revisions of the “T” Descriptors in the Forthcoming Ninth Edition of the TNM Classification for Pleural Mesothelioma

Author

Gill, Ritu R., Nowak, Anna K., Giroux, Dorothy J., Eisele, Megan, Rosenthal, Adam, Kindler, Hedy, Wolf, Andrea, Ripley, Robert T., Billé, Andre, Rice, David, Opitz, Isabelle, Rimner, Andreas, de Perrot, Marc, Pass, Harvey I., and Rusch, Valerie W.

Published
2024
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12. The International Association for the Study of Lung Cancer Pleural Mesothelioma Staging Project: Expanded Database to Inform Revisions in the Ninth Edition of the TNM Classification of Pleural Mesothelioma

Author

Wolf, Andrea S., Eisele, Megan, Giroux, Dorothy J., Gill, Ritu, Nowak, Anna K., Bille, Andrea, Rice, David, Ripley, Robert T., Opitz, Isabelle, Galateau-Salle, Francoise, Hasegawa, Seiki, Kindler, Hedy L., Pass, Harvey I., and Rusch, Valerie W.

Published
2024
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13. Inflammation in the tumor-adjacent lung as a predictor of clinical outcome in lung adenocarcinoma

Author

Dolgalev, Igor, Zhou, Hua, Murrell, Nina, Le, Hortense, Sakellaropoulos, Theodore, Coudray, Nicolas, Zhu, Kelsey, Vasudevaraja, Varshini, Yeaton, Anna, Goparaju, Chandra, Li, Yonghua, Sulaiman, Imran, Tsay, Jun-Chieh J., Meyn, Peter, Mohamed, Hussein, Sydney, Iris, Shiomi, Tomoe, Ramaswami, Sitharam, Narula, Navneet, Kulicke, Ruth, Davis, Fred P., Stransky, Nicolas, Smolen, Gromoslaw A., Cheng, Wei-Yi, Cai, James, Punekar, Salman, Velcheti, Vamsidhar, Sterman, Daniel H., Poirier, J. T., Neel, Ben, Wong, Kwok-Kin, Chiriboga, Luis, Heguy, Adriana, Papagiannakopoulos, Thales, Nadorp, Bettina, Snuderl, Matija, Segal, Leopoldo N., Moreira, Andre L., Pass, Harvey I., and Tsirigos, Aristotelis

Published
2023
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14. Pleural fluid microbiota as a biomarker for malignancy and prognosis

Author

Kwok, Benjamin, Wu, Benjamin G., Kocak, Ibrahim F., Sulaiman, Imran, Schluger, Rosemary, Li, Yonghua, Anwer, Raheel, Goparaju, Chandra, Ryan, Daniel J., Sagatelian, Marla, Dreier, Matthew S., Murthy, Vivek, Rafeq, Samaan, Michaud, Gaetane C., Sterman, Daniel H., Bessich, Jamie L., Pass, Harvey I., Segal, Leopoldo N., and Tsay, Jun-Chieh J.

Published
2023
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15. Pig-to-human heart xenotransplantation in two recently deceased human recipients

Author

Moazami, Nader, Stern, Jeffrey M., Khalil, Karen, Kim, Jacqueline I., Narula, Navneet, Mangiola, Massimo, Weldon, Elaina P., Kagermazova, Larisa, James, Les, Lawson, Nikki, Piper, Greta L., Sommer, Philip M., Reyentovich, Alex, Bamira, Daniel, Saraon, Tajinderpal, Kadosh, Bernard S., DiVita, Michael, Goldberg, Randal I., Hussain, Syed T., Chan, Justin, Ngai, Jennie, Jan, Thomas, Ali, Nicole M., Tatapudi, Vasishta S., Segev, Dorry L., Bisen, Shivani, Jaffe, Ian S., Piegari, Benjamin, Kowalski, Haley, Kokkinaki, Maria, Monahan, Jeffrey, Sorrells, Lori, Burdorf, Lars, Boeke, Jef D., Pass, Harvey, Goparaju, Chandra, Keating, Brendan, Ayares, David, Lorber, Marc, Griesemer, Adam, Mehta, Sapna A., Smith, Deane E., and Montgomery, Robert A.

Published
2023
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16. Prospective Cohort Study to Compare Long-Term Lung Cancer-Specific and All-Cause Survival of Clinical Early Stage (T1a–b; ≤20 mm) NSCLC Treated by Stereotactic Body Radiation Therapy and Surgery

Author

Flores, Raja, Kaufman, Andrew, Lee, Dong-Seok, Nicastri, Daniel, Wolf, Andrea, Song, Kimberly, Rosenzweig, Kenneth, Gomez, Jorge, Samstein, Robert, Dutta, Pinaki, Beasley, Mary Beth, Zakowski, Maureen, Chung, Michael, Yankelevitz, David F., Henschke, Claudia I., Taioli, Emanuela, Schwartz, Rebecca, Chan, Huiwen, Zhu, Jeffrey, Kantor, Sydney, Woode, Sydney, Hakami, Ardeshir, Buyuk, Arzu, Friedman, Adie, Dreifuss, Ronald, Verzosa, Stacey, Yakubox, Mariya, Aloferdova, Karina, Stacey, Patricia, De Nobrega, Simone, Lentini, Lauren, Pass, Harvey, Cooper, Benjamin, Moreirea, Andre, Sorensen, Audrey, Kohman, Leslie, Dunton, Robert, Wallen, Jason, Curtiss, Christopher, Scalzetti, Ernest, Ellinwood, Linda, Tannous, Henry, Connery, Cliff P., Torres, Emilo, Cruzer, Dan, Gendron, Bruce, Alyea, Sonya, Krumholtz, Pramila, Watkins, Ammara, Servais, Elliot, Stock, Cameron, McKee, Andrea, Lopez, Edilin, Hsu, Howard, Hunter, Kaudia, Lemons, Jeffrey, Nixon, Asa, Osa, Etin-Osa, Lee, Paul, Hyman, Kevin, Jurado, Julisa, Zeltman, David, Glassman, Lawrence, Sharma, Rajiv, Singh, Vijay, Milhelis, Efstathia, Karan, Nandanee, Rzyman, Witold, Dziedzic, Robert, Henschke, Claudia, Yankelevitz, David, Jirapatnakul, Artit, Yip, Rowena, Zulueta, Javier J., Reeves, A.P., Altorki, Nasser K., Smith, James P., Libby, Daniel M., Pasmantier, Mark, Markowitz, Steven, Miller, Albert, Deval, Jose Cervera, Shaham, Dorith, Seijo, Luis, Bastarika, Gorka, Montuenga, Luis M., Spring, Silver, Aylesworth, Cheryl, Klingler, Karl, Schöb, Othmar, Andaz, Shahriyour, Straznicka, Michaela, Chin, Cynthia, Weiser, Todd, Sone, Shusuke, Hanaoka, Takaomi, Roberts, Heidi, Patsios, Demetris, Scopetuolo, M., Brown, Andrew, Wu, Ning, Cole, Enser, Yeh, Diana, Luedke, Dan, Liu, Xueguo, Herzog, Gary, Aye, Ralph, Rifkin, Matthew, Veronesi, Giula, Infante, Maurizio, Vafai, Davood, Kopel, Samuel, Taylor, Jana, Thurer, Richard, Villamizar, Nestor, Austin, John H.M., Pearson, Gregory D.N., Klippenstein, Donald, Litwin, Alan, Loud, Peter A., Kohman, Leslie J., Scalzetti, Ernest M., Khan, Arfa, Shah, Rakesh, Mayfield, William, Frumiento, Carmine, Smith, Michael V., Thorsen, M. Kristin, Hansen, Richard, Naidich, David, McGuinness, Georgeann, Widmann, Mark, Korst, Robert, Lowry, Joseph, Salvatore, Mary, Walsh, James, Bertsch, David, Scheinberg, Paul, Sheppard, Barry, Cecchi, Gary, Ginsberg, Michelle S., Welch, Laura, Raz, Dan J., Rotter, Arnold, Connery, Cliff, Matalon, Terence A.S., Cheung, Edson H., Glassberg, Robert, Olsen, David, Mullen, David, Odzer, Shari-Lynn, Wiernik, Peter H., Ray, Daniel, DeCunzo, Louis, Endress, Carmen, Vacca, Anthony, Kondapaneni, M., Lim, Melissa, Kalafer, Michael, Green, Jeremy, Yoder, Mark, Shah, Palmi, Camacho, Elmer, O’Brien, James, Willey, James C., Gordon, David, Kocha, Albert, Sun, Qi, Li, Pengfei, and Flores, Raja M.

Published
2024
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18. Pathomic Features Reveal Immune and Molecular Evolution From Lung Preneoplasia to Invasive Adenocarcinoma

Author

Chen, Pingjun, Rojas, Frank R., Hu, Xin, Serrano, Alejandra, Zhu, Bo, Chen, Hong, Hong, Lingzhi, Bandyoyadhyay, Rukhmini, Aminu, Muhammad, Kalhor, Neda, Lee, J. Jack, El Hussein, Siba, Khoury, Joseph D., Pass, Harvey I., Moreira, Andre L., Velcheti, Vamsidhar, Sterman, Daniel H., Fukuoka, Junya, Tabata, Kazuhiro, Su, Dan, Ying, Lisha, Gibbons, Don L., Heymach, John V., Wistuba, Ignacio I., Fujimoto, Junya, Solis Soto, Luisa M., Zhang, Jianjun, and Wu, Jia

Published
2023
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20. KEAP1 mutation in lung adenocarcinoma promotes immune evasion and immunotherapy resistance

Author

Zavitsanou, Anastasia-Maria, Pillai, Ray, Hao, Yuan, Wu, Warren L., Bartnicki, Eric, Karakousi, Triantafyllia, Rajalingam, Sahith, Herrera, Alberto, Karatza, Angeliki, Rashidfarrokhi, Ali, Solis, Sabrina, Ciampricotti, Metamia, Yeaton, Anna H., Ivanova, Ellie, Wohlhieter, Corrin A., Buus, Terkild B., Hayashi, Makiko, Karadal-Ferrena, Burcu, Pass, Harvey I., Poirier, John T., Rudin, Charles M., Wong, Kwok-Kin, Moreira, Andre L., Khanna, Kamal M., Tsirigos, Aristotelis, Papagiannakopoulos, Thales, and Koralov, Sergei B.

Published
2023
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21. Immune response after pig-to-human kidney xenotransplantation: a multimodal phenotyping study

Author

Loupy, Alexandre, Goutaudier, Valentin, Giarraputo, Alessia, Mezine, Fariza, Morgand, Erwan, Robin, Blaise, Khalil, Karen, Mehta, Sapna, Keating, Brendan, Dandro, Amy, Certain, Anaïs, Tharaux, Pierre-Louis, Narula, Navneet, Tissier, Renaud, Giraud, Sébastien, Hauet, Thierry, Pass, Harvey I, Sannier, Aurélie, Wu, Ming, Griesemer, Adam, Ayares, David, Tatapudi, Vasishta, Stern, Jeffrey, Lefaucheur, Carmen, Bruneval, Patrick, Mangiola, Massimo, and Montgomery, Robert A

Published
2023
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23. Tumour predisposition and cancer syndromes as models to study gene-environment interactions.

Author

Carbone, Michele, Arron, Sarah T, Beutler, Bruce, Bononi, Angela, Cavenee, Webster, Cleaver, James E, Croce, Carlo M, D'Andrea, Alan, Foulkes, William D, Gaudino, Giovanni, Groden, Joanna L, Henske, Elizabeth P, Hickson, Ian D, Hwang, Paul M, Kolodner, Richard D, Mak, Tak W, Malkin, David, Monnat, Raymond J, Novelli, Flavia, Pass, Harvey I, Petrini, John H, Schmidt, Laura S, and Yang, Haining

Subjects
Animals, Humans, Neoplasms, Genetic Predisposition to Disease, Germ-Line Mutation, Gene-Environment Interaction, Genetics, Cancer, Prevention, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, Aetiology, Medical and Health Sciences, Oncology & Carcinogenesis
Abstract

Cell division and organismal development are exquisitely orchestrated and regulated processes. The dysregulation of the molecular mechanisms underlying these processes may cause cancer, a consequence of cell-intrinsic and/or cell-extrinsic events. Cellular DNA can be damaged by spontaneous hydrolysis, reactive oxygen species, aberrant cellular metabolism or other perturbations that cause DNA damage. Moreover, several environmental factors may damage the DNA, alter cellular metabolism or affect the ability of cells to interact with their microenvironment. While some environmental factors are well established as carcinogens, there remains a large knowledge gap of others owing to the difficulty in identifying them because of the typically long interval between carcinogen exposure and cancer diagnosis. DNA damage increases in cells harbouring mutations that impair their ability to correctly repair the DNA. Tumour predisposition syndromes in which cancers arise at an accelerated rate and in different organs - the equivalent of a sensitized background - provide a unique opportunity to examine how gene-environment interactions influence cancer risk when the initiating genetic defect responsible for malignancy is known. Understanding the molecular processes that are altered by specific germline mutations, environmental exposures and related mechanisms that promote cancer will allow the design of novel and effective preventive and therapeutic strategies.

Published
2020

24. IASLC Lung Cancer Staging Project: The New Database to Inform Revisions in the Ninth Edition of the TNM Classification of Lung Cancer

Author

Asamura, Hisao, Rusch, Valerie, Rami-Porta, Ramón, Araujo, Luiz Henrique, Beer, David, Bertoglio, Pietro, Beyruti, Ricardo, Billè, Andrea, Boubia, Souheil, Brambilla, Elisabeth, Cangir, A.K., Carbone, David, Cilento, Vanessa, Connolly, Casey, Darling, Gail, Detterbeck, Frank, Dibaba, Daniel, D’Journo, Xavier Benoit, Donington, Jessica, Eberhardt, Wilfried, Edwards, John, Erasmus, Jeremy, Fang, Wentao, Fennell, Dean, Fong, Kwun, Galateau-Sallé, Françoise, Gautschi, Oliver, Gill, Ritu R., Giroux, Dorothy, Giuliani, Meredith, Goo, Jin Mo, Hasegawa, Seiki, Hirsch, Fred, Hoffman, Hans, Hofstetter, Wayne, Huang, James, Joubert, Philippe, Kernstine, Kemp, Kerr, Keith, Kim, Young Tae, Kim, Dong Kwan, Kindler, Hedy, Lievens, Yolande, Liu, Hui, Low, Donald E., Lyons, Gustavo, MacMahon, Heber, Mahar, Alyson, Marino, Mirella, Marom, Edith M., Matilla, José-María, van Meerbeeck, Jan, Montuenga, Luis M., Nicholson, Andrew, Nishimura, Katie, Nowak, Anna, Opitz, Isabelle, Okumura, Meinoshin, Osarogiagbon, Raymond U., Pass, Harvey, de Perrot, Marc, Prosch, Helmut, Rice, David, Rimner, Andreas, Rosenthal, Adam, Ruffini, Enrico, Sakai, Shuji, Van Schil, Paul, Singh, Navneet, Suárez, Francisco, Terra, Ricardo M., Travis, William D., Tsao, Ming S., Ugalde, Paula, Watanabe, Shun-ichi, Wistuba, Ignacio, Wynes, Murry, Yatabe, Yasushi, Nishimura, Katherine K., Giroux, Dorothy J., Chansky, Kari, and Hoering, Antje

Published
2023
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25. BAP1 forms a trimer with HMGB1 and HDAC1 that modulates gene × environment interaction with asbestos

Author

Novelli, Flavia, Bononi, Angela, Wang, Qian, Bai, Fang, Patergnani, Simone, Kricek, Franz, Haglund, Ellinor, Suarez, Joelle S., Tanji, Mika, Xu, Ronghui, Takanishi, Yasutaka, Minaai, Michael, Pastorino, Sandra, Morris, Paul, Sakamoto, Greg, Pass, Harvey I., Barbour, Haithem, Gaudino, Giovanni, Giorgi, Carlotta, Pinton, Paolo, Onuchic, Jose N., Yang, Haining, and Carbone, Michele

Published
2021

26. Mesothelioma: Scientific clues for prevention, diagnosis, and therapy.

Author

Carbone, Michele, Adusumilli, Prasad S, Alexander, H Richard, Baas, Paul, Bardelli, Fabrizio, Bononi, Angela, Bueno, Raphael, Felley-Bosco, Emanuela, Galateau-Salle, Francoise, Jablons, David, Mansfield, Aaron S, Minaai, Michael, de Perrot, Marc, Pesavento, Patricia, Rusch, Valerie, Severson, David T, Taioli, Emanuela, Tsao, Anne, Woodard, Gavitt, Yang, Haining, Zauderer, Marjorie G, and Pass, Harvey I

Subjects
Pleura, Humans, Mesothelioma, Pleural Neoplasms, Genetic Predisposition to Disease, Asbestos, Ubiquitin Thiolesterase, Tumor Suppressor Proteins, Diagnostic Errors, Prognosis, Combined Modality Therapy, Pneumonectomy, Incidence, Inhalation Exposure, Occupational Exposure, Germ-Line Mutation, International Cooperation, United States, Australia, Europe, Molecular Targeted Therapy, Carcinogenesis, Biomarkers, Tumor, Global Burden of Disease, Antineoplastic Agents, Immunological, BRCA1-associated protein 1, asbestos, cancer syndromes, chromothripsis, gene-environment interaction, immunotherapy, mesothelioma, Lung, Rare Diseases, Lung Cancer, Cancer, Prevention, Good Health and Well Being, Clinical Sciences, Public Health and Health Services, Oncology & Carcinogenesis
Abstract

Mesothelioma affects mostly older individuals who have been occupationally exposed to asbestos. The global mesothelioma incidence and mortality rates are unknown, because data are not available from developing countries that continue to use large amounts of asbestos. The incidence rate of mesothelioma has decreased in Australia, the United States, and Western Europe, where the use of asbestos was banned or strictly regulated in the 1970s and 1980s, demonstrating the value of these preventive measures. However, in these same countries, the overall number of deaths from mesothelioma has not decreased as the size of the population and the percentage of old people have increased. Moreover, hotspots of mesothelioma may occur when carcinogenic fibers that are present in the environment are disturbed as rural areas are being developed. Novel immunohistochemical and molecular markers have improved the accuracy of diagnosis; however, about 14% (high-resource countries) to 50% (developing countries) of mesothelioma diagnoses are incorrect, resulting in inadequate treatment and complicating epidemiological studies. The discovery that germline BRCA1-asssociated protein 1 (BAP1) mutations cause mesothelioma and other cancers (BAP1 cancer syndrome) elucidated some of the key pathogenic mechanisms, and treatments targeting these molecular mechanisms and/or modulating the immune response are being tested. The role of surgery in pleural mesothelioma is controversial as it is difficult to predict who will benefit from aggressive management, even when local therapies are added to existing or novel systemic treatments. Treatment outcomes are improving, however, for peritoneal mesothelioma. Multidisciplinary international collaboration will be necessary to improve prevention, early detection, and treatment.

Published
2019

27. Integrative Molecular Characterization of Malignant Pleural Mesothelioma

Author

Hmeljak, Julija, Sanchez-Vega, Francisco, Hoadley, Katherine A, Shih, Juliann, Stewart, Chip, Heiman, David, Tarpey, Patrick, Danilova, Ludmila, Drill, Esther, Gibb, Ewan A, Bowlby, Reanne, Kanchi, Rupa, Osmanbeyoglu, Hatice U, Sekido, Yoshitaka, Takeshita, Jumpei, Newton, Yulia, Graim, Kiley, Gupta, Manaswi, Gay, Carl M, Diao, Lixia, Gibbs, David L, Thorsson, Vesteinn, Iype, Lisa, Kantheti, Havish, Severson, David T, Ravegnini, Gloria, Desmeules, Patrice, Jungbluth, Achim A, Travis, William D, Dacic, Sanja, Chirieac, Lucian R, Galateau-Sallé, Françoise, Fujimoto, Junya, Husain, Aliya N, Silveira, Henrique C, Rusch, Valerie W, Rintoul, Robert C, Pass, Harvey, Kindler, Hedy, Zauderer, Marjorie G, Kwiatkowski, David J, Bueno, Raphael, Tsao, Anne S, Creaney, Jenette, Lichtenberg, Tara, Leraas, Kristen, Bowen, Jay, Felau, Ina, Zenklusen, Jean Claude, Akbani, Rehan, Cherniack, Andrew D, Byers, Lauren A, Noble, Michael S, Fletcher, Jonathan A, Robertson, A Gordon, Shen, Ronglai, Aburatani, Hiroyuki, Robinson, Bruce W, Campbell, Peter, Ladanyi, Marc, Ally, Adrian, Anur, Pavana, Armenia, Joshua, Auman, J Todd, Balasundaram, Miruna, Balu, Saianand, Baylin, Stephen B, Becich, Michael, Behrens, Carmen, Beroukhim, Rameen, Bielski, Craig, Bodenheimer, Tom, Bootwalla, Moiz S, Brooks, Denise, Byers, Lauren Averett, Cárcano, Flávio M, Carlsen, Rebecca, Carvalho, Andre L, Cheung, Dorothy, Chirieac, Lucian, Cho, Juok, Chuah, Eric, Chudamani, Sudha, Cibulskis, Carrie, Cope, Leslie, Crain, Daniel, Curley, Erin, Rienzo, Assunta De, DeFreitas, Timothy, Demchok, John A, and Dhalla, Noreen

Subjects
Rare Diseases, Lung Cancer, Biotechnology, Lung, Cancer, Human Genome, Genetics, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Aged, Biomarkers, Tumor, Female, Histone-Lysine N-Methyltransferase, Humans, Kaplan-Meier Estimate, Lung Neoplasms, Male, Mesothelioma, Middle Aged, Mutation, Pleural Neoplasms, Prognosis, Protein Methyltransferases, Tumor Suppressor Proteins, Ubiquitin Thiolesterase, TCGA Research Network, Oncology and Carcinogenesis
Abstract

Malignant pleural mesothelioma (MPM) is a highly lethal cancer of the lining of the chest cavity. To expand our understanding of MPM, we conducted a comprehensive integrated genomic study, including the most detailed analysis of BAP1 alterations to date. We identified histology-independent molecular prognostic subsets, and defined a novel genomic subtype with TP53 and SETDB1 mutations and extensive loss of heterozygosity. We also report strong expression of the immune-checkpoint gene VISTA in epithelioid MPM, strikingly higher than in other solid cancers, with implications for the immune response to MPM and for its immunotherapy. Our findings highlight new avenues for further investigation of MPM biology and novel therapeutic options. SIGNIFICANCE: Through a comprehensive integrated genomic study of 74 MPMs, we provide a deeper understanding of histology-independent determinants of aggressive behavior, define a novel genomic subtype with TP53 and SETDB1 mutations and extensive loss of heterozygosity, and discovered strong expression of the immune-checkpoint gene VISTA in epithelioid MPM.See related commentary by Aggarwal and Albelda, p. 1508.This article is highlighted in the In This Issue feature, p. 1494.

Published
2018

28. Summarizing performance for genome scale measurement of miRNA: reference samples and metrics

Author

Pine, P Scott, Lund, Steven P, Parsons, Jerod R, Vang, Lindsay K, Mahabal, Ashish A, Cinquini, Luca, Kelly, Sean C, Kincaid, Heather, Crichton, Daniel J, Spira, Avrum, Liu, Gang, Gower, Adam C, Pass, Harvey I, Goparaju, Chandra, Dubinett, Steven M, Krysan, Kostyantyn, Stass, Sanford A, Kukuruga, Debra, Van Keuren-Jensen, Kendall, Courtright-Lim, Amanda, Thompson, Karol L, Rosenzweig, Barry A, Sorbara, Lynn, Srivastava, Sudhir, and Salit, Marc L

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Biotechnology, Bioengineering, Human Genome, Genetics, 4.2 Evaluation of markers and technologies, Brain, Female, Gene Expression Profiling, Genome, Human, High-Throughput Nucleotide Sequencing, Humans, Liver, MicroRNAs, Placenta, Pregnancy, Reference Standards, microRNA, miRNA, Reference samples, Process controls, Dashboard, Information and Computing Sciences, Medical and Health Sciences, Bioinformatics, Biological sciences, Biomedical and clinical sciences
Abstract

BackgroundThe potential utility of microRNA as biomarkers for early detection of cancer and other diseases is being investigated with genome-scale profiling of differentially expressed microRNA. Processes for measurement assurance are critical components of genome-scale measurements. Here, we evaluated the utility of a set of total RNA samples, designed with between-sample differences in the relative abundance of miRNAs, as process controls.ResultsThree pure total human RNA samples (brain, liver, and placenta) and two different mixtures of these components were evaluated as measurement assurance control samples on multiple measurement systems at multiple sites and over multiple rounds. In silico modeling of mixtures provided benchmark values for comparison with physical mixtures. Biomarker development laboratories using next-generation sequencing (NGS) or genome-scale hybridization assays participated in the study and returned data from the samples using their routine workflows. Multiplexed and single assay reverse-transcription PCR (RT-PCR) was used to confirm in silico predicted sample differences. Data visualizations and summary metrics for genome-scale miRNA profiling assessment were developed using this dataset, and a range of performance was observed. These metrics have been incorporated into an online data analysis pipeline and provide a convenient dashboard view of results from experiments following the described design. The website also serves as a repository for the accumulation of performance values providing new participants in the project an opportunity to learn what may be achievable with similar measurement processes.ConclusionsThe set of reference samples used in this study provides benchmark values suitable for assessing genome-scale miRNA profiling processes. Incorporation of these metrics into an online resource allows laboratories to periodically evaluate their performance and assess any changes introduced into their measurement process.

Published
2018

29. New or enlarging hiatal hernias after thoracic surgery for early lung cancer

Author

Flores, Raja, Kaufman, Andrew, Lee, Dong-Seok, Nicastri, Daniel, Wolf, Andrea, Song, Kimberly, Rosenzweig, Kenneth, Gomez, Jorge, Beasley, Mary Beth, Zakowski, Maureen, Chung, Michael, Yankelevitz, David F., Henschke, Claudia I., Taioli, Emanuela, Schwartz, Rebecca, Chan, Huiwen, Zhu, Jeffrey, Kantor, Sydney, Adler, Shana, Raad, Wissam, Buyuk, Zrzu, Friedman, Adie, Dreifuss, Ronald, Verzosa, Stacey, Yakubox, Mariya, Aloferdova, Karina, Stacey, Patricia, De Nobrega, Simone, Hakami, Ardeshir, Pass, Harvey, Crawford, Berne, Donnington, Jessica, Cooper, Benjamin, Moreirea, Andre, Sorensen, Audrey, Kohman, Leslie, Dunton, Robert, Wallen, Jason, Curtiss, Christopher, Scalzetti, Ernest, Ellinwood, Linda, Connery, Clifford P., Torres, Emilo, Cruzer, Dan, Gendron, Bruce, Alyea, Sonya, Lackaye, Daniel, Studer, Lauren, Henschke, Claudia, Yankelevitz, David, Becker, Betsy, Jirapatnakul, Artit, Yip, Rowena, You, Nan, Libby, Daniel M., Smith, James P., Pasmantier, Mark, Reeves, A.P., Markowitz, Steven, Miller, Albert, Deval, Jose Cervera, Roberts, Heidi, Patsios, Demetris, Sone, Shusuke, Hanaoka, Takaomi, Zulueta, Javier, de-Torres, Juan P., Lozano, Maria D., Aye, Ralph, Manning, Kristin, Care, Christiana, Bauer, Thomas, Canitano, Stefano, Giunta, Salvatore, Cole, Enser, Klingler, Karl, Austin, John H.M., Pearson, Gregory D.N., Shaham, Dorith, Aylesworth, Cheryl, Meyers, Patrick, Andaz, Shahriyour, Vafai, Davood, Naidich, David, McGuinness, Georgeann, Sheppard, Barry, Rifkin, Matthew, Thorsen, M. Kristin, Hansen, Richard, Kopel, Samuel, Mayfield, William, Luedke, Dan, Klippenstein, Donald, Litwin, Alan, Loud, Peter A., Kohman, Leslie J., Scalzetti, Ernest M., Thurer, Richard, Villamizar, Nestor, Khan, Arfa, Shah, Rakesh, Liu, Xueguo, Herzog, Gary, Yeh, Diana, Wu, Ning, Lowry, Joseph, Salvatore, Mary, Frumiento, Carmine, Mendelson, David S., Smith, Michael V., Korst, Robert, Taylor, Jana, Ginsberg, Michelle S., Straznicka, Michaela, Widmann, Mark, Cecchi, Gary, Matalon, Terence A.S., Scheinberg, Paul, Odzer, Shari-Lynn, Olsen, David, Grannis, Fred, Rotter, Arnold, Ray, Daniel, Mullen, David, Wiernik, Peter H., Cheung, Edson H., Lim, Melissa, DeCunzo, Louis, Glassberg, Robert, Endress, Carmen, Yoder, Mark, Shah, Palmi, Welch, Laura, Kalafer, Michael, Green, Jeremy, Walsh, James, Bertsch, David, Camacho, Elmer, Chin, Cynthia, O'Brien, James, Willey, James C., Song, Kimberly J., Cai, Qiang, Zhu, Yeqing, Singh, Ayushi, and Lewis, Erik E.

Published
2022
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32. Heterozygous germline BLM mutations increase susceptibility to asbestos and mesothelioma

Author

Bononi, Angela, Goto, Keisuke, Ak, Guntulu, Yoshikawa, Yoshie, Emi, Mitsuru, Pastorino, Sandra, Carparelli, Lorenzo, Ferro, Angelica, Nasu, Masaki, Kim, Jin-Hee, Suarez, Joelle S., Xu, Ronghui, Tanji, Mika, Takinishi, Yasutaka, Minaai, Michael, Novelli, Flavia, Pagano, Ian, Gaudino, Giovanni, Pass, Harvey I., Groden, Joanna, Grzymski, Joseph J., Metintas, Muzaffer, Akarsu, Muhittin, Morrow, Betsy, Hassan, Raffit, Yang, Haining, and Carbone, Michele

Published
2020

33. The evolution of lung adenocarcinoma precursors is associated with chromosomal instability and transition from innate to adaptive immune response/evasion

Author

Zhang, Jianjun, primary, Hu, Xin, additional, Zhu, Bo, additional, Vokes, Natalie, additional, Fukuoka, Junya, additional, Alvarez, Frank Rojas, additional, Heeke, Simon, additional, Moreira, Andre, additional, Solis, Luisa, additional, Haymaker, Cara, additional, Velcheti, Vamsidhar, additional, Sterman, Daniel, additional, Pass, Harvey, additional, Cheng, Chao, additional, Lee, Jack, additional, Zhang, Jianhua, additional, Wei, Zhubo, additional, Wu, Jia, additional, Li, Xiuning, additional, Ostrin, Edwin, additional, Toumazis, Iakovos, additional, Gibbons, Don, additional, Su, Dan, additional, Antonoff, Mara, additional, Gerber, David, additional, Li, Chenyang, additional, Kadara, Humam, additional, Wang, Linghua, additional, Davis, Mark, additional, Heymach, John, additional, Hanash, Samir, additional, Wistuba, Ignacio, additional, Dubinett, Steven, additional, Alexandrov, Ludmil, additional, Lippman, Scott, additional, Spira, Avrum, additional, Futreal, Andrew, additional, and Reuben, Alexandre, additional

Published
2024
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34. Asbestos induces mesothelial cell transformation via HMGB1-driven autophagy

Author

Xue, Jiaming, Patergnani, Simone, Giorgi, Carlotta, Suarez, Joelle, Goto, Keisuke, Bononi, Angela, Tanji, Mika, Novelli, Flavia, Pastorino, Sandra, Xu, Ronghui, Caroccia, Natascia, Dogan, A. Umran, Pass, Harvey I., Tognon, Mauro, Pinton, Paolo, Gaudino, Giovanni, Mak, Tak W., Carbone, Michele, and Yang, Haining

Published
2020

35. The importance of low-dose CT screening to identify emphysema in asymptomatic participants with and without a prior diagnosis of COPD

Author

Henschke, Claudia I., Yankelevitz, David F., Yip, Rowena, Jirapatnakul, Artit, Flores, Raja, Wolf, Andrea, Libby, Daniel M., Smith, James P., Pasmantier, Mark, Reeves, A.P., Markowitz, Steven, Miller, Albert, Deval, Jose Cervera, Roberts, Heidi, Patsios, Demetris, Sone, Shusuke, Hanaoka, Takaomi, Zulueta, Javier, de-Torres, Juan P., Lozano, Maria D., Aye, Ralph, Manning, Kristin, Bauer, Thomas, Canitano, Stefano, Giunta, Salvatore, Cole, Enser, Klingler, Karl, Austin, John H.M., Pearson, Gregory D.N., Shaham, Dorith, Aylesworth, Cheryl, Meyers, Patrick, Andaz, Shahriyour, Vafai, Davood, Naidich, David, McGuinness, Georgeann, Sheppard, Barry, Rifkin, Matthew, Thorsen, M. Kristin, Hansen, Richard, Kopel, Samuel, Mayfield, William, Luedke, Dan, Klippenstein, Donald, Litwin, Alan, Loud, Peter A., Kohman, Leslie J., Scalzetti, Ernest M., Thurer, Richard, Villamizar, Nestor, Khan, Arfa, Shah, Rakesh, Liu, Xueguo, Herzog, Gary, Yeh, Diana, Wu, Ning, Lowry, Joseph, Salvatore, Mary, Frumiento, Carmine, Mendelson, David S., Smith, Michael V., Korst, Robert, Taylor, Jana, Ginsberg, Michelle S., Straznicka, Michaela, Widmann, Mark, Cecchi, Gary, Matalon, Terence A.S., Scheinberg, Paul, Odzer, Shari-Lynn, Olsen, David, Grannis, Fred, Rotter, Arnold, Ray, Daniel, Mullen, David, Wiernik, Peter H., Cheung, Edson H., Lim, Melissa, DeCunzo, Louis, Glassberg, Robert, Pass, Harvey, Endress, Carmen, Yoder, Mark, Shah, Palmi, Welch, Laura, Kalafer, Michael, Green, Jeremy, Walsh, James, Bertsch, David, Camacho, Elmer, Chin, Cynthia, O'Brien, James, Willey, James C., Steiger, David, and Siddiqi, M. Faisal

Published
2021
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37. 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

38. Proteomic profiling of lung adenocarcinoma indicates heightened DNA repair, antioxidant mechanisms and identifies LASP1 as a potential negative predictor of survival

Author

Fahrmann, Johannes F, Grapov, Dmitry, Phinney, Brett S, Stroble, Carol, DeFelice, Brian C, Rom, William, Gandara, David R, Zhang, Yanhong, Fiehn, Oliver, Pass, Harvey, and Miyamoto, Suzanne

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Lung Cancer, Prevention, Lung, Cancer, Lung adenocarcinoma, Proteomics, Biomarker, Biochemistry & Molecular Biology, Biochemistry and cell biology, Clinical sciences, Medical biochemistry and metabolomics
Abstract

BackgroundLung cancer is the leading cause of cancer mortality in the United States. Non-small cell lung cancer accounts for 85% of all lung cancers for which adenocarcinoma is the most common histological type. Management of lung cancer is hindered by high false-positive rates due to difficulty resolving between benign and malignant tumors. Better molecular analysis comparing malignant and non-malignant tissues will provide important evidence of the underlying biology contributing to tumorigenesis.MethodsWe utilized a proteomics approach to analyze 38 malignant and non-malignant paired tissue samples obtained from current or former smokers with early stage (Stage IA/IB) lung adenocarcinoma. Statistical mixed effects modeling and orthogonal partial least squares discriminant analysis were used to identify key cancer-associated perturbations in the adenocarcinoma proteome. Identified proteins were subsequently assessed against clinicopathological variables.ResultsTop cancer-associated protein alterations were characterized by: (1) elevations in APEX1, HYOU1 and PDIA4, indicative of increased DNA repair machinery and heightened anti-oxidant defense mechanisms; (2) increased LRPPRC, STOML2, COPG1 and EPRS, suggesting altered tumor metabolism and inflammation; (3) reductions in SPTB, SPTA1 and ANK1 implying dysregulation of membrane integrity; and (4) decreased SLCA41 suggesting altered pH regulation. Increased protein levels of HYOU1, EPRS and LASP1 in NSCLC adenocarcinoma was independently validated by tissue microarray immunohistochemistry. Immunohistochemistry for HYOU1 and EPRS indicated AUCs of 0.952 and 0.841, respectively, for classifying tissue as malignant. Increased LASP1 correlated with poor overall survival (HR 3.66 per unit increase; CI 1.37-9.78; p = 0.01).ConclusionThese results reveal distinct proteomic changes associated with early stage lung adenocarcinoma that may be useful prognostic indicators and therapeutic targets.

Published
2016

42. A Grading System for Invasive Pulmonary Adenocarcinoma: A Proposal From the International Association for the Study of Lung Cancer Pathology Committee

Author

Moreira, Andre L., Ocampo, Paolo S.S., Xia, Yuhe, Zhong, Hua, Russell, Prudence A., Minami, Yuko, Cooper, Wendy A., Yoshida, Akihiko, Bubendorf, Lukas, Papotti, Mauro, Pelosi, Giuseppe, Lopez-Rios, Fernando, Kunitoki, Keiko, Ferrari-Light, Dana, Sholl, Lynette M., Beasley, Mary Beth, Borczuk, Alain, Botling, Johan, Brambilla, Elisabeth, Chen, Gang, Chou, Teh-Ying, Chung, Jin-Haeng, Dacic, Sanja, Jain, Deepali, Hirsch, Fred R., Hwang, David, Lantuejoul, Sylvie, Lin, Dongmei, Longshore, John W., Motoi, Noriko, Noguchi, Masayuki, Poleri, Claudia, Rekhtman, Natasha, Tsao, Ming-Sound, Thunnissen, Erik, Travis, William D., Yatabe, Yasushi, Roden, Anja C., Daigneault, Jillian B., Wistuba, Ignacio I., Kerr, Keith M., Pass, Harvey, Nicholson, Andrew G., and Mino-Kenudson, Mari

Published
2020
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43. The IASLC Lung Cancer Staging Project: Analysis of Resection Margin Status and Proposals for Residual Tumor Descriptors for Non–Small Cell Lung Cancer

Author

Asamura, Hisao, Rusch, Valerie, Rami-Porta, Ramón, Araujo, Luiz Henrique, Beer, David, Bertoglio, Pietro, Beyruti, Ricardo, Bille, Andrea, Bolejack, Vanessa, Boubia, Souheil, Brambilla, Elisabeth, Brierley, James D., Cangir, A.K., Carbone, David, Chansky, Kari, Crowley, John, Darling, Gail, Detterbeck, Frank, D’Journo, Xavier Benoit, Donnington, Jessica, Eberhardt, Wilfried, Edwards, John, Erasmus, Jeremy, Falkson, Conrad, Fang, Wentao, Fennell, Dean, Fong, Kwun, Galateau-Salle, Françoise, Gautschi, Oliver, Gill, Ritu, Giroux, Dorothy, Giuliani, Meredith, Goo, Jin Mo, Hasegawa, Seiki, Hirsch, Fred, Hoffman, Hans, Hofstetter, Wayne, Huang, James, Joubert, Philippe, Kernstine, Kemp, Kerr, Keith, Kim, Young Tae, Kim, Hong Kwan, Kindler, Hedy, Lievens, Yolande, Liu, Hui, Low, Donald E., Lyons, Gustavo, MacMahon, Heber, Marino, Mirella, Marom, Edith, Matilla, José-María, van Meerbeeck, Jan, Montuenga, Luis M., Nicholson, Andrew, Nishimura, Katie, Nowak, Anna, Opitz, Isabelle, Okumura, Meinoshin, Osarogiagbon, Raymond U., Pass, Harvey, de Perrot, Marc, Prosch, Helmut, Rice, David, Rimner, Andreas, Ruffini, Enrico, Sakai, Shuji, Van Schil, Paul, Singh, Navneet, Stoll-D’Astice, Amy, Su´rez, Francisco, Terra, Ricardo M., Travis, William D., Tsao, Ming S., Ugalde, Paula, Waller, David, Watanabe, Shun-ichi, Wiens, Jacinta, Wistuba, Ignacio, Yatabe, Yasushi, Jiang, Liyan, Kubota, Kaoru, Turna, Akif, Weksler, Benny, Tzukazan, Maria Teresa, Tammemägi, Martin, Powell, Charles, Naidich, David, Liu, Hongxu, Armato, Samuel, Brunelli, Alex, Cardillo, Giuseppe, David, Elizabeth, Fournier, Brigitte, Krasnik, Mark, Kubota, Kauro, Labbe, Catherine, Lim, Eric, Putora, Paul Martin, Rocco, Gaetano, Filosso, Pier Luigi, Kondo, Kazuya, Kim, Dong Kwan, Giaccone, Giuseppe, Lucchi, Marco, Infante, Maurizio, Rice, Thomas, Ferguson, Mark, Adsusmilli, Prasad, Travis, William, Suárez, Francisco, Kubota, Kaura, Shun-ichi, Watanabe, Hisao Asamura, Nicholson, Andrew G., Ramón, Rami-Porta, Edith Marom, Tsao, Ming, Shun-ichi, Watanabe, Ming Tsao, Guiliani, Meredith, Brierley, James, Terra, Ricardo, Osarogiagbon, Ray, Montuenga, Luis, Wang, Hongwei, Nakajima, Jun, Galateau, Françoise, Ostrowski, Marcin, Goo, Jim Mo, Travis, Bill, Matilla, Jose Maria, St. Pierre, Carolle, Tzukazan, Ma Teresa, Girard, Nicholas, Rimmer, Andreas, Galateau, Francoise, Adusumilli, Prasad, D’Journo, Xavier, Low, Donald, Rosenthal, Adam, Edwards, John G., Donington, Jessica, Galateau-Sallé, Françoise, Hoffmann, Hans, Marom, Edith M., Tsao, Ming-Sound, Giroux, Dorothy J., Shemanski, Lynn, and Krasnik, Marc

Published
2020
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44. EURACAN/IASLC Proposals for Updating the Histologic Classification of Pleural Mesothelioma: Towards a More Multidisciplinary Approach

Author

Nicholson, Andrew G., Sauter, Jennifer L., Nowak, Anna K., Kindler, Hedy L., Gill, Ritu R., Remy-Jardin, Martine, Armato, Samuel G., III, Fernandez-Cuesta, Lynnette, Bueno, Raphael, Alcala, Nicolas, Foll, Matthieu, Pass, Harvey, Attanoos, Richard, Baas, Paul, Beasley, Mary Beth, Brcic, Luka, Butnor, Kelly J., Chirieac, Lucian R., Churg, Andrew, Courtiol, Pierre, Dacic, Sanja, De Perrot, Marc, Frauenfelder, Thomas, Gibbs, Allen, Hirsch, Fred R., Hiroshima, Kenzo, Husain, Aliya, Klebe, Sonja, Lantuejoul, Sylvie, Moreira, Andre, Opitz, Isabelle, Perol, Maurice, Roden, Anja, Roggli, Victor, Scherpereel, Arnaud, Tirode, Frank, Tazelaar, Henry, Travis, William D., Tsao, Ming-Sound, van Schil, Paul, Vignaud, Jean Michel, Weynand, Birgit, Lang-Lazdunski, Loic, Cree, Ian, Rusch, Valerie W., Girard, Nicolas, and Galateau-Salle, Francoise

Published
2020
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45. The International Association for the Study of Lung Cancer Consensus Statement on Optimizing Management of EGFR Mutation-Positive Non-Small Cell Lung Cancer: Status in 2016.

Author

Tan, Daniel SW, Yom, Sue S, Tsao, Ming S, Pass, Harvey I, Kelly, Karen, Peled, Nir, Yung, Rex C, Wistuba, Ignacio I, Yatabe, Yasushi, Unger, Michael, Mack, Philip C, Wynes, Murry W, Mitsudomi, Tetsuya, Weder, Walter, Yankelevitz, David, Herbst, Roy S, Gandara, David R, Carbone, David P, Bunn, Paul A, Mok, Tony SK, and Hirsch, Fred R

Subjects
Humans, Carcinoma, Non-Small-Cell Lung, Brain Neoplasms, Lung Neoplasms, Protein Kinase Inhibitors, Consensus, Drug Resistance, Neoplasm, Mutation, ErbB Receptors, Brain metastases, EGFR mutation, Non–small cell lung cancer, Resistance, Therapy, Tyrosine kinase inhibitor, Non-small cell lung cancer, Carcinoma, Non-Small-Cell Lung, Drug Resistance, Neoplasm, Receptor, Epidermal Growth Factor, Lung Cancer, Lung, Cancer, Clinical Research, Oncology & Carcinogenesis, Clinical Sciences, Cardiorespiratory Medicine and Haematology, Oncology and Carcinogenesis
Abstract

Mutations in the epidermal growth factor receptor gene (EGFR) represent one of the most frequent "actionable" alterations in non-small cell lung cancer (NSCLC). Typified by high response rates to targeted therapies, EGFR tyrosine kinase inhibitors (TKIs) are now established first-line treatment options and have transformed the treatment paradigm for NSCLC. With the recent breakthrough designation and approval of the third-generation EGFR TKI osimertinib, available systemic and local treatment options have expanded, requiring new clinical algorithms that take into account individual patient molecular and clinical profiles. In this International Association for the Study of Lung Cancer commissioned consensus statement, key pathologic, diagnostic, and therapeutic considerations, such as optimal choice of EGFR TKI and management of brain metastasis, are discussed. In addition, recommendations are made for clinical guidelines and research priorities, such as the role of repeat biopsies and use of circulating free DNA for molecular studies. With the rapid pace of progress in treating EGFR-mutant NSCLC, this statement provides a state-of-the-art review of the contemporary issues in managing this unique subgroup of patients.

Published
2016

46. Dysregulation of a family of short noncoding RNAs, tsRNAs, in human cancer

Author

Pekarsky, Yuri, Balatti, Veronica, Palamarchuk, Alexey, Rizzotto, Lara, Veneziano, Dario, Nigita, Giovanni, Rassenti, Laura Z, Pass, Harvey I, Kipps, Thomas J, Liu, Chang-Gong, and Croce, Carlo M

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biotechnology, Genetics, Lung Cancer, Lymphoma, Lung, Human Genome, Rare Diseases, Cancer, Hematology, 2.1 Biological and endogenous factors, Aetiology, Gene Expression Regulation, Neoplastic, Genetic Markers, Genetic Predisposition to Disease, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Lung Neoplasms, Multigene Family, RNA, Neoplasm, RNA, Small Untranslated, RNA, Transfer, tsRNAs, ts-4521, ts-3676
Abstract

Chronic lymphocytic leukemia (CLL) is the most common human leukemia, and transgenic mouse studies indicate that activation of the T-cell leukemia/lymphoma 1 (TCL1) oncogene is a contributing event in the pathogenesis of the aggressive form of this disease. While studying the regulation of TCL1 expression, we identified the microRNA cluster miR-4521/3676 and discovered that these two microRNAs are associated with tRNA sequences and that this region can produce two small RNAs, members of a recently identified class of small noncoding RNAs, tRNA-derived small RNAs (tsRNAs). We further proved that miR-3676 and miR-4521 are tsRNAs using Northern blot analysis. We found that, like ts-3676, ts-4521 is down-regulated and mutated in CLL. Analysis of lung cancer samples revealed that both ts-3676 and ts-4521 are down-regulated and mutated in patient tumor samples. Because tsRNAs are similar in nature to piRNAs [P-element-induced wimpy testis (Piwi)-interacting small RNAs], we investigated whether ts-3676 and ts-4521 can interact with Piwi proteins and found these two tsRNAs in complexes containing Piwi-like protein 2 (PIWIL2). To determine whether other tsRNAs are involved in cancer, we generated a custom microarray chip containing 120 tsRNAs 16 bp or more in size. Microarray hybridization experiments revealed tsRNA signatures in CLL and lung cancer, indicating that, like microRNAs, tsRNAs may have an oncogenic and/or tumor-suppressor function in hematopoietic malignancies and solid tumors. Thus, our results show that tsRNAs are dysregulated in human cancer.

Published
2016

47. 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

48. Prospective Cohort Study to Compare Long-Term Lung Cancer-Specific and All-Cause Survival of Clinical Early Stage (T1a–b; ≤20 mm) NSCLC Treated by Stereotactic Body Radiation Therapy and Surgery

Author

Henschke, Claudia I., Yip, Rowena, Sun, Qi, Li, Pengfei, Kaufman, Andrew, Samstein, Robert, Connery, Cliff, Kohman, Leslie, Lee, Paul, Tannous, Henry, Yankelevitz, David F., Taioli, Emanuela, Rosenzweig, Kenneth, Flores, Raja M., Flores, Raja, Kaufman, Andrew, Lee, Dong-Seok, Nicastri, Daniel, Wolf, Andrea, Song, Kimberly, Rosenzweig, Kenneth, Gomez, Jorge, Samstein, Robert, Dutta, Pinaki, Beasley, Mary Beth, Zakowski, Maureen, Chung, Michael, Yankelevitz, David F., Henschke, Claudia I., Taioli, Emanuela, Schwartz, Rebecca, Chan, Huiwen, Zhu, Jeffrey, Kantor, Sydney, Woode, Sydney, Nicastri, Daniel, Hakami, Ardeshir, Buyuk, Arzu, Friedman, Adie, Dreifuss, Ronald, Verzosa, Stacey, Yakubox, Mariya, Aloferdova, Karina, Stacey, Patricia, De Nobrega, Simone, Zhu, Jeffrey, Kantor, Sydney, Woode, Sydney, Hakami, Ardeshir, Zhu, Jeffrey, Kantor, Sydney, Woode, Sydney, Lentini, Lauren, Pass, Harvey, Cooper, Benjamin, Moreirea, Andre, Sorensen, Audrey, Kohman, Leslie, Dunton, Robert, Wallen, Jason, Curtiss, Christopher, Scalzetti, Ernest, Ellinwood, Linda, Tannous, Henry, Connery, Cliff P., Torres, Emilo, Cruzer, Dan, Gendron, Bruce, Alyea, Sonya, Krumholtz, Pramila, Watkins, Ammara, Servais, Elliot, Stock, Cameron, McKee, Andrea, Lopez, Edilin, Hsu, Howard, Hunter, Kaudia, Lemons, Jeffrey, Nixon, Asa, Osa, Etin-Osa, Lee, Paul, Hyman, Kevin, Jurado, Julisa, Zeltman, David, Glassman, Lawrence, Sharma, Rajiv, Singh, Vijay, Milhelis, Efstathia, Karan, Nandanee, Rzyman, Witold, Dziedzic, Robert, Flores, Raja, Henschke, Claudia, Taioli, Emanuela, Yankelevitz, David, Schwartz, Rebecca, Jirapatnakul, Artit, Yip, Rowena, Chan, Huiwen, Henschke, Claudia I., Yankelevitz, David F., Yip, Rowena, Jirapatnakul, Artit, Flores, Raja, Kaufman, Andrew, Wolf, Andrea, Nicastri, Daniel, Zulueta, Javier J., Taioli, Emanuela, Reeves, A.P., Altorki, Nasser K., Smith, James P., Libby, Daniel M., Pasmantier, Mark, Markowitz, Steven, Miller, Albert, Deval, Jose Cervera, Shaham, Dorith, Seijo, Luis, Bastarika, Gorka, Montuenga, Luis M., Spring, Silver, Aylesworth, Cheryl, Klingler, Karl, Schöb, Othmar, Andaz, Shahriyour, Straznicka, Michaela, Chin, Cynthia, Weiser, Todd, Sone, Shusuke, Hanaoka, Takaomi, Roberts, Heidi, Patsios, Demetris, Scopetuolo, M., Brown, Andrew, Wu, Ning, Cole, Enser, Yeh, Diana, Luedke, Dan, Liu, Xueguo, Herzog, Gary, Aye, Ralph, Rifkin, Matthew, Veronesi, Giula, Infante, Maurizio, Vafai, Davood, Kopel, Samuel, Taylor, Jana, Thurer, Richard, Villamizar, Nestor, Austin, John H.M., Pearson, Gregory D.N., Klippenstein, Donald, Litwin, Alan, Loud, Peter A., Kohman, Leslie J., Scalzetti, Ernest M., Khan, Arfa, Shah, Rakesh, Mayfield, William, Frumiento, Carmine, Smith, Michael V., Thorsen, M. Kristin, Hansen, Richard, Naidich, David, McGuinness, Georgeann, Widmann, Mark, Korst, Robert, Lowry, Joseph, Salvatore, Mary, Walsh, James, Bertsch, David, Scheinberg, Paul, Sheppard, Barry, Cecchi, Gary, Ginsberg, Michelle S., Welch, Laura, Raz, Dan J., Rotter, Arnold, Connery, Cliff, Matalon, Terence A.S., Cheung, Edson H., Glassberg, Robert, Olsen, David, Mullen, David, Odzer, Shari-Lynn, Wiernik, Peter H., Ray, Daniel, DeCunzo, Louis, Pass, Harvey, Endress, Carmen, Vacca, Anthony, Kondapaneni, M., Lim, Melissa, Kalafer, Michael, Green, Jeremy, Yoder, Mark, Shah, Palmi, Camacho, Elmer, O’Brien, James, Willey, James C., Gordon, David, and Kocha, Albert

Abstract

We aimed to compare outcomes of patients with first primary clinical T1a-bN0M0 NSCLC treated with surgery or stereotactic body radiation therapy (SBRT).

Published
2024
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49. Evolution of DNA methylome from precancerous lesions to invasive lung adenocarcinomas

Author

Hu, Xin, Estecio, Marcos R., Chen, Runzhe, Reuben, Alexandre, Wang, Linghua, Fujimoto, Junya, Carrot-Zhang, Jian, McGranahan, Nicholas, Ying, Lisha, Fukuoka, Junya, Chow, Chi-Wan, Pham, Hoa H. N., Godoy, Myrna C. B., Carter, Brett W., Behrens, Carmen, Zhang, Jianhua, Antonoff, Mara B., Sepesi, Boris, Lu, Yue, Pass, Harvey I., Kadara, Humam, Scheet, Paul, Vaporciyan, Ara A., Heymach, John V., Wistuba, Ignacio I., Lee, J. Jack, Futreal, P. Andrew, Su, Dan, Issa, Jean-Pierre J., and Zhang, Jianjun

Published
2021
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50. Author Correction: Multi-region exome sequencing reveals genomic evolution from preneoplasia to lung adenocarcinoma

Author

Hu, Xin, Fujimoto, Junya, Ying, Lisha, Fukuoka, Junya, Ashizawa, Kazuto, Sun, Wenyong, Reuben, Alexandre, Chow, Chi-Wan, McGranahan, Nicholas, Chen, Runzhe, Hu, Jinlin, Godoy, Myrna C., Tabata, Kazuhiro, Kuroda, Kishio, Shi, Lei, Li, Jun, Behrens, Carmen, Parra, Edwin Roger, Little, Latasha D., Gumbs, Curtis, Mao, Xizeng, Song, Xingzhi, Tippen, Samantha, Thornton, Rebecca L., Kadara, Humam, Scheet, Paul, Roarty, Emily, Ostrin, Edwin Justin, Wang, Xu, Carter, Brett W., Antonoff, Mara B., Zhang, Jianhua, Vaporciyan, Ara A., Pass, Harvey, Swisher, Stephen G., Heymach, John V., Lee, J. Jack, Wistuba, Ignacio I., Hong, Waun Ki, Futreal, P. Andrew, Su, Dan, and Zhang, Jianjun

Published
2021
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