Search

Your search keyword '"Wolpin, Brian"' showing total 1,479 results
Start Over Author "Wolpin, Brian" Publication Year Range Last 50 years
1,479 results on '"Wolpin, Brian"'

1. Cancer tissue of origin constrains the growth and metabolism of metastases

Author

Sivanand, Sharanya, Gultekin, Yetis, Winter, Peter S., Vermeulen, Sidney Y., Tchourine, Konstantine M., Abbott, Keene L., Danai, Laura V., Gourgue, Florian, Do, Brian T., Crowder, Kayla, Kunchok, Tenzin, Lau, Allison N., Darnell, Alicia M., Jefferson, Alexandria, Morita, Satoru, Duda, Dan G., Aguirre, Andrew J., Wolpin, Brian M., Henning, Nicole, Spanoudaki, Virginia, Maiorino, Laura, Irvine, Darrell J., Yilmaz, Omer H., Lewis, Caroline A., Vitkup, Dennis, Shalek, Alex K., and Vander Heiden, Matthew G.

Published
2024
Full Text
View/download PDF

2. Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer

Author

Wasko, Urszula N., Jiang, Jingjing, Dalton, Tanner C., Curiel-Garcia, Alvaro, Edwards, A. Cole, Wang, Yingyun, Lee, Bianca, Orlen, Margo, Tian, Sha, Stalnecker, Clint A., Drizyte-Miller, Kristina, Menard, Marie, Dilly, Julien, Sastra, Stephen A., Palermo, Carmine F., Hasselluhn, Marie C., Decker-Farrell, Amanda R., Chang, Stephanie, Jiang, Lingyan, Wei, Xing, Yang, Yu C., Helland, Ciara, Courtney, Haley, Gindin, Yevgeniy, Muonio, Karl, Zhao, Ruiping, Kemp, Samantha B., Clendenin, Cynthia, Sor, Rina, Vostrejs, William P., Hibshman, Priya S., Amparo, Amber M., Hennessey, Connor, Rees, Matthew G., Ronan, Melissa M., Roth, Jennifer A., Brodbeck, Jens, Tomassoni, Lorenzo, Bakir, Basil, Socci, Nicholas D., Herring, Laura E., Barker, Natalie K., Wang, Junning, Cleary, James M., Wolpin, Brian M., Chabot, John A., Kluger, Michael D., Manji, Gulam A., Tsai, Kenneth Y., Sekulic, Miroslav, Lagana, Stephen M., Califano, Andrea, Quintana, Elsa, Wang, Zhengping, Smith, Jacqueline A. M., Holderfield, Matthew, Wildes, David, Lowe, Scott W., Badgley, Michael A., Aguirre, Andrew J., Vonderheide, Robert H., Stanger, Ben Z., Baslan, Timour, Der, Channing J., Singh, Mallika, and Olive, Kenneth P.

Published
2024
Full Text
View/download PDF

3. Sex-Specific Associations between Adiponectin and Leptin Signaling and Pancreatic Cancer Survival.

Author

Babic, Ana, Wang, Qiao-Li, Lee, Alice, Yuan, Chen, Rifai, Nader, Luo, Juhua, Tabung, Fred, Wactawski-Wende, Jean, Saquib, Nazmus, Kim, Jihye, Kraft, Peter, Sesso, Howard, Buring, Julie, Giovannucci, Edward, Manson, JoAnn, Stampfer, Meir, Ng, Kimmie, Fuchs, Charles, Wolpin, Brian, and Shadyab, Aladdin

Subjects
Male, Humans, Female, Leptin, Adiponectin, Adipokines, Receptors, Adiponectin, Pancreatic Neoplasms, Polymorphism, Single Nucleotide, Receptors, Leptin
Abstract

BACKGROUND: Circulating adiponectin and leptin have been associated with risk of pancreatic cancer. However, the relationship between long-term exposure to these adipokines in the prediagnostic period with patient survival has not been investigated. METHODS: Adipokine levels were measured in prospectively collected samples from 472 patients with pancreatic cancer. Because of sex-specific differences in adipokine levels, associations were evaluated separately for men and women. In a subset of 415 patients, we genotyped 23 SNPs in adiponectin receptor genes (ADIPOR1 and ADIPOR2) and 30 SNPs in the leptin receptor gene (LEPR). RESULTS: Adiponectin levels were inversely associated with survival in women [HR, 1.71; 95% confidence interval (CI), 1.15-2.54]; comparing top with bottom quartile but not in men (HR, 0.89; 95% CI, 0.46-1.70). The SNPs rs10753929 and rs1418445 in ADIPOR1 were associated with survival in the combined population (per minor allele HR, 0.66; 95% CI, 0.51-0.84, and HR, 1.33; 95% CI, 1.12-1.58, respectively). Among SNPs in LEPR, rs12025906, rs3790431, and rs17127601 were associated with survival in the combined population [HRs, 1.54 (95% CI, 1.25-1.90), 0.72 (95% CI, 0.59-0.88), and 0.70 (95% CI, 0.56-0.89), respectively], whereas rs11585329 was associated with survival in men only (HR, 0.39; 95% CI, 0.23-0.66; Pinteraction = 0.0002). CONCLUSIONS: High levels of adiponectin in the prediagnostic period were associated with shorter survival among women, but not among men with pancreatic cancer. Several polymorphisms in ADIPOR1 and LEPR are associated with patient survival. IMPACT: Our findings reveal the association between adipokine signaling and pancreatic cancer survival and demonstrate the importance of examining obesity-associated pathways in relation to pancreatic cancer in a sex-specific manner.

Published
2023

4. Genetic Susceptibility to Nonalcoholic Fatty Liver Disease and Risk for Pancreatic Cancer: Mendelian Randomization.

Author

Canzian, Federico, Du, Mengmeng, Gallinger, Steven, Giles, Graham, Goodman, Phyllis, Haiman, Christopher, Kogevinas, Manolis, Kooperberg, Charles, LeMarchand, Loic, Neale, Rachel, Visvanathan, Kala, White, Emily, Albanes, Demetrius, Andreotti, Gabriella, Babic, Ana, Berndt, Sonja, Brais, Lauren, Brennan, Paul, Buring, Julie, Rabe, Kari, Bamlet, William, Chanock, Stephen, Fuchs, Charles, Gaziano, J, Giovannucci, Edward, Hackert, Thilo, Hassan, Manal, Katzke, Verena, Kurtz, Robert, Lee, I-Min, Malats, Núria, Murphy, Neil, Oberg, Ann, Orlow, Irene, Porta, Miquel, Real, Francisco, Rothman, Nathaniel, Sesso, Howard, Silverman, Debra, Thompson, Ian, Wactawski-Wende, Jean, Wang, Xiaoliang, Wentzensen, Nicolas, Yu, Herbert, Zeleniuch-Jacquotte, Anne, Yu, Kai, Wolpin, Brian, Duell, Eric, Li, Donghui, Hung, Rayjean, Perdomo, Sandra, McCullough, Marjorie, Freedman, Neal, Patel, Alpa, Peters, Ulrike, Riboli, Elio, Sund, Malin, Tjønneland, Anne, Zhong, Jun, Van Den Eeden, Stephen, Kraft, Peter, Risch, Harvey, Amundadottir, Laufey, Klein, Alison, Stolzenberg-Solomon, Rachael, Antwi, Samuel, King, Sontoria, Veliginti, Swathi, Brouwers, Martijn, Ren, Zhewen, Zheng, Wei, Setiawan, Veronica, Wilkens, Lynne, Shu, Xiao-Ou, Arslan, Alan, Beane Freeman, Laura, and Bracci, Paige

Subjects
Humans, Non-alcoholic Fatty Liver Disease, Genetic Predisposition to Disease, Genome-Wide Association Study, Mendelian Randomization Analysis, Pancreatic Neoplasms, Obesity, Polymorphism, Single Nucleotide
Abstract

BACKGROUND: There are conflicting data on whether nonalcoholic fatty liver disease (NAFLD) is associated with susceptibility to pancreatic cancer. Using Mendelian randomization (MR), we investigated the relationship between genetic predisposition to NAFLD and risk for pancreatic cancer. METHODS: Data from genome-wide association studies (GWAS) within the Pancreatic Cancer Cohort Consortium (PanScan; cases n = 5,090, controls n = 8,733) and the Pancreatic Cancer Case Control Consortium (PanC4; cases n = 4,163, controls n = 3,792) were analyzed. We used data on 68 genetic variants with four different MR methods [inverse variance weighting (IVW), MR-Egger, simple median, and penalized weighted median] separately to predict genetic heritability of NAFLD. We then assessed the relationship between each of the four MR methods and pancreatic cancer risk, using logistic regression to calculate ORs and 95% confidence intervals (CI), adjusting for PC risk factors, including obesity and diabetes. RESULTS: No association was found between genetically predicted NAFLD and pancreatic cancer risk in the PanScan or PanC4 samples [e.g., PanScan, IVW OR, 1.04; 95% confidence interval (CI), 0.88-1.22; MR-Egger OR, 0.89; 95% CI, 0.65-1.21; PanC4, IVW OR, 1.07; 95% CI, 0.90-1.27; MR-Egger OR, 0.93; 95% CI, 0.67-1.28]. None of the four MR methods indicated an association between genetically predicted NAFLD and pancreatic cancer risk in either sample. CONCLUSIONS: Genetic predisposition to NAFLD is not associated with pancreatic cancer risk. IMPACT: Given the close relationship between NAFLD and metabolic conditions, it is plausible that any association between NAFLD and pancreatic cancer might reflect host metabolic perturbations (e.g., obesity, diabetes, or metabolic syndrome) and does not necessarily reflect a causal relationship between NAFLD and pancreatic cancer.

Published
2023

6. Genome-wide analyses characterize shared heritability among cancers and identify novel cancer susceptibility regions

Author

Lindström, Sara, Wang, Lu, Feng, Helian, Majumdar, Arunabha, Huo, Sijia, Macdonald, James, Harrison, Tabitha, Turman, Constance, Chen, Hongjie, Mancuso, Nicholas, Bammler, Theo, Consortium, Breast Cancer Association, Gallinger, Steve, Gruber, Stephen B, Gunter, Marc J, Le Marchand, Loic, Moreno, Victor, Offit, Kenneth, Study, Genetics And Epidemiology Of Colorectal Cancer Consortium Colorectal Transdisciplinary Study Colon Cancer Family Registry, De Vivo, Immaculata, O’Mara, Tracy A, Spurdle, Amanda B, Tomlinson, Ian, Consortium, Endometrial Cancer Association, Fitzgerald, Rebecca, Gharahkhani, Puya, Gockel, Ines, Jankowski, Janusz, Macgregor, Stuart, Schumacher, Johannes, Barnholtz-Sloan, Jill, Bondy, Melissa L, Houlston, Richard S, Jenkins, Robert B, Melin, Beatrice, Wrensch, Margaret, Brennan, Paul, Christiani, David C, Johansson, Mattias, Mckay, James, Aldrich, Melinda C, Amos, Christopher I, Landi, Maria Teresa, Tardon, Adonina, Consortium, International Lung Cancer, Bishop, D Timothy, Demenais, Florence, Goldstein, Alisa M, Iles, Mark M, Kanetsky, Peter A, Law, Matthew H, Consortium, Ovarian Cancer Association, Amundadottir, Laufey T, Stolzenberg-Solomon, Rachael, Wolpin, Brian M, Consortium, Pancreatic Cancer Cohort, Klein, Alison, Petersen, Gloria, Risch, Harvey, Consortium, The PRACTICAL Consortium Pancreatic Cancer Case-Control, Chanock, Stephen J, Purdue, Mark P, Scelo, Ghislaine, Pharoah, Paul, Kar, Siddhartha, Hung, Rayjean J, Pasaniuc, Bogdan, and Kraft, Peter

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Human Genome, Genetics, Digestive Diseases, Prevention, Clinical Research, Urologic Diseases, Cancer, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Male, Humans, Genome-Wide Association Study, Genetic Predisposition to Disease, Neoplasms, Risk Factors, Transcriptome, Polymorphism, Single Nucleotide, Breast Cancer Association Consortium, Colorectal Transdisciplinary Study (CORECT), Colon Cancer Family Registry Study (CCFR), Genetics And Epidemiology Of Colorectal Cancer Consortium, Endometrial Cancer Association Consortium, International Lung Cancer Consortium, Ovarian Cancer Association Consortium, Pancreatic Cancer Cohort Consortium, Pancreatic Cancer Case-Control Consortium (Panc4), The PRACTICAL Consortium, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundThe shared inherited genetic contribution to risk of different cancers is not fully known. In this study, we leverage results from 12 cancer genome-wide association studies (GWAS) to quantify pairwise genome-wide genetic correlations across cancers and identify novel cancer susceptibility loci.MethodsWe collected GWAS summary statistics for 12 solid cancers based on 376 759 participants with cancer and 532 864 participants without cancer of European ancestry. The included cancer types were breast, colorectal, endometrial, esophageal, glioma, head and neck, lung, melanoma, ovarian, pancreatic, prostate, and renal cancers. We conducted cross-cancer GWAS and transcriptome-wide association studies to discover novel cancer susceptibility loci. Finally, we assessed the extent of variant-specific pleiotropy among cancers at known and newly identified cancer susceptibility loci.ResultsWe observed widespread but modest genome-wide genetic correlations across cancers. In cross-cancer GWAS and transcriptome-wide association studies, we identified 15 novel cancer susceptibility loci. Additionally, we identified multiple variants at 77 distinct loci with strong evidence of being associated with at least 2 cancer types by testing for pleiotropy at known cancer susceptibility loci.ConclusionsOverall, these results suggest that some genetic risk variants are shared among cancers, though much of cancer heritability is cancer-specific and thus tissue-specific. The increase in statistical power associated with larger sample sizes in cross-disease analysis allows for the identification of novel susceptibility regions. Future studies incorporating data on multiple cancer types are likely to identify additional regions associated with the risk of multiple cancer types.

Published
2023

7. Closed-loop automated drug infusion regulator: A clinically translatable, closed-loop drug delivery system for personalized drug dosing

Author

DeRidder, Louis B., Hare, Kyle A., Lopes, Aaron, Jenkins, Josh, Fitzgerald, Nina, MacPherson, Emmeline, Fabian, Niora, Morimoto, Josh, Chu, Jacqueline N., Kirtane, Ameya R., Madani, Wiam, Ishida, Keiko, Kuosmanen, Johannes L.P., Zecharias, Naomi, Colangelo, Christopher M., Huang, Hen-Wei, Chilekwa, Makaya, Lal, Nikhil B., Srinivasan, Shriya S., Hayward, Alison M., Wolpin, Brian M., Trumper, David, Quast, Troy, Rubinson, Douglas A., Langer, Robert, and Traverso, Giovanni

Published
2024
Full Text
View/download PDF

10. Adipose tissue and skeletal muscle wasting precede clinical diagnosis of pancreatic cancer

Author

Babic, Ana, Rosenthal, Michael H., Sundaresan, Tilak K., Khalaf, Natalia, Lee, Valerie, Brais, Lauren K., Loftus, Maureen, Caplan, Leah, Denning, Sarah, Gurung, Anamol, Harrod, Joanna, Schawkat, Khoschy, Yuan, Chen, Wang, Qiao-Li, Lee, Alice A., Biller, Leah H., Yurgelun, Matthew B., Ng, Kimmie, Nowak, Jonathan A., Aguirre, Andrew J., Bhatia, Sangeeta N., Vander Heiden, Matthew G., Van Den Eeden, Stephen K., Caan, Bette J., and Wolpin, Brian M.

Published
2023
Full Text
View/download PDF

13. A deep learning algorithm to predict risk of pancreatic cancer from disease trajectories

Author

Placido, Davide, Yuan, Bo, Hjaltelin, Jessica X., Zheng, Chunlei, Haue, Amalie D., Chmura, Piotr J., Yuan, Chen, Kim, Jihye, Umeton, Renato, Antell, Gregory, Chowdhury, Alexander, Franz, Alexandra, Brais, Lauren, Andrews, Elizabeth, Marks, Debora S., Regev, Aviv, Ayandeh, Siamack, Brophy, Mary T., Do, Nhan V., Kraft, Peter, Wolpin, Brian M., Rosenthal, Michael H., Fillmore, Nathanael R., Brunak, Søren, and Sander, Chris

Published
2023
Full Text
View/download PDF

14. Retrospective Case Series Analysis of RAF Family Alterations in Pancreatic Cancer: Real-World Outcomes From Targeted and Standard Therapies

Author

Hendifar, Andrew, Blais, Edik M, Wolpin, Brian, Subbiah, Vivek, Collisson, Eric, Singh, Isha, Cannon, Timothy, Shaw, Kenna, Petricoin, Emanuel F, Klempner, Samuel, Lyons, Emily, Wang-Gillam, Andrea, Pishvaian, Michael J, and O'Reilly, Eileen M

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Rare Diseases, Pancreatic Cancer, Clinical Research, Genetics, Orphan Drug, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Aged, Exons, Female, Humans, MAP Kinase Signaling System, Male, Middle Aged, Mutation, Neoplasm Metastasis, Pancreatic Neoplasms, Protein Kinase Inhibitors, Proto-Oncogene Proteins B-raf, Retrospective Studies, Survival Analysis, Oncology and carcinogenesis
Abstract

PurposeIn pancreatic cancer (PC), the RAF family alterations define a rare subset of patients that may predict response to inhibition of the BRAF/MEK/ERK signaling pathway. A comprehensive understanding of the molecular and clinical characteristics of RAF-mutated PC may support future development of RAF-directed strategies.MethodsClinical outcomes were assessed across a multi-institutional case series of 81 patients with RAF family-mutated PC. Mutational subgroups were defined on the basis of RAF alteration hotspots and therapeutic implications.ResultsThe frequency of RAF alterations in PC was 2.2% (84 of 3,781) within a prevalence cohort derived from large molecular databases where BRAF V600E (Exon 15), BRAF ΔNVTAP (Exon 11), and SND1-BRAF fusions were the most common variants. In our retrospective case series, we identified 17 of 81 (21.0%) molecular profiles with a BRAF V600/Exon 15 mutation without any confounding drivers, 25 of 81 (30.9%) with BRAF or RAF1 fusions, and 18 of 81 (22.2%) with Exon 11 mutations. The remaining 21 of 81 (25.9%) profiles had atypical RAF variants and/or multiple oncogenic drivers. Clinical benefit from BRAF/MEK/ERK inhibitors was observed in 3 of 3 subjects within the V600 subgroup (two partial responses), 4 of 6 with fusions (two partial responses), 2 of 6 with Exon 11 mutations (one partial response), and 0 of 3 with confounding drivers. Outcomes analyses also suggested a trend favoring fluorouracil-based regimens over gemcitabine/nab-paclitaxel within the fusion subgroup (P = .027).ConclusionProspective evaluation of RAF-directed therapies is warranted in RAF-mutated PC; however, differential responses to targeted agents or standard regimens for each mutational subgroup should be a consideration when designing clinical trials.

Published
2021

15. Prediagnostic Inflammation and Pancreatic Cancer Survival.

Author

Yuan, Chen, Morales-Oyarvide, Vicente, Khalaf, Natalia, Perez, Kimberly, Tabung, Fred K, Ho, Gloria YF, Kooperberg, Charles, Shadyab, Aladdin H, Qi, Lihong, Kraft, Peter, Sesso, Howard D, Giovannucci, Edward L, Manson, JoAnn E, Stampfer, Meir J, Ng, Kimmie, Fuchs, Charles S, Wolpin, Brian M, and Babic, Ana

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Clinical Research, Rare Diseases, Cancer, Pancreatic Cancer, Digestive Diseases, Humans, Inflammation, Pancreatic Neoplasms, Proportional Hazards Models, Prospective Studies, Risk Factors, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundChronic inflammation may promote initiation and progression of pancreatic cancer, but no studies have examined the association between inflammation in the period before diagnosis and pancreatic cancer survival.MethodsWe prospectively examined the association of prediagnostic plasma levels of C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 2 with survival among 492 participants from 5 large US prospective cohort studies who developed pancreatic cancer. Using an empirical dietary inflammatory pattern (EDIP) score, we evaluated whether long-term proinflammatory diets were associated with survival among 1153 patients from 2 of the 5 cohorts. Cox proportional hazards regression was used to estimate hazard ratios for death with adjustment for potential confounders. All statistical tests were 2-sided.ResultsHigher prediagnostic levels of C-reactive protein, interleukin-6, and tumor necrosis factor-α receptor 2 were individually associated with reduced survival (Ptrend = .03, .01, and .04, respectively). Compared with patients with a combined inflammatory biomarker score of 0 (all 3 marker levels below medians), those with a score of 3 (all 3 marker levels above medians) had a hazard ratio for death of 1.57 (95% confidence interval = 1.16 to 2.12; Ptrend = .003), corresponding to median overall survival times of 8 vs 5 months. Patients consuming the most proinflammatory diets (EDIP quartile 4) in the prediagnostic period had a hazard ratio for death of 1.34 (95% confidence interval = 1.13 to 1.59; Ptrend = .01), compared with those consuming the least proinflammatory diets (EDIP quartile 1).ConclusionPrediagnostic levels of inflammatory biomarkers and long-term proinflammatory diets were inversely associated with pancreatic cancer survival.

Published
2021

16. Artificial Intelligence and Early Detection of Pancreatic Cancer: 2020 Summative Review.

Author

Kenner, Barbara, Chari, Suresh T, Kelsen, David, Klimstra, David S, Pandol, Stephen J, Rosenthal, Michael, Rustgi, Anil K, Taylor, James A, Yala, Adam, Abul-Husn, Noura, Andersen, Dana K, Bernstein, David, Brunak, Søren, Canto, Marcia Irene, Eldar, Yonina C, Fishman, Elliot K, Fleshman, Julie, Go, Vay Liang W, Holt, Jane M, Field, Bruce, Goldberg, Ann, Hoos, William, Iacobuzio-Donahue, Christine, Li, Debiao, Lidgard, Graham, Maitra, Anirban, Matrisian, Lynn M, Poblete, Sung, Rothschild, Laura, Sander, Chris, Schwartz, Lawrence H, Shalit, Uri, Srivastava, Sudhir, and Wolpin, Brian

Subjects
Humans, Carcinoma, Pancreatic Ductal, Pancreatic Neoplasms, Prognosis, Survival Analysis, Interdisciplinary Communication, Genomics, Artificial Intelligence, Early Detection of Cancer, Biomarkers, Tumor, Cancer, Rare Diseases, Prevention, Pancreatic Cancer, Digestive Diseases, Good Health and Well Being, artificial intelligence, machine learning, pancreatic cancer, early detection, Clinical Sciences, Gastroenterology & Hepatology
Abstract

AbstractDespite considerable research efforts, pancreatic cancer is associated with a dire prognosis and a 5-year survival rate of only 10%. Early symptoms of the disease are mostly nonspecific. The premise of improved survival through early detection is that more individuals will benefit from potentially curative treatment. Artificial intelligence (AI) methodology has emerged as a successful tool for risk stratification and identification in general health care. In response to the maturity of AI, Kenner Family Research Fund conducted the 2020 AI and Early Detection of Pancreatic Cancer Virtual Summit (www.pdac-virtualsummit.org) in conjunction with the American Pancreatic Association, with a focus on the potential of AI to advance early detection efforts in this disease. This comprehensive presummit article was prepared based on information provided by each of the interdisciplinary participants on one of the 5 following topics: Progress, Problems, and Prospects for Early Detection; AI and Machine Learning; AI and Pancreatic Cancer-Current Efforts; Collaborative Opportunities; and Moving Forward-Reflections from Government, Industry, and Advocacy. The outcome from the robust Summit conversations, to be presented in a future white paper, indicate that significant progress must be the result of strategic collaboration among investigators and institutions from multidisciplinary backgrounds, supported by committed funders.

Published
2021

17. A blood-based metabolomic signature predictive of risk for pancreatic cancer

Author

Irajizad, Ehsan, Kenney, Ana, Tang, Tiffany, Vykoukal, Jody, Wu, Ranran, Murage, Eunice, Dennison, Jennifer B., Sans, Marta, Long, James P., Loftus, Maureen, Chabot, John A., Kluger, Michael D., Kastrinos, Fay, Brais, Lauren, Babic, Ana, Jajoo, Kunal, Lee, Linda S., Clancy, Thomas E., Ng, Kimmie, Bullock, Andrea, Genkinger, Jeanine M., Maitra, Anirban, Do, Kim-Anh, Yu, Bin, Wolpin, Brian M., Hanash, Sam, and Fahrmann, Johannes F.

Published
2023
Full Text
View/download PDF

18. Assessment of polygenic architecture and risk prediction based on common variants across fourteen cancers.

Author

Zhang, Yan Dora, Hurson, Amber N, Zhang, Haoyu, Choudhury, Parichoy Pal, Easton, Douglas F, Milne, Roger L, Simard, Jacques, Hall, Per, Michailidou, Kyriaki, Dennis, Joe, Schmidt, Marjanka K, Chang-Claude, Jenny, Gharahkhani, Puya, Whiteman, David, Campbell, Peter T, Hoffmeister, Michael, Jenkins, Mark, Peters, Ulrike, Hsu, Li, Gruber, Stephen B, Casey, Graham, Schmit, Stephanie L, O'Mara, Tracy A, Spurdle, Amanda B, Thompson, Deborah J, Tomlinson, Ian, De Vivo, Immaculata, Landi, Maria Teresa, Law, Matthew H, Iles, Mark M, Demenais, Florence, Kumar, Rajiv, MacGregor, Stuart, Bishop, D Timothy, Ward, Sarah V, Bondy, Melissa L, Houlston, Richard, Wiencke, John K, Melin, Beatrice, Barnholtz-Sloan, Jill, Kinnersley, Ben, Wrensch, Margaret R, Amos, Christopher I, Hung, Rayjean J, Brennan, Paul, McKay, James, Caporaso, Neil E, Berndt, Sonja I, Birmann, Brenda M, Camp, Nicola J, Kraft, Peter, Rothman, Nathaniel, Slager, Susan L, Berchuck, Andrew, Pharoah, Paul DP, Sellers, Thomas A, Gayther, Simon A, Pearce, Celeste L, Goode, Ellen L, Schildkraut, Joellen M, Moysich, Kirsten B, Amundadottir, Laufey T, Jacobs, Eric J, Klein, Alison P, Petersen, Gloria M, Risch, Harvey A, Stolzenberg-Solomon, Rachel Z, Wolpin, Brian M, Li, Donghui, Eeles, Rosalind A, Haiman, Christopher A, Kote-Jarai, Zsofia, Schumacher, Fredrick R, Al Olama, Ali Amin, Purdue, Mark P, Scelo, Ghislaine, Dalgaard, Marlene D, Greene, Mark H, Grotmol, Tom, Kanetsky, Peter A, McGlynn, Katherine A, Nathanson, Katherine L, Turnbull, Clare, Wiklund, Fredrik, Breast Cancer Association Consortium (BCAC), Barrett’s and Esophageal Adenocarcinoma Consortium (BEACON), Colon Cancer Family Registry (CCFR), Transdisciplinary Studies of Genetic Variation in Colorectal Cancer (CORECT), Endometrial Cancer Association Consortium (ECAC), Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO), Melanoma Genetics Consortium (GenoMEL), Glioma International Case-Control Study (GICC), International Lung Cancer Consortium (ILCCO), Integrative Analysis of Lung Cancer Etiology and Risk (INTEGRAL) Consortium, International Consortium of Investigators Working on Non-Hodgkin’s Lymphoma Epidemiologic Studies (InterLymph), Ovarian Cancer Association Consortium (OCAC), Oral Cancer GWAS, Pancreatic Cancer Case-Control Consortium (PanC4), Pancreatic Cancer Cohort Consortium (PanScan), and Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL)

Subjects
Breast Cancer Association Consortium, Barrett’s and Esophageal Adenocarcinoma Consortium, Colon Cancer Family Registry, Transdisciplinary Studies of Genetic Variation in Colorectal Cancer, Endometrial Cancer Association Consortium, Genetics and Epidemiology of Colorectal Cancer Consortium, Melanoma Genetics Consortium, Glioma International Case-Control Study, International Lung Cancer Consortium, Integrative Analysis of Lung Cancer Etiology and Risk (INTEGRAL) Consortium, International Consortium of Investigators Working on Non-Hodgkin’s Lymphoma Epidemiologic Studies, Ovarian Cancer Association Consortium, Oral Cancer GWAS, Pancreatic Cancer Case-Control Consortium, Pancreatic Cancer Cohort Consortium, Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome, Renal Cancer GWAS, Testicular Cancer Consortium, Animals, Humans, Neoplasms, Genetic Predisposition to Disease, Incidence, Risk Assessment, Risk Factors, Multifactorial Inheritance, Polymorphism, Single Nucleotide, Models, Genetic, Female, Male, Genome-Wide Association Study, Human Genome, Prevention, Cancer, Prostate Cancer, Genetics, Urologic Diseases, 2.1 Biological and endogenous factors
Abstract

Genome-wide association studies (GWAS) have led to the identification of hundreds of susceptibility loci across cancers, but the impact of further studies remains uncertain. Here we analyse summary-level data from GWAS of European ancestry across fourteen cancer sites to estimate the number of common susceptibility variants (polygenicity) and underlying effect-size distribution. All cancers show a high degree of polygenicity, involving at a minimum of thousands of loci. We project that sample sizes required to explain 80% of GWAS heritability vary from 60,000 cases for testicular to over 1,000,000 cases for lung cancer. The maximum relative risk achievable for subjects at the 99th risk percentile of underlying polygenic risk scores (PRS), compared to average risk, ranges from 12 for testicular to 2.5 for ovarian cancer. We show that PRS have potential for risk stratification for cancers of breast, colon and prostate, but less so for others because of modest heritability and lower incidence.

Published
2020

19. USP9X mediates an acute adaptive response to MAPK suppression in pancreatic cancer but creates multiple actionable therapeutic vulnerabilities

Author

Perurena, Naiara, Lock, Rebecca, Davis, Rachel A., Raghavan, Srivatsan, Pilla, Natalie F., Ng, Raymond, Loi, Patrick, Guild, Caroline J., Miller, Abigail L., Sicinska, Ewa, Cleary, James M., Rubinson, Douglas A., Wolpin, Brian M., Gray, Nathanael S., Santagata, Sandro, Hahn, William C., Morton, Jennifer P., Sansom, Owen J., Aguirre, Andrew J., and Cichowski, Karen

Published
2023
Full Text
View/download PDF

21. Early results of the PASS-01 trial: Pancreatic adenocarcinoma signature stratification for treatment-01.

Author

Knox, Jennifer J., primary, Jaffee, Elizabeth M., additional, O'Kane, Grainne M., additional, King, Daniel, additional, Laheru, Dan, additional, Yu, Kenneth H., additional, Perez, Kimberly, additional, Habowski, Amber N, additional, Grant, Robert C, additional, Fischer, Sandra, additional, Aguirre, Andrew, additional, Jang, Raymond Woo-Jun, additional, Devoe, Craig E., additional, O'Reilly, Eileen M., additional, Dodd, Anna, additional, Wolpin, Brian M., additional, Ye, Xiang Y, additional, Notta, Faiyaz, additional, Gallinger, Steven, additional, and Tuveson, David A., additional

Published
2024
Full Text
View/download PDF

22. Fully-Automated Analysis of Body Composition from CT in Cancer Patients Using Convolutional Neural Networks

Author

Bridge, Christopher P., Rosenthal, Michael, Wright, Bradley, Kotecha, Gopal, Fintelmann, Florian, Troschel, Fabian, Miskin, Nityanand, Desai, Khanant, Wrobel, William, Babic, Ana, Khalaf, Natalia, Brais, Lauren, Welch, Marisa, Zellers, Caitlin, Tenenholtz, Neil, Michalski, Mark, Wolpin, Brian, and Andriole, Katherine

Subjects
Computer Science - Computer Vision and Pattern Recognition
Abstract

The amounts of muscle and fat in a person's body, known as body composition, are correlated with cancer risks, cancer survival, and cardiovascular risk. The current gold standard for measuring body composition requires time-consuming manual segmentation of CT images by an expert reader. In this work, we describe a two-step process to fully automate the analysis of CT body composition using a DenseNet to select the CT slice and U-Net to perform segmentation. We train and test our methods on independent cohorts. Our results show Dice scores (0.95-0.98) and correlation coefficients (R=0.99) that are favorable compared to human readers. These results suggest that fully automated body composition analysis is feasible, which could enable both clinical use and large-scale population studies.

Published
2018
Full Text
View/download PDF

23. Helicobacter pylori Seropositivity, ABO Blood Type, and Pancreatic Cancer Risk from 5 Prospective Cohorts

Author

Lee, Alice A., Wang, Qiao-Li, Kim, Jihye, Babic, Ana, Zhang, Xuehong, Perez, Kimberly, Ng, Kimmie, Nowak, Jonathan, Rifazzzzzzzzgi, Nader, Sesso, Howard D., Buring, Julie E., Anderson, Garnet L., Wactawski-Wende, Jean, Wallace, Robert, Manson, JoAnn E., Giovannucci, Edward L., Stampfer, Meir J., Kraft, Peter, Fuchs, Charles S., Yuan, Chen, and Wolpin, Brian M.

Published
2023
Full Text
View/download PDF

24. Pancreas Cancer‐Associated Weight Loss

Author

Hendifar, Andrew E, Petzel, Maria QB, Zimmers, Teresa A, Denlinger, Crystal S, Matrisian, Lynn M, Picozzi, Vincent J, Rahib, Lola, Hendifar, Andrew, Tuli, Richard, Wolpin, Brian, Hidalgo, Manuel, Ryan, David, Hingorani, Sunil, Chiorean, Elena Gabriela, Coveler, Andrew, O'Reilly, Eileen, Balachandran, Vinod, Simeone, Diane, Lowy, Andrew, Fanta, Paul, Kurzrock, Razelle, Reid, Tony, Ko, Andrew, Collisson, Eric, Tempero, Margaret, Kindler, Hedy, George, Thomas, Trevino, Jose, Vonderheide, Robert, Beatty, Gregory, Picozzi, Vincent, Mandelson, Margaret, Wang‐Gillam, Andrea, Hawkins, William, Fleshman, Julie, Maitra, Anirban, Manax, Victoria, and Matrisian, Lynn

Subjects
Pancreatic Cancer, Cancer, Clinical Research, Digestive Diseases, Rare Diseases, Prevention, Nutrition, Clinical Trials and Supportive Activities, Cachexia, Humans, Pancreatic Neoplasms, Prevalence, Quality of Life, Weight Loss, Pancreatic cancer, Weight loss, Anorexia, Malabsorption, Supportive care, Precision Promise Consortium, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

Unintentional weight loss in patients with pancreatic cancer is highly prevalent and contributes to low therapeutic tolerance, reduced quality of life, and overall mortality. Weight loss in pancreatic cancer can be due to anorexia, malabsorption, and/or cachexia. Proper supportive care can stabilize or reverse weight loss in patients and improve outcomes. We review the literature on supportive care relevant to pancreatic cancer patients, and offer evidence-based recommendations that include expert nutritional assessment, counseling, supportive measures to ensure adequate caloric intake, pancreatic enzyme supplementation, nutritional supplement replacement, orexigenic agents, and exercise. Pancreatic Cancer Action Network-supported initiatives will spearhead the dissemination and adoption of these best supportive care practices. IMPLICATIONS FOR PRACTICE: Weight loss in pancreatic cancer patients is endemic, as 85% of pancreatic cancer patients meet the classic definition of cancer cachexia. Despite its significant prevalence and associated morbidity, there is no established approach to this disease entity. It is believed that this is due to an important knowledge gap in understanding the underlying biology and lack of optimal treatment approaches. This article reviews the literature regarding pancreas cancer-associated weight loss and establishes a new framework from which to view this complex clinical problem. An improved approach and understanding will help educate clinicians, improve clinical care, and provide more clarity for future clinical investigation.

Published
2019

27. Low glycaemic diets alter lipid metabolism to influence tumour growth

Author

Lien, Evan C., Westermark, Anna M., Zhang, Yin, Yuan, Chen, Li, Zhaoqi, Lau, Allison N., Sapp, Kiera M., Wolpin, Brian M., and Vander Heiden, Matthew G.

Subjects
Tumors -- Diet therapy, Dextrose -- Physiological aspects, Glucose -- Physiological aspects, Lipid metabolism -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Dietary interventions can change metabolite levels in the tumour microenvironment, which might then affect cancer cell metabolism to alter tumour growth.sup.1-5. Although caloric restriction (CR) and a ketogenic diet (KD) are often thought to limit tumour progression by lowering blood glucose and insulin levels.sup.6-8, we found that only CR inhibits the growth of select tumour allografts in mice, suggesting that other mechanisms contribute to tumour growth inhibition. A change in nutrient availability observed with CR, but not with KD, is lower lipid levels in the plasma and tumours. Upregulation of stearoyl-CoA desaturase (SCD), which synthesises monounsaturated fatty acids, is required for cancer cells to proliferate in a lipid-depleted environment, and CR also impairs tumour SCD activity to cause an imbalance between unsaturated and saturated fatty acids to slow tumour growth. Enforcing cancer cell SCD expression or raising circulating lipid levels through a higher-fat CR diet confers resistance to the effects of CR. By contrast, although KD also impairs tumour SCD activity, KD-driven increases in lipid availability maintain the unsaturated to saturated fatty acid ratios in tumours, and changing the KD fat composition to increase tumour saturated fatty acid levels cooperates with decreased tumour SCD activity to slow tumour growth. These data suggest that diet-induced mismatches between tumour fatty acid desaturation activity and the availability of specific fatty acid species determine whether low glycaemic diets impair tumour growth. Lien et al. show that low glycemic diets can reduce tumour growth by deregulating lipid metabolism., Author(s): Evan C. Lien [sup.1] , Anna M. Westermark [sup.1] , Yin Zhang [sup.2] [sup.3] , Chen Yuan [sup.2] , Zhaoqi Li [sup.1] [sup.4] , Allison N. Lau [sup.1] , [...]

Published
2021
Full Text
View/download PDF

28. Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer.

Author

Tiriac, Hervé, Belleau, Pascal, Engle, Dannielle D, Plenker, Dennis, Deschênes, Astrid, Somerville, Tim DD, Froeling, Fieke EM, Burkhart, Richard A, Denroche, Robert E, Jang, Gun-Ho, Miyabayashi, Koji, Young, C Megan, Patel, Hardik, Ma, Michelle, LaComb, Joseph F, Palmaira, Randze Lerie D, Javed, Ammar A, Huynh, Jasmine C, Johnson, Molly, Arora, Kanika, Robine, Nicolas, Shah, Minita, Sanghvi, Rashesh, Goetz, Austin B, Lowder, Cinthya Y, Martello, Laura, Driehuis, Else, LeComte, Nicolas, Askan, Gokce, Iacobuzio-Donahue, Christine A, Clevers, Hans, Wood, Laura D, Hruban, Ralph H, Thompson, Elizabeth, Aguirre, Andrew J, Wolpin, Brian M, Sasson, Aaron, Kim, Joseph, Wu, Maoxin, Bucobo, Juan Carlos, Allen, Peter, Sejpal, Divyesh V, Nealon, William, Sullivan, James D, Winter, Jordan M, Gimotty, Phyllis A, Grem, Jean L, DiMaio, Dominick J, Buscaglia, Jonathan M, Grandgenett, Paul M, Brody, Jonathan R, Hollingsworth, Michael A, O'Kane, Grainne M, Notta, Faiyaz, Kim, Edward, Crawford, James M, Devoe, Craig, Ocean, Allyson, Wolfgang, Christopher L, Yu, Kenneth H, Li, Ellen, Vakoc, Christopher R, Hubert, Benjamin, Fischer, Sandra E, Wilson, Julie M, Moffitt, Richard, Knox, Jennifer, Krasnitz, Alexander, Gallinger, Steven, and Tuveson, David A

Subjects
Organoids, Tumor Cells, Cultured, Humans, Pancreatic Neoplasms, Antineoplastic Agents, Drug Screening Assays, Antitumor, Prospective Studies, Gene Expression Profiling, Sequence Analysis, RNA, Gene Expression Regulation, Neoplastic, Drug Resistance, Neoplasm, Gene Regulatory Networks, Molecular Targeted Therapy, Standard of Care, Precision Medicine, Genetics, Pancreatic Cancer, Rare Diseases, Digestive Diseases, Orphan Drug, Cancer, Detection, screening and diagnosis, Development of treatments and therapeutic interventions, 4.1 Discovery and preclinical testing of markers and technologies, 5.1 Pharmaceuticals, Good Health and Well Being, Oncology and Carcinogenesis
Abstract

Pancreatic cancer is the most lethal common solid malignancy. Systemic therapies are often ineffective, and predictive biomarkers to guide treatment are urgently needed. We generated a pancreatic cancer patient-derived organoid (PDO) library that recapitulates the mutational spectrum and transcriptional subtypes of primary pancreatic cancer. New driver oncogenes were nominated and transcriptomic analyses revealed unique clusters. PDOs exhibited heterogeneous responses to standard-of-care chemotherapeutics and investigational agents. In a case study manner, we found that PDO therapeutic profiles paralleled patient outcomes and that PDOs enabled longitudinal assessment of chemosensitivity and evaluation of synchronous metastases. We derived organoid-based gene expression signatures of chemosensitivity that predicted improved responses for many patients to chemotherapy in both the adjuvant and advanced disease settings. Finally, we nominated alternative treatment strategies for chemorefractory PDOs using targeted agent therapeutic profiling. We propose that combined molecular and therapeutic profiling of PDOs may predict clinical response and enable prospective therapeutic selection.Significance: New approaches to prioritize treatment strategies are urgently needed to improve survival and quality of life for patients with pancreatic cancer. Combined genomic, transcriptomic, and therapeutic profiling of PDOs can identify molecular and functional subtypes of pancreatic cancer, predict therapeutic responses, and facilitate precision medicine for patients with pancreatic cancer. Cancer Discov; 8(9); 1112-29. ©2018 AACR.See related commentary by Collisson, p. 1062This article is highlighted in the In This Issue feature, p. 1047.

Published
2018

29. Covariate selection for association screening in multiphenotype genetic studies

Author

Aschard, Hugues, Guillemot, Vincent, Vilhjalmsson, Bjarni, Patel, Chirag J, Skurnik, David, Ye, Chun J, Wolpin, Brian, Kraft, Peter, and Zaitlen, Noah

Subjects
Biological Sciences, Genetics, Clinical Research, Algorithms, Genetic Association Studies, Genetic Variation, Genome-Wide Association Study, Genotype, Humans, Models, Genetic, Multivariate Analysis, Phenotype, Reproducibility of Results, Sample Size, Medical and Health Sciences, Developmental Biology, Agricultural biotechnology, Bioinformatics and computational biology
Abstract

Testing for associations in big data faces the problem of multiple comparisons, wherein true signals are difficult to detect on the background of all associations queried. This difficulty is particularly salient in human genetic association studies, in which phenotypic variation is often driven by numerous variants of small effect. The current strategy to improve power to identify these weak associations consists of applying standard marginal statistical approaches and increasing study sample sizes. Although successful, this approach does not leverage the environmental and genetic factors shared among the multiple phenotypes collected in contemporary cohorts. Here we developed covariates for multiphenotype studies (CMS), an approach that improves power when correlated phenotypes are measured on the same samples. Our analyses of real and simulated data provide direct evidence that correlated phenotypes can be used to achieve increases in power to levels often surpassing the power gained by a twofold increase in sample size.

Published
2017

30. Supplementary Figure 1 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

31. Supplementary Table 1 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

32. Supplementary Table 8 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

33. Supplementary Table 5 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

34. Supplementary Figure 5 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

35. Supplementary Table 2 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

36. Supplementary Table 9 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

37. Supplementary Table 7 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

38. Supplementary Figure 6 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

39. Supplementary Table 3 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

40. Supplementary Methods 1 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

41. Supplementary Figure 3 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

42. Supplementary Table 6 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

43. Supplementary Figure 2 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

44. Supplementary Table 4 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

45. Supplementary Figure 4 from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

46. Data from RAS/RAF Comutation and ERBB2 Copy Number Modulates HER2 Heterogeneity and Responsiveness to HER2-directed Therapy in Colorectal Cancer

Author

Singh, Harshabad, primary, Sahgal, Pranshu, primary, Kapner, Kevin, primary, Corsello, Steven M., primary, Gupta, Hersh, primary, Gujrathi, Rahul, primary, Li, Yvonne Y., primary, Cherniack, Andrew D., primary, El Alam, Raquelle, primary, Kerfoot, Joseph, primary, Andrews, Elizabeth, primary, Lee, Annette, primary, Nambiar, Chetan, primary, Hannigan, Alison M., primary, Remland, Joshua, primary, Brais, Lauren, primary, Leahy, Meghan E., primary, Rubinson, Douglas A., primary, Schlechter, Benjamin L., primary, Meyerson, Matthew, primary, Kuang, Yanan, primary, Paweletz, Cloud P., primary, Lee, Jessica K., primary, Quintanilha, Julia C.F., primary, Aguirre, Andrew J., primary, Perez, Kimberly J., primary, Huffman, Brandon M., primary, Rossi, Humberto, primary, Abrams, Thomas A., primary, Kabraji, Sheheryar, primary, Trusolino, Livio, primary, Bertotti, Andrea, primary, Sicinska, Ewa T., primary, Parikh, Aparna R., primary, Wolpin, Brian M., primary, Schrock, Alexa B., primary, Giannakis, Marios, primary, Ng, Kimmie, primary, Meyerhardt, Jeffrey A., primary, Hornick, Jason L., primary, Sethi, Nilay S., primary, and Cleary, James M., primary

Published
2024
Full Text
View/download PDF

47. Identifying regulators of aberrant stem cell and differentiation activity in colorectal cancer using a dual endogenous reporter system

Author

Spisak, Sandor, primary, Chen, David, additional, Likasitwatanakul, Pornlada, additional, Doan, Paul, additional, Li, Zhixin, additional, Bala, Pratyusha, additional, Vizkeleti, Laura, additional, Tisza, Viktoria, additional, De Silva, Pushpamali, additional, Giannakis, Marios, additional, Wolpin, Brian, additional, Qi, Jun, additional, and Sethi, Nilay S., additional

Published
2024
Full Text
View/download PDF

48. Machine learning links T-cell function and spatial localization to neoadjuvant immunotherapy and clinical outcome in pancreatic cancer

Author

Blise, Katie E., primary, Sivagnanam, Shamilene, additional, Betts, Courtney B., additional, Betre, Konjit, additional, Kirchberger, Nell, additional, Tate, Benjamin J., additional, Furth, Emma E., additional, Dias Costa, Andressa, additional, Nowak, Jonathan A., additional, Wolpin, Brian M., additional, Vonderheide, Robert H., additional, Goecks, Jeremy, additional, Coussens, Lisa M., additional, and Byrne, Katelyn T., additional

Published
2024
Full Text
View/download PDF

49. Data from Neoadjuvant Selicrelumab, an Agonist CD40 Antibody, Induces Changes in the Tumor Microenvironment in Patients with Resectable Pancreatic Cancer

Author

Byrne, Katelyn T., primary, Betts, Courtney B., primary, Mick, Rosemarie, primary, Sivagnanam, Shamilene, primary, Bajor, David L., primary, Laheru, Daniel A., primary, Chiorean, E. Gabriela, primary, O'Hara, Mark H., primary, Liudahl, Shannon M., primary, Newcomb, Craig, primary, Alanio, Cécile, primary, Ferreira, Ana P., primary, Park, Byung S., primary, Ohtani, Takuya, primary, Huffman, Austin P., primary, Väyrynen, Sara A., primary, Dias Costa, Andressa, primary, Kaiser, Judith C., primary, Lacroix, Andreanne M., primary, Redlinger, Colleen, primary, Stern, Martin, primary, Nowak, Jonathan A., primary, Wherry, E. John, primary, Cheever, Martin A., primary, Wolpin, Brian M., primary, Furth, Emma E., primary, Jaffee, Elizabeth M., primary, Coussens, Lisa M., primary, and Vonderheide, Robert H., primary

Published
2024
Full Text
View/download PDF

50. Supplementary Table 2 from Neoadjuvant Selicrelumab, an Agonist CD40 Antibody, Induces Changes in the Tumor Microenvironment in Patients with Resectable Pancreatic Cancer

Author

Byrne, Katelyn T., primary, Betts, Courtney B., primary, Mick, Rosemarie, primary, Sivagnanam, Shamilene, primary, Bajor, David L., primary, Laheru, Daniel A., primary, Chiorean, E. Gabriela, primary, O'Hara, Mark H., primary, Liudahl, Shannon M., primary, Newcomb, Craig, primary, Alanio, Cécile, primary, Ferreira, Ana P., primary, Park, Byung S., primary, Ohtani, Takuya, primary, Huffman, Austin P., primary, Väyrynen, Sara A., primary, Dias Costa, Andressa, primary, Kaiser, Judith C., primary, Lacroix, Andreanne M., primary, Redlinger, Colleen, primary, Stern, Martin, primary, Nowak, Jonathan A., primary, Wherry, E. John, primary, Cheever, Martin A., primary, Wolpin, Brian M., primary, Furth, Emma E., primary, Jaffee, Elizabeth M., primary, Coussens, Lisa M., primary, and Vonderheide, Robert H., primary

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results