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1. The Current State of Robot-Assisted Minimally Invasive Esophagectomy (RAMIE): Outcomes from the Upper GI International Robotic Association (UGIRA) Esophageal Registry

Author

Kooij, Cezanne D., de Jongh, Cas, Kingma, B. Feike, van Berge Henegouwen, Mark I., Gisbertz, Suzanne S., Chao, Yin-Kai, Chiu, Philip W., Rouanet, Philippe, Mourregot, Anne, Immanuel, Arul, Mala, Tom, van Boxel, Gijs I., Carter, Nicholas C., Li, Hecheng, Fuchs, Hans F., Bruns, Christiane J., Giacopuzzi, Simone, Kalff, Jörg C., Hölzen, Jens-Peter, Juratli, Mazen A., Benedix, Frank, Lorenz, Eric, Egberts, Jan-Hendrik, Haveman, Jan W., van Etten, Boudewijn, Müller, Beat P., Grimminger, Peter P., Berlth, Felix, Piessen, Guillaume, van den Berg, Jan W., Milone, Marco, Luketich, James D., Sarkaria, Inderpal S., Sallum, Rubens A. A., van Det, Marc J., Kouwenhoven, Ewout A., Brüwer, Matthias, Harustiak, Tomas, Kinoshita, Takahiro, Fujita, Takeo, Daiko, Hiroyuki, Li, Zhigang, Ruurda, Jelle P., and van Hillegersberg, Richard

Published
2024
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4. ASO Visual Abstract: The Current State of Robot-Assisted Minimally Invasive Esophagectomy (RAMIE)—Outcomes from the Upper GI International Robotic Association (UGIRA) Esophageal Registry

Author

Kooij, Cezanne D., de Jongh , Cas, Kingma, B. Feike, van Berge Henegouwen, Mark I., Gisbertz, Suzanne S., Chao, Yin-Kai, Chiu, Philip W., Rouanet, Philippe, Mourregot, Anne, Immanuel, Arul, Mala, Tom, van Boxel, Gijs I., Carter, Nicholas C., Li, Hecheng, Fuchs, Hans F., Bruns, Christiane J., Giacopuzzi, Simone, Kalff, Jörg C., Hölzen, Jens-Peter, Juratli, Mazen A., Benedix, Frank, Lorenz, Eric, Egberts, Jan-Hendrik, Haveman, Jan W., van Etten, Boudewijn, Müller, Beat P., Grimminger, Peter P., Berlth, Felix, Piessen, Guillaume, van den Berg, Jan W., Milone, Marco, Luketich, James D., Sarkaria, Inderpal S., Sallum, Rubens A. A., van Det, Marc J., Kouwenhoven, Ewout A., Brüwer, Matthias, Harustiak, Tomas, Kinoshita, Takahiro, Fujita, Takeo, Daiko, Hiroyuki, Li, Zhigang, Ruurda, Jelle P., and van Hillegersberg, Richard

Published
2024
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5. ATM inhibition exploits checkpoint defects and ATM-dependent double strand break repair in TP53-mutant glioblastoma

Author

Daniel J. Laverty, Shiv K. Gupta, Gary A. Bradshaw, Alexander S. Hunter, Brett L. Carlson, Nery Matias Calmo, Jiajia Chen, Shulan Tian, Jann N. Sarkaria, and Zachary D. Nagel

Subjects
Science
Abstract

Abstract Determining the balance between DNA double strand break repair (DSBR) pathways is essential for understanding treatment response in cancer. We report a method for simultaneously measuring non-homologous end joining (NHEJ), homologous recombination (HR), and microhomology-mediated end joining (MMEJ). Using this method, we show that patient-derived glioblastoma (GBM) samples with acquired temozolomide (TMZ) resistance display elevated HR and MMEJ activity, suggesting that these pathways contribute to treatment resistance. We screen clinically relevant small molecules for DSBR inhibition with the aim of identifying improved GBM combination therapy regimens. We identify the ATM kinase inhibitor, AZD1390, as a potent dual HR/MMEJ inhibitor that suppresses radiation-induced phosphorylation of DSBR proteins, blocks DSB end resection, and enhances the cytotoxic effects of TMZ in treatment-naïve and treatment-resistant GBMs with TP53 mutation. We further show that a combination of G2/M checkpoint deficiency and reliance upon ATM-dependent DSBR renders TP53 mutant GBMs hypersensitive to TMZ/AZD1390 and radiation/AZD1390 combinations. This report identifies ATM-dependent HR and MMEJ as targetable resistance mechanisms in TP53-mutant GBM and establishes an approach for simultaneously measuring multiple DSBR pathways in treatment selection and oncology research.

Published
2024
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6. Alliance A071401: Phase II Trial of Focal Adhesion Kinase Inhibition in Meningiomas With Somatic NF2 Mutations.

Author

Monga, Varun, Fadul, Camilo, Schiff, David, Taylor, Jennie, Chowdhary, Sajeel, Bettegowda, Chetan, Ansstas, George, De La Fuente, Macarena, Anderson, Mark, Shonka, Nicole, Damek, Denise, Carrillo, Jose, Kunschner-Ronan, Lara, Chaudhary, Rekha, Jaeckle, Kurt, Senecal, Francis, Kaley, Thomas, Morrison, Tara, Thomas, Alissa, Welch, Mary, Iwamoto, Fabio, Cachia, David, Cohen, Adam, Vora, Shivangi, Knopp, Michael, Dunn, Ian, Kumthekar, Priya, Sarkaria, Jann, Geyer, Susan, Carrero, Xiomara, Martinez-Lage, Maria, Cahill, Daniel, Brown, Paul, Giannini, Caterina, Santagata, Sandro, Barker, Frederick, Galanis, Evanthia, Brastianos, Priscilla, Twohy, Erin, Gerstner, Elizabeth, Kaufmann, Timothy, Iafrate, A, Lennerz, Jochen, Jeyapalan, Suriya, and Piccioni, David

Subjects
Humans, Focal Adhesion Protein-Tyrosine Kinases, Meningeal Neoplasms, Meningioma, Mutation, Neoplasm Recurrence, Local
Abstract

PURPOSE: Patients with progressive or recurrent meningiomas have limited systemic therapy options. Focal adhesion kinase (FAK) inhibition has a synthetic lethal relationship with NF2 loss. Given the predominance of NF2 mutations in meningiomas, we evaluated the efficacy of GSK2256098, a FAK inhibitor, as part of the first genomically driven phase II study in recurrent or progressive grade 1-3 meningiomas. PATIENTS AND METHODS: Eligible patients whose tumors screened positively for NF2 mutations were treated with GSK2256098, 750 mg orally twice daily, until progressive disease. Efficacy was evaluated using two coprimary end points: progression-free survival at 6 months (PFS6) and response rate by Macdonald criteria, where PFS6 was evaluated separately within grade-based subgroups: grade 1 versus 2/3 meningiomas. Per study design, the FAK inhibitor would be considered promising in this patient population if either end point met the corresponding decision criteria for efficacy. RESULTS: Of 322 patients screened for all mutation cohorts of the study, 36 eligible and evaluable patients with NF2 mutations were enrolled and treated: 12 grade 1 and 24 grade 2/3 patients. Across all grades, one patient had a partial response and 24 had stable disease as their best response to treatment. In grade 1 patients, the observed PFS6 rate was 83% (10/12 patients; 95% CI, 52 to 98). In grade 2/3 patients, the observed PFS6 rate was 33% (8/24 patients; 95% CI, 16 to 55). The study met the PFS6 efficacy end point both for the grade 1 and the grade 2/3 cohorts. Treatment was well tolerated; seven patients had a maximum grade 3 adverse event that was at least possibly related to treatment with no grade 4 or 5 events. CONCLUSION: GSK2256098 was well tolerated and resulted in an improved PFS6 rate in patients with recurrent or progressive NF2-mutated meningiomas, compared with historical controls. The criteria for promising activity were met, and FAK inhibition warrants further evaluation for this patient population.

Published
2023

7. Detection of Alternative Lengthening of Telomeres via Chromogenic In Situ Hybridization for the Prognostication of PanNETs and Other Neoplasms

Author

Heaphy, Christopher M., Patel, Simmi, Smith, Katelyn, Wondisford, Anne R., Lynskey, Michelle L., O’Sullivan, Roderick J., Fuhrer, Kimberly, Han, Xiaoli, Seethala, Raja R., Liu, Ta-Chiang, Cao, Dengfeng, Ertunc, Onur, Zheng, Qizhi, Stojanova, Marija, Zureikat, Amer H., Paniccia, Alessandro, Lee, Kenneth, Ongchin, Melanie C., Pingpank, James F., Zeh, Herbert J., Hogg, Melissa E., Geller, David, Marsh, James Wallis, Brand, Randall E., Chennat, Jennifer S., Das, Rohit, Fasanella, Kenneth E., Gabbert, Charles, Khalid, Asif, McGrath, Kevin, Lennon, Anne Marie, Sarkaria, Savreet, Singh, Harkirat, Slivka, Adam, Hsu, Dennis, Zhang, Janie Y., Nacev, Benjamin A., Nikiforova, Marina N., Wald, Abigail I., Vaddi, Neel, De Marzo, Angelo M., Singhi, Anju H., Bell, Phoenix D., and Singhi, Aatur D.

Published
2025
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9. Blockade of tumor cell-intrinsic PD-L1 signaling enhances AURKA-targeted therapy in triple negative breast cancer

Author

Andrew Takchi, Minzhi Zhang, Mohammad Jalalirad, Roberto Leon Ferre, Royal Shrestha, Tufia Haddad, Jann Sarkaria, Ann Tuma, Jodi Carter, Hillman David, Karthik Giridhar, Liewei Wang, Carol Lange, Urban Lendahl, James Ingle, Matthew Goetz, and Antonino Bonaventura D’Assoro

Subjects
triple negative breast cancer, immunotherapy, cancer cell plasticity, small molecule inhibitor, organ metastases, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
Abstract

Triple negative breast cancer (TNBC) accounts for 15–20% of all breast cancers and mainly affects pre-menopausal and minority women. Because of the lack of ER, PR or HER2 expression in TNBC, there are limited options for tailored therapies. While TNBCs respond initially to standard of care chemotherapy, tumor recurrence commonly occurs within 1 to 3 years post-chemotherapy and is associated with early organ metastasis and a high incidence of mortality. One of the major mechanisms responsible for drug resistance and emergence of organ metastasis is activation of epithelial to mesenchymal transition (EMT) reprogramming. EMT-mediated cancer cell plasticity also promotes the enrichment of cancer cells with a CD44high/CD24low and/or ALDHhigh cancer stem-like phenotype [cancer stem cells (CSCs)], characterized by an increased capacity for tumor self-renewal, intrinsic drug resistance, immune evasion and metastasis. In this study we demonstrate for the first time a positive feedback loop between AURKA and intra-tumoral PD-L1 oncogenic pathways in TNBC. Genetic targeting of intra-tumoral PD-L1 expression impairs the enrichment of ALDHhigh CSCs and enhances the therapeutic efficacy of AURKA-targeted therapy. Moreover, dual AURKA and PD-L1 pharmacological blockade resulted in the strongest inhibition of tumor growth and organ metastatic burden. Taken together, our findings provide a compelling preclinical rationale for the development of novel combinatorial therapeutic strategies aimed to inhibit cancer cell plasticity, immune evasion capacity and organ metastasis in patients with advanced TNBC.

Published
2024
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12. Endoscopic Management of Anastomotic Leaks

Author

Ackerman, James M., Levy, Ryan M., Sarkaria, Inderpal S., Nguyen, Ninh T., editor, Clarke, John O., editor, Lipham, John C., editor, Chang, Kenneth J., editor, Schnoll-Sussman, Felice, editor, Bell, Reginald C.W., editor, and Kahrilas, Peter J., editor

Published
2023
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14. From the Operating Room to the Laboratory: Role of the Neuroscience Tissue Biorepository in the Clinical, Translational, and Basic Science Research Pipeline

Author

Quiñones-Hinojosa, Alfredo, Basil, Aleeshba, Moniz-Garcia, Diogo, Suarez-Meade, Paola, Ramos, Andres, Jentoft, Mark, Middlebrooks, Erik, Grewal, Sanjeet, Abode-Iyamah, Kingsley, Bydon, Mohamad, Sarkaria, Jann, Dickson, Dennis, Swanson, Kristin, Rosenfeld, Steven, Schiapparelli, Paula, Guerrero-Cazares, Hugo, Chaichana, Kaisorn, and Meyer, Fredric

Published
2024
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18. Blood-brain barrier disruption defines the extracellular metabolome of live human high-grade gliomas

Author

Riviere-Cazaux, Cecile, Carlstrom, Lucas P., Rajani, Karishma, Munoz-Casabella, Amanda, Rahman, Masum, Gharibi-Loron, Ali, Brown, Desmond A., Miller, Kai J., White, Jaclyn J., Himes, Benjamin T., Jusue-Torres, Ignacio, Ikram, Samar, Ransom, Seth C., Hirte, Renee, Oh, Ju-Hee, Elmquist, William F., Sarkaria, Jann N., Vaubel, Rachael A., Rodriguez, Moses, Warrington, Arthur E., Kizilbash, Sani H., and Burns, Terry C.

Published
2023
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19. Blood-brain barrier disruption defines the extracellular metabolome of live human high-grade gliomas

Author

Cecile Riviere-Cazaux, Lucas P. Carlstrom, Karishma Rajani, Amanda Munoz-Casabella, Masum Rahman, Ali Gharibi-Loron, Desmond A. Brown, Kai J. Miller, Jaclyn J. White, Benjamin T. Himes, Ignacio Jusue-Torres, Samar Ikram, Seth C. Ransom, Renee Hirte, Ju-Hee Oh, William F. Elmquist, Jann N. Sarkaria, Rachael A. Vaubel, Moses Rodriguez, Arthur E. Warrington, Sani H. Kizilbash, and Terry C. Burns

Subjects
Biology (General), QH301-705.5
Abstract

Abstract The extracellular microenvironment modulates glioma behaviour. It remains unknown if blood-brain barrier disruption merely reflects or functionally supports glioma aggressiveness. We utilised intra-operative microdialysis to sample the extracellular metabolome of radiographically diverse regions of gliomas and evaluated the global extracellular metabolome via ultra-performance liquid chromatography tandem mass spectrometry. Among 162 named metabolites, guanidinoacetate (GAA) was 126.32x higher in enhancing tumour than in adjacent brain. 48 additional metabolites were 2.05–10.18x more abundant in enhancing tumour than brain. With exception of GAA, and 2-hydroxyglutarate in IDH-mutant gliomas, differences between non-enhancing tumour and brain microdialysate were modest and less consistent. The enhancing, but not the non-enhancing glioma metabolome, was significantly enriched for plasma-associated metabolites largely comprising amino acids and carnitines. Our findings suggest that metabolite diffusion through a disrupted blood-brain barrier may largely define the enhancing extracellular glioma metabolome. Future studies will determine how the altered extracellular metabolome impacts glioma behaviour.

Published
2023
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22. Hybrid laparoscopic versus fully robot-assisted minimally invasive esophagectomy: an international propensity-score matched analysis of perioperative outcome

Author

Jung, Jin-On, de Groot, Eline M., Kingma, B. Feike, Babic, Benjamin, Ruurda, Jelle P., Grimminger, Peter P., Hölzen, Jens P., Chao, Yin-Kai, Haveman, Jan W., van Det, Marc J., Rouanet, Philippe, Benedix, Frank, Li, Hecheng, Sarkaria, Inderpal, van Berge Henegouwen, Mark I., van Boxel, Gijs I., Chiu, Philip, Egberts, Jan-Hendrik, Sallum, Rubens, Immanuel, Arul, Turner, Paul, Low, Donald E., Hubka, Michal, Perez, Daniel, Strignano, Paolo, Biebl, Matthias, Chaudry, M. Asif, Bruns, Christiane J., van Hillegersberg, Richard, and Fuchs, Hans F.

Published
2023
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25. Baseline requirements for novel agents being considered for phase II/III brain cancer efficacy trials: conclusions from the Adult Brain Tumor Consortium’s first workshop on CNS drug delivery

Author

Grossman, Stuart A, Romo, Carlos G, Rudek, Michelle A, Supko, Jeffrey, Fisher, Joy, Nabors, L Burt, Wen, Patrick Y, Peereboom, David M, Ellingson, Benjamin M, Elmquist, William, Barker, Fred G, Kamson, David, Sarkaria, Jann N, Timmer, William, Bindra, Ranjit S, and Ye, Xiaobu

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Adult, Brain Neoplasms, Clinical Trials, Phase II as Topic, Clinical Trials, Phase III as Topic, Drug Delivery Systems, Humans, Pharmaceutical Preparations, Neurosciences, Oncology & Carcinogenesis, Oncology and carcinogenesis
Published
2020

27. Autoimmunity

Author

Jeskey, Jack, Fill, Lauren, Huq, Madiha, Sarkaria, Sandeep, Saab, Remie, Hostoffer, Robert, and Mahmoudi, Massoud, editor

Published
2022
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29. A Combined DNA/RNA-based Next-Generation Sequencing Platform to Improve the Classification of Pancreatic Cysts and Early Detection of Pancreatic Cancer Arising From Pancreatic Cysts

Author

Nikiforova, Marina N., Wald, Abigail I., Spagnolo, Daniel M., Melan, Melissa A., Grupillo, Maria, Lai, Yi-Tak, Brand, Randall E., O’Broin-Lennon, Anne Marie, McGrath, Kevin, Park, Walter G., Pfau, Patrick R., Polanco, Patricio M., Kubiliun, Nisa, DeWitt, John, Easler, Jeffrey J., Dam, Aamir, Mok, Shaffer R., Wallace, Michael B., Kumbhari, Vivek, Boone, Brian A., Marsh, Wallis, Thakkar, Shyam, Fairley, Kimberly J., Afghani, Elham, Bhat, Yasser, Ramrakhiani, Sanjay, Nasr, John, Skef, Wasseem, Thiruvengadam, Nikhil R., Khalid, Asif, Fasanella, Kenneth, Chennat, Jennifer, Das, Rohit, Singh, Harkirat, Sarkaria, Savreet, Slivka, Adam, Gabbert, Charles, Sawas, Tarek, Tielleman, Thomas, Vanderveldt, Hendrikus Dutch, Tavakkoli, Anna, Smith, Lynette M., Smith, Katelyn, Bell, Phoenix D., Hruban, Ralph H., Paniccia, Alessandro, Zureikat, Amer, Lee, Kenneth K., Ongchin, Melanie, Zeh, Herbert, Minter, Rebecca, He, Jin, Nikiforov, Yuri E., and Singhi, Aatur D.

Published
2023
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31. Prospective, Multi-Institutional, Real-Time Next-Generation Sequencing of Pancreatic Cyst Fluid Reveals Diverse Genomic Alterations That Improve the Clinical Management of Pancreatic Cysts

Author

Paniccia, Alessandro, Polanco, Patricio M., Boone, Brian A., Wald, Abigail I., McGrath, Kevin, Brand, Randall E., Khalid, Asif, Kubiliun, Nisa, O'Broin-Lennon, Anne Marie, Park, Walter G., Klapman, Jason, Tharian, Benjamin, Inamdar, Sumant, Fasanella, Kenneth, Nasr, John, Chennat, Jennifer, Das, Rohit, DeWitt, John, Easler, Jeffrey J., Bick, Benjamin, Singh, Harkirat, Fairley, Kimberly J., Sarkaria, Savreet, Sawas, Tarek, Skef, Wasseem, Slivka, Adam, Tavakkoli, Anna, Thakkar, Shyam, Kim, Victoria, Vanderveldt, Hendrikus Dutch, Richardson, Allyson, Wallace, Michael B., Brahmbhatt, Bhaumik, Engels, Megan, Gabbert, Charles, Dugum, Mohannad, El-Dika, Samer, Bhat, Yasser, Ramrakhiani, Sanjay, Bakis, Gennadiy, Rolshud, Daniil, Millspaugh, Gordon, Tielleman, Thomas, Schmidt, Carl, Mansour, John, Marsh, Wallis, Ongchin, Melanie, Centeno, Barbara, Monaco, Sara E., Ohori, N. Paul, Lajara, Sigfred, Thompson, Elizabeth D., Hruban, Ralph H., Bell, Phoenix D., Smith, Katelyn, Permuth, Jennifer B., Vandenbussche, Christopher, Ernst, Wayne, Grupillo, Maria, Kaya, Cihan, Hogg, Melissa, He, Jin, Wolfgang, Christopher L., Lee, Kenneth K., Zeh, Herbert, Zureikat, Amer, Nikiforova, Marina N., and Singhi, Aatur D.

Published
2023
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32. A Syx-RhoA-Dia1 signaling axis regulates cell cycle progression, DNA damage, and therapy resistance in glioblastoma

Author

Wan-Hsin Lin, Ryan W. Feathers, Lisa M. Cooper, Laura J. Lewis-Tuffin, Jiaxiang Chen, Jann N. Sarkaria, and Panos Z. Anastasiadis

Subjects
Oncology, Medicine
Abstract

Glioblastomas (GBM) are aggressive tumors that lack effective treatments. Here, we show that the Rho family guanine nucleotide exchange factor Syx promotes GBM cell growth both in vitro and in orthotopic xenografts derived from patients with GBM. Growth defects upon Syx depletion are attributed to prolonged mitosis, increased DNA damage, G2/M cell cycle arrest, and cell apoptosis, mediated by altered mRNA and protein expression of various cell cycle regulators. These effects are phenocopied by depletion of the Rho downstream effector Dia1 and are due, at least in part, to increased phosphorylation, cytoplasmic retention, and reduced activity of the YAP/TAZ transcriptional coactivators. Furthermore, targeting Syx signaling cooperates with radiation treatment and temozolomide (TMZ) to decrease viability in GBM cells, irrespective of their inherent response to TMZ. The data indicate that a Syx-RhoA-Dia1-YAP/TAZ signaling axis regulates cell cycle progression, DNA damage, and therapy resistance in GBM and argue for its targeting for cancer treatment.

Published
2023
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33. EGFR ligand shifts the role of EGFR from oncogene to tumour suppressor in EGFR-amplified glioblastoma by suppressing invasion through BIN3 upregulation

Author

Guo, Gao, Gong, Ke, Beckley, Nicole, Zhang, Yue, Yang, Xiaoyao, Chkheidze, Rati, Hatanpaa, Kimmo J., Garzon-Muvdi, Tomas, Koduru, Prasad, Nayab, Arifa, Jenks, Jennifer, Sathe, Adwait Amod, Liu, Yan, Xing, Chao, Wu, Shwu-Yuan, Chiang, Cheng-Ming, Mukherjee, Bipasha, Burma, Sandeep, Wohlfeld, Bryan, Patel, Toral, Mickey, Bruce, Abdullah, Kalil, Youssef, Michael, Pan, Edward, Gerber, David E., Tian, Shulan, Sarkaria, Jann N., McBrayer, Samuel K., Zhao, Dawen, and Habib, Amyn A.

Published
2022
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34. The medical necessity of advanced molecular testing in the diagnosis and treatment of brain tumor patients

Author

Horbinski, Craig, Ligon, Keith L, Brastianos, Priscilla, Huse, Jason T, Venere, Monica, Chang, Susan, Buckner, Jan, Cloughesy, Timothy, Jenkins, Robert B, Giannini, Caterina, Stupp, Roger, Nabors, L Burt, Wen, Patrick Y, Aldape, Kenneth J, Lukas, Rimas V, Galanis, Evanthia, Eberhart, Charles G, Brat, Daniel J, and Sarkaria, Jann N

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Brain Cancer, Clinical Research, Cancer, Genetics, Human Genome, Neurosciences, Brain Disorders, Neurological, Good Health and Well Being, Biomarkers, Tumor, Brain Neoplasms, Humans, Pathology, Molecular, Prognosis, embryona, ependymoma, glioma, meningioma, molecular, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

Accurate pathologic diagnoses and molecularly informed treatment decisions for a wide variety of cancers depend on robust clinical molecular testing that uses genomic, epigenomic, and transcriptomic-based tools. Nowhere is this more essential than in the workup of brain tumors, as emphasized by the incorporation of molecular criteria into the 2016 World Health Organization classification of central nervous system tumors and the updated official guidelines of the National Comprehensive Cancer Network. Despite the medical necessity of molecular testing in brain tumors, access to and utilization of molecular diagnostics is still highly variable across institutions, and a lack of reimbursement for such testing remains a significant obstacle. The objectives of this review are (i) to identify barriers to adoption of molecular testing in brain tumors, (ii) to describe the current molecular tools recommended for the clinical evaluation of brain tumors, and (iii) to summarize how molecular data are interpreted to guide clinical care, so as to improve understanding and justification for their coverage in the routine workup of adult and pediatric brain tumor cases.

Published
2019

35. Forced Marriage

Author

Campbell, Gerry, Roberts, Karl A., Sarkaria, Neelam, Campbell, Gerry, Roberts, Karl A., and Sarkaria, Neelam

Published
2020
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40. Breast Ironing

Author

Campbell, Gerry, Roberts, Karl A., Sarkaria, Neelam, Campbell, Gerry, Roberts, Karl A., and Sarkaria, Neelam

Published
2020
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46. Introduction

Author

Campbell, Gerry, Roberts, Karl A., Sarkaria, Neelam, Campbell, Gerry, Roberts, Karl A., and Sarkaria, Neelam

Published
2020
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47. Cardiopulmonary Toxicity Following Intensity-Modulated Proton Therapy (IMPT) Versus Intensity-Modulated Radiation Therapy (IMRT) for Stage III Non-Small Cell Lung Cancer

Author

Yu, Nathan Y., DeWees, Todd A., Voss, Molly M., Breen, William G., Chiang, Jennifer S., Ding, Julia X., Daniels, Thomas B., Owen, Dawn, Olivier, Kenneth R., Garces, Yolanda I., Park, Sean S., Sarkaria, Jann N., Yang, Ping, Savvides, Panayiotis S., Ernani, Vinicius, Liu, Wei, Schild, Steven E., Merrell, Kenneth W., and Sio, Terence T.

Published
2022
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