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Churpek, Jane E

0000-0001-7998-5479

Mayo Clinic

Division of Hematology, Medical Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health and University of Wisconsin Carbone Cancer Center, Madison, Wisconsin, USA.

Citations 6

NCCN Guidelines® Insights: Genetic/Familial High-Risk Assessment: Breast, Ovarian, Pancreatic, and Prostate, Version 2.2026
Cheng, Heather H., Goggins, Michael, Yurgelun, Matthew B. , Karlan, Beth Y., Norquist, Barbara S., Daly, MB, Pal, Tuya, AlHilli, Zahraa, Arun, Banu , Churpek, Jane, Colonna, Sarah, Domchek, Susan M., Escobar, Mauricio R., Friedman, S, Hagemann, Andrea, Hendrix, Ashley, Huo, Dezheng, Hutton, Mollie L., Kassem, Nawal , Kurian, Allison W., Laronga, Christine , Mak, Julie S, McDonnell, Kevin, Mersch, Jacqueline, Offit, Kenneth, Plichta, Jennifer K. , Rash, Dominique , Reiser, Gwen , Senter-Jamieson, Leigha, Shannon, K. McWeeney, Welborn, Jeanna, Wick, Myra , Wood, Marie , Darlow, Susan, Diwan, Zeenat, Dwyer, Mary, Churpek, Jane E. , Kurian, Allison W. , Kurian, Allison W , Plichta, Jennifer K , Churpek, Jane E , Churpek, Jane , Giri, Veda N. , Goggins, Michael, Karlan, Beth Y , Norquist, Barbara, Pal, Tuya , Al‐Hilli, Zahraa , Arun, Banu , Colonna, Sarah V. , Domchek, Susan M. , Fejerman, Laura , Hagemann, Andrea, Huo, Dezheng , Khan, Seema A. , Mak, Julie , Maxwell, Kara N. , McDonnell, Kevin , Merajver, Sofía D. , Mersch, Jacqueline A, Offit, Kenneth , Darlow, Susan

Journal of the National Comprehensive Cancer Network | February 9, 2026 | Volume: 24 | Issue: 2 | Pages: 2-10

10.6004/jnccn.2026.0007 Get It

The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Genetic/Familial High-Risk Assessment: Breast, Ovarian, Pancreatic, and Prostate are intended to serve as a resource for health care providers to identify individuals who may benefit from cancer risk assessment and genetic counseling and testing; help guide decisions related to genetic testing; and facilitate a multidisciplinary approach in the comprehensive care of individuals at increased risk for hereditary breast, ovarian, pancreatic, and prostate cancer. The current guidelines focus primarily on assessment of pathogenic and likely pathogenic (P/LP) variants associated with increased risk of breast, ovarian, pancreatic, and prostate cancer and recommended approaches to genetic counseling/testing and care strategies in individuals with these P/LP variants associated with increased risk of these cancers. These NCCN Guidelines Insights summarize the panel’s most recent recommendations regarding screening for prostate cancer and pancreas cancer, as well as testing criteria for nonepithelial ovarian cancer.
Reducing clinical trial eligibility barriers for patients with MDS: an icMDS position statement
Borate, Uma , Pugh, Kelly , Waller, Allyson, Welkie, Rina Li , Huang, Ying , Stahl, Maximilian , Platzbecker, Uwe , Wei, Andrew H. , Buckstein, Rena , Hasserjian, Robert P. , Fenaux, Pierre , Sallman, David A. , Nimer, Stephen D. , Little, Richard F. , Garcia‐Manero, Guillermo , Odenike, Olatoyosi, Kim, Tae Kon , Greenberg, Peter L. , Xu, Mina L. , Patnaik, Mrinal M. , Padron, Eric , Gore, Steven D. , Churpek, Jane E. , Bennett, John M., Brunner, Andrew M. , Zeidan, Amer M., Zeidan, Amer M. , Platzbecker, Uwe , Sekeres, Mikkael A , Wei, Andrew H , Roboz, Gail J , Loghavi, Sanam , Hasserjian, Robert P , Sallman, David A , Hourigan, Christopher S , Della Porta, Matteo Giovanni , Little, Richard F , Santini, Valeria , Taylor, Justin , Kim, Tae Kon , Halene, Stephanie , Komrokji, Rami S , Griffiths, Elizabeth A. , Greenberg, Peter L , Xie, Zhuoer , Sanz, Guillermo F , Patnaik, Mrinal , Carraway, Hetty E. , Boultwood, Jacqueline , Daver, Naval , Zeidan, Amer M , Churpek, Jane E , Bewersdorf, Jan Philipp , Dezern, Amy Elizabeth , Sekeres, Mikkael A. , Roboz, Gail J. , Savona, Michael R. , Loghavi, Sanam , Hourigan, Christopher S. , Santini, Valeria , Efficace, Fabio , Odenike, Olatoyosi , Komrokji, Rami S. , Xie, Zhuoer , Bejar, Rafael , Sanz, Guillermo , Figueroa, María E. , Abdel‐Wahab, Omar , Starczynowski, Daniel T. , Boultwood, Jacqueline , Daver, Naval , Majeti, Ravindra , List, Alan F. , Brunner, Andrew M., Churpek, Jane

Blood | March 27, 2025 | Volume: 145 | Issue: 13 | Pages: 1369-1381

10.1182/blood.2023023717 Get It

Abstract Excessively restrictive inclusion and exclusion criteria in clinical trials are one of many barriers to clinical trial enrollment for patients with myelodysplastic syndromes/neoplasms (MDSs). Many organizations are developing efforts to increase clinical trial eligibility; yet, several recent publications focused on patients with MDS suggest that many patients with this disease may be excluded from clinical trials unnecessarily. Clinical trial eligibility should reflect the phase of the study and risks of the agent being studied. Phase 3 trials should be less restrictive than early-phase trials to represent the real-world population as closely as possible. We hypothesize that many clinical trials, particularly phase 3 trials, have unnecessarily restrictive eligibility criteria. This study aims to evaluate the most common eligibility criteria according to phase of trial and to determine whether criteria correspond with drug safety signals. We identified MDS clinical trials registered on ClinicalTrials.gov from 1 January 2000 to 1 September 2023 and analyzed the eligibility criteria of 191 therapeutic MDS trials. We found that categorical inclusion and exclusion criteria are remarkably similar in representation across trial phases. Additionally, only 13% of trials are concordant with drug safety signals, suggesting that the eligibility criteria are often arbitrary. On behalf of the icMDS (International Consortium for Myelodysplastic Syndromes), an association of international MDS experts, we provide a position statement on restrictive eligibility criteria for MDS clinical trials that should be avoided with the aim of removing barriers to clinical trial enrollment.
NCCN Guidelines® Insights: Genetic/Familial High-Risk Assessment: Breast, Ovarian, and Pancreatic, Version 2.2024
Churpek, Jane , Kohlmann, Wendy , Al‐Hilli, Zahraa , Friedman, Susan , Hagemann, Andrea R. , Hendrix, Ashley, Hutton, Mollie L., Kassem, Nawal , Khan, Seema, Khoury, Katia , Kurian, Allison W. , Laronga, Christine , Mak, Julie , Mansour, John C. , McDonnell, Kevin , Menendez, Carolyn S. , Merajver, Sofía D. , Norquist, Barbara S., Offit, Kenneth , Rash, Dominique , Reiser, Gwen , Senter-Jamieson, Leigha, Shannon, Kristen M. , Visvanathan, Kala , Welborn, Jeanna, Wick, Myra , Wood, Marie , Yurgelun, Matthew B. , Dwyer, Mary A., Darlow, Susan, Norquist, Barbara M. , Churpek, Jane E. , Visvanathan, Kala , Kurian, Allison W , Norquist, Barbara , Churpek, Jane E , Daly, Mary Beryl , Pal, Tuya , Maxwell, Kara N. , Arun, Banu , Buys, Saundra S. , Cheng, Heather H. , Domchek, Susan M. , Giri, Veda N. , Goggins, Michael , Karlan, Beth Y.

Journal of the National Comprehensive Cancer Network | October 12, 2023 | Volume: 21 | Issue: 10 | Pages: 1000-1010

10.6004/jnccn.2023.0051 Get It

The NCCN Guidelines for Genetic/Familial High-Risk Assessment: Breast, Ovarian, and Pancreatic focus primarily on assessment of pathogenic/likely pathogenic (P/LP) variants associated with increased risk of breast, ovarian, pancreatic, and prostate cancer, including BRCA1 , BRCA2 , CDH1 , PALB2 , PTEN , and TP53 , and recommended approaches to genetic counseling/testing and care strategies in individuals with these P/LP variants. These NCCN Guidelines Insights summarize important updates regarding: (1) a new section for transgender, nonbinary and gender diverse people who have a hereditary predisposition to cancer focused on risk reduction strategies for ovarian cancer, uterine cancer, prostate cancer, and breast cancer; and (2) testing criteria and management associated with TP53 P/LP variants and Li-Fraumeni syndrome.
An agenda to advance research in myelodysplastic syndromes: a TOP 10 priority list from the first international workshop in MDS
Stahl, Maximilian , Wei, Andrew H. , Savona, Michael R. , Xu, Mina L. , Xie, Zhuoer , Sanz, Guillermo , Sallman, David A. , Patnaik, Mrinal M. , Padron, Eric , Odenike, Olatoyosi , Nazha, Aziz , Nimer, Stephen D. , Majeti, Ravindra , Little, Richard F. , Gore, Steven D. , Kutchroo, Vijay, Kim, Tae Kon , Kim, Nina , Hasserjian, Robert P. , Greenberg, Peter L. , Fenaux, Pierre , Churpek, Jane E. , Brunner, Andrew M. , Borate, Uma , Bennett, John M. , Platzbecker, Uwe , Buckstein, Rena , Zeidan, Amer M. , Wei, Andrew H , Savona, Michael R , Xie, Zhuoer , Taylor, Justin , Sanz, Guillermo F , Santini, Valeria , Roboz, Gail J , Patnaik, Mrinal , Little, Richard F , Komrokji, Rami S , Kim, Tae Kon , Kim, Nina , Hourigan, Christopher S , Halene, Stephanie , Griffiths, Elizabeth A. , Greenberg, Peter L , Daver, Naval , Carraway, Hetty E. , Bejar, Rafael , Boultwood, Jacqueline , Loghavi, Sanam , Platzbecker, Uwe , Steensma, David P , Majeti, Ravindra , Zeidan, Amer M , Churpek, Jane E , Abdel‐Wahab, Omar , Starczynowski, Daniel T. , Santini, Valeria , Roboz, Gail J. , List, Alan F. , Komrokji, Rami S. , Hourigan, Christopher S. , Figueroa, María E. , Efficace, Fabio , Dezern, Amy Elizabeth , Della Porta, Matteo Giovanni , Daver, Naval , Boultwood, Jacqueline , Loghavi, Sanam , Bewersdorf, Jan Philipp , Steensma, David P. , Sekeres, Mikkael A. , Churpek, Jane

Blood Advances | October 19, 2022 | Volume: 7 | Issue: 12 | Pages: 2709-2714

10.1182/bloodadvances.2022008747 Get It

Germline Lysine-Specific Demethylase 1 ( LSD1/KDM1A ) Mutations Confer Susceptibility to Multiple Myeloma
Wei, Xiaomu , Calvo-Vidal, M. Nieves, Chen, Siwei , Wu, Gang , Revuelta, María V. , Zhang, Jinghui , Walsh, Michael F. , Nichols, Kim E. , Vijai, Joseph , Snyder, Carrie, Vachon, Celine M. , McKay, James , Wang, Shuping , Jayabalan, David , Jacobs, Lauren , Becirovic, Dina, Waller, Rosalie G., Artomov, Mykyta , Viale, Agnès , Patel, Jayeshkumar , Curtin, Karen , Salama, Mohamed E. , Atanackovic, Djordje , Niesvizky, Rubén, Godley, Lucy A. , Churpek, Jane E. , Dumontet, Charles , Lynch, Henry T., Camp, Nicola J. , Offit, Kenneth , Klein, Robert J. , Lipkin, Steven M. , Waller, Rosalie G. , Griffin, R. L. , Joseph, Vijai , Revuelta, Maria , Waller, Rosalie G , Godley, Lucy A , Sun, Jian Hua , Vachon, Celine M. , Waller, Rosalie G., Phillip, Jude M. , Chen‐Kiang, Selina , Landgren, Ola , Slager, Susan L. , Garber, Judy E. , Anderson, Kenneth C. , Daly, Mark J. , Roeder, Robert G. , Mullighan, Charles G. , Yu, Haiyuan , Cerchietti, Leandro C. A. , Wu, Gang , Nichols, Kim E , Griffin, Rosalie , Klein, Robert , Churpek, Jane E , Churpek, Jane

Cancer Research | March 20, 2018 | Volume: 78 | Issue: 10 | Pages: 2747-2759

10.1158/0008-5472.can-17-1900 Get It

Abstract Given the frequent and largely incurable occurrence of multiple myeloma, identification of germline genetic mutations that predispose cells to multiple myeloma may provide insight into disease etiology and the developmental mechanisms of its cell of origin, the plasma cell (PC). Here, we identified familial and early-onset multiple myeloma kindreds with truncating mutations in lysine-specific demethylase 1 (LSD1/KDM1A), an epigenetic transcriptional repressor that primarily demethylates histone H3 on lysine 4 and regulates hematopoietic stem cell self-renewal. In addition, we found higher rates of germline truncating and predicted deleterious missense KDM1A mutations in patients with multiple myeloma unselected for family history compared with controls. Both monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma cells have significantly lower KDM1A transcript levels compared with normal PCs. Transcriptome analysis of multiple myeloma cells from KDM1A mutation carriers shows enrichment of pathways and MYC target genes previously associated with myeloma pathogenesis. In mice, antigen challenge followed by pharmacologic inhibition of KDM1A promoted PC expansion, enhanced secondary immune response, elicited appearance of serum paraprotein, and mediated upregulation of MYC transcriptional targets. These changes are consistent with the development of MGUS. Collectively, our findings show that KDM1A is the first autosomal-dominant multiple myeloma germline predisposition gene providing new insights into its mechanistic roles as a tumor suppressor during post-germinal center B-cell differentiation. Significance: KDM1A is the first germline autosomal dominant predisposition gene identified in multiple myeloma and provides new insights into multiple myeloma etiology and the mechanistic role of KDM1A as a tumor suppressor during post-germinal center B-cell differentiation. Cancer Res; 78(10); 2747–59. ©2018 AACR.