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4. Combined Associations of a Polygenic Risk Score and Classical Risk Factors With Breast Cancer Risk.

Author

Kapoor, Pooja Middha, Mavaddat, Nasim, Choudhury, Parichoy Pal, Wilcox, Amber N, Lindström, Sara, Behrens, Sabine, Michailidou, Kyriaki, Dennis, Joe, Bolla, Manjeet K, Wang, Qin, Jung, Audrey, Abu-Ful, Zomoroda, Ahearn, Thomas, Andrulis, Irene L, Anton-Culver, Hoda, Arndt, Volker, Aronson, Kristan J, Auer, Paul L, Freeman, Laura E Beane, Becher, Heiko, Beckmann, Matthias W, Beeghly-Fadiel, Alicia, Benitez, Javier, Bernstein, Leslie, Bojesen, Stig E, Brauch, Hiltrud, Brenner, Hermann, Brüning, Thomas, Cai, Qiuyin, Campa, Daniele, Canzian, Federico, Carracedo, Angel, Carter, Brian D, Castelao, Jose E, Chanock, Stephen J, Chatterjee, Nilanjan, Chenevix-Trench, Georgia, Clarke, Christine L, Couch, Fergus J, Cox, Angela, Cross, Simon S, Czene, Kamila, Dai, James Y, Earp, H Shelton, Ekici, Arif B, Eliassen, A Heather, Eriksson, Mikael, Evans, D Gareth, Fasching, Peter A, Figueroa, Jonine, Fritschi, Lin, Gabrielson, Marike, Gago-Dominguez, Manuela, Gao, Chi, Gapstur, Susan M, Gaudet, Mia M, Giles, Graham G, González-Neira, Anna, Guénel, Pascal, Haeberle, Lothar, Haiman, Christopher A, Håkansson, Niclas, Hall, Per, Hamann, Ute, Hatse, Sigrid, Heyworth, Jane, Holleczek, Bernd, Hoover, Robert N, Hopper, John L, Howell, Anthony, Hunter, David J, ABCTB Investigators, kConFab/AOCS Investigators, John, Esther M, Jones, Michael E, Kaaks, Rudolf, Keeman, Renske, Kitahara, Cari M, Ko, Yon-Dschun, Koutros, Stella, Kurian, Allison W, Lambrechts, Diether, Le Marchand, Loic, Lee, Eunjung, Lejbkowicz, Flavio, Linet, Martha, Lissowska, Jolanta, Llaneza, Ana, MacInnis, Robert J, Martinez, Maria Elena, Maurer, Tabea, McLean, Catriona, Neuhausen, Susan L, Newman, William G, Norman, Aaron, O'Brien, Katie M, Olshan, Andrew F, Olson, Janet E, Olsson, Håkan, and Orr, Nick

Subjects
ABCTB Investigators, kConFab/AOCS Investigators, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract

We evaluated the joint associations between a new 313-variant PRS (PRS313) and questionnaire-based breast cancer risk factors for women of European ancestry, using 72 284 cases and 80 354 controls from the Breast Cancer Association Consortium. Interactions were evaluated using standard logistic regression and a newly developed case-only method for breast cancer risk overall and by estrogen receptor status. After accounting for multiple testing, we did not find evidence that per-standard deviation PRS313 odds ratio differed across strata defined by individual risk factors. Goodness-of-fit tests did not reject the assumption of a multiplicative model between PRS313 and each risk factor. Variation in projected absolute lifetime risk of breast cancer associated with classical risk factors was greater for women with higher genetic risk (PRS313 and family history) and, on average, 17.5% higher in the highest vs lowest deciles of genetic risk. These findings have implications for risk prevention for women at increased risk of breast cancer.

Published
2021

5. Assessment of interactions between 205 breast cancer susceptibility loci and 13 established risk factors in relation to breast cancer risk, in the Breast Cancer Association Consortium

Author

Kapoor, Pooja Middha, Lindström, Sara, Behrens, Sabine, Wang, Xiaoliang, Michailidou, Kyriaki, Bolla, Manjeet K, Wang, Qin, Dennis, Joe, Dunning, Alison M, Pharoah, Paul DP, Schmidt, Marjanka K, Kraft, Peter, García-Closas, Montserrat, Easton, Douglas F, Milne, Roger L, Chang-Claude, Jenny, Ahearn, Thomas, Andrulis, Irene L, Anton-Culver, Hoda, Arndt, Volker, Aronson, Kristan J, Auer, Paul L, Augustinsson, Annelie, Freeman, Laura E Beane, Beckmann, Matthias W, Benitez, Javier, Bernstein, Leslie, Berrandou, Takiy, Bojesen, Stig E, Brauch, Hiltrud, Brenner, Hermann, Brock, Ian W, Broeks, Annegien, Brooks-Wilson, Angela, Butterbach, Katja, Cai, Qiuyin, Campa, Daniele, Canzian, Federico, Carter, Brian D, Castelao, Jose E, Chanock, Stephen J, Chenevix-Trench, Georgia, Cheng, Ting-Yuan David, Clarke, Christine L, Cordina-Duverger, Emilie, Couch, Fergus J, Cox, Angela, Cross, Simon S, Czene, Kamila, Dai, James Y, Dite, Gillian S, Earp, H Shelton, Eliassen, A Heather, Eriksson, Mikael, Evans, D Gareth, Fasching, Peter A, Figueroa, Jonine, Flyger, Henrik, Fritschi, Lin, Gabrielson, Marike, Gago-Dominguez, Manuela, Gapstur, Susan M, Gaudet, Mia M, Giles, Graham G, González-Neira, Anna, Grundy, Anne, Guénel, Pascal, Haeberle, Lothar, Haiman, Christopher A, Håkansson, Niclas, Hall, Per, Hamann, Ute, Hankinson, Susan E, Harkness, Elaine F, Harstad, Tricia, He, Wei, Heyworth, Jane, Hoover, Robert N, Hopper, John L, Humphreys, Keith, Hunter, David J, Marrón, Pablo Isidro, John, Esther M, Jones, Michael E, Jung, Audrey, Kaaks, Rudolf, Keeman, Renske, Kitahara, Cari M, Ko, Yon-Dschun, Koutros, Stella, Krüger, Ute, Lambrechts, Diether, Le Marchand, Loic, Lee, Eunjung, Lejbkowicz, Flavio, Linet, Martha, Lissowska, Jolanta, Llaneza, Ana, Lo, Wing-Yee, and Makalic, Enes

Subjects
Genetics, Estrogen, Clinical Research, Cancer, Breast Cancer, Prevention, 2.1 Biological and endogenous factors, Aetiology, Alleles, Breast Neoplasms, Case-Control Studies, Europe, Factor XIII, Female, Gene-Environment Interaction, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Polymorphism, Single Nucleotide, Receptors, Estrogen, Risk Factors, White People, Breast Cancer Association Consortium, Europeans, Gene-environment interaction, breast cancer, epidemiology, risk factors, single nucleotide polymorphism, Statistics, Public Health and Health Services, Epidemiology
Abstract

BackgroundPrevious gene-environment interaction studies of breast cancer risk have provided sparse evidence of interactions. Using the largest available dataset to date, we performed a comprehensive assessment of potential effect modification of 205 common susceptibility variants by 13 established breast cancer risk factors, including replication of previously reported interactions.MethodsAnalyses were performed using 28 176 cases and 32 209 controls genotyped with iCOGS array and 44 109 cases and 48 145 controls genotyped using OncoArray from the Breast Cancer Association Consortium (BCAC). Gene-environment interactions were assessed using unconditional logistic regression and likelihood ratio tests for breast cancer risk overall and by estrogen-receptor (ER) status. Bayesian false discovery probability was used to assess the noteworthiness of the meta-analysed array-specific interactions.ResultsNoteworthy evidence of interaction at ≤1% prior probability was observed for three single nucleotide polymorphism (SNP)-risk factor pairs. SNP rs4442975 was associated with a greater reduction of risk of ER-positive breast cancer [odds ratio (OR)int = 0.85 (0.78-0.93), Pint = 2.8 x 10-4] and overall breast cancer [ORint = 0.85 (0.78-0.92), Pint = 7.4 x 10-5) in current users of estrogen-progesterone therapy compared with non-users. This finding was supported by replication using OncoArray data of the previously reported interaction between rs13387042 (r2 = 0.93 with rs4442975) and current estrogen-progesterone therapy for overall disease (Pint = 0.004). The two other interactions suggested stronger associations between SNP rs6596100 and ER-negative breast cancer with increasing parity and younger age at first birth.ConclusionsOverall, our study does not suggest strong effect modification of common breast cancer susceptibility variants by established risk factors.

Published
2020

7. Associations of obesity and circulating insulin and glucose with breast cancer risk: a Mendelian randomization analysis.

Author

Shu, Xiang, Wu, Lang, Khankari, Nikhil K, Shu, Xiao-Ou, Wang, Thomas J, Michailidou, Kyriaki, Bolla, Manjeet K, Wang, Qin, Dennis, Joe, Milne, Roger L, Schmidt, Marjanka K, Pharoah, Paul DP, Andrulis, Irene L, Hunter, David J, Simard, Jacques, Easton, Douglas F, Zheng, Wei, Alicia, Beeghly-Fadiel J, Anton-Culver, Hoda, Antonenkova, Natalia N, Arndt, Volker, Aronson, Kristan J, Auer, Paul L, Barrdahl, Myrto, Baynes, Caroline, Beane Freeman, Laura E, Beckmann, Matthias W, Behrens, Sabine, Benitez, Javier, Bermisheva, Marina, Blomqvist, Carl, Bogdanova, Natalia V, Bojesen, Stig E, Brauch, Hiltrud, Brenner, Hermann, Brinton, Louise, Broberg, Per, Brucker, Sara Y, Brüning, Thomas, Burwinkel, Barbara, Cai, Qiuyin, Caldés, Trinidad, Canzian, Federico, Carter, Brian D, Castelao, Jose E, Chang-Claude, Jenny, Chenevix-Trench, Georgia, David Cheng, Ting-Yuan, Clarke, Christine L, Conroy, Don M, Couch, Fergus J, Cox, David G, Cox, Angela, Cross, Simon S, Cunningham, Julie M, Czene, Kamila, Daly, Mary B, Doheny, Kimberly F, Dörk, Thilo, dos-Santos-Silva, Isabel, Dumont, Martine, Dunning, Alison M, Dwek, Miriam, Earp, H Shelton, Eccles, Diana M, Heather Eliassen, A, Engel, Christoph, Eriksson, Mikael, Gareth Evans, D, Fachal, Laura, Fasching, Peter A, Figueroa, Jonine, Fletcher, Olivia, Flyger, Henrik, Fritschi, Lin, Gabrielson, Marike, Gago-Dominguez, Manuela, Gapstur, Susan M, García-Closas, Montserrat, Gaudet, Mia M, Ghoussaini, Maya, Giles, Graham G, Goldberg, Mark S, Goldgar, David E, González-Neira, Anna, Guénel, Pascal, Hahnen, Eric, Haiman, Christopher A, Håkansson, Niclas, Hall, Per, Hallberg, Emily, Hamann, Ute, Harrington, Patricia, He, Wei, Hein, Alexander, Hicks, Belynda, Hillemanns, Peter, Hogervorst, Frans B, Hollestelle, Antoinette, and Hoover, Robert N

Subjects
Clinical Research, Diabetes, Prevention, Nutrition, Obesity, Cancer, Aging, Breast Cancer, Genetics, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Adult, Aged, Blood Glucose, Body Mass Index, Breast Neoplasms, Diabetes Mellitus, Type 2, Female, Humans, Insulin, Mendelian Randomization Analysis, Middle Aged, Obesity, Abdominal, Waist-Hip Ratio, Breast cancer, insulin, glucose, obesity, genetics, Mendelian randomization analysis, Breast Cancer Association Consortium, Statistics, Public Health and Health Services, Epidemiology
Abstract

BackgroundIn addition to the established association between general obesity and breast cancer risk, central obesity and circulating fasting insulin and glucose have been linked to the development of this common malignancy. Findings from previous studies, however, have been inconsistent, and the nature of the associations is unclear.MethodsWe conducted Mendelian randomization analyses to evaluate the association of breast cancer risk, using genetic instruments, with fasting insulin, fasting glucose, 2-h glucose, body mass index (BMI) and BMI-adjusted waist-hip-ratio (WHRadj BMI). We first confirmed the association of these instruments with type 2 diabetes risk in a large diabetes genome-wide association study consortium. We then investigated their associations with breast cancer risk using individual-level data obtained from 98 842 cases and 83 464 controls of European descent in the Breast Cancer Association Consortium.ResultsAll sets of instruments were associated with risk of type 2 diabetes. Associations with breast cancer risk were found for genetically predicted fasting insulin [odds ratio (OR) = 1.71 per standard deviation (SD) increase, 95% confidence interval (CI) = 1.26-2.31, p  =  5.09  ×  10-4], 2-h glucose (OR = 1.80 per SD increase, 95% CI = 1.3 0-2.49, p  =  4.02  ×  10-4), BMI (OR = 0.70 per 5-unit increase, 95% CI = 0.65-0.76, p  =  5.05  ×  10-19) and WHRadj BMI (OR = 0.85, 95% CI = 0.79-0.91, p  =  9.22  ×  10-6). Stratified analyses showed that genetically predicted fasting insulin was more closely related to risk of estrogen-receptor [ER]-positive cancer, whereas the associations with instruments of 2-h glucose, BMI and WHRadj BMI were consistent regardless of age, menopausal status, estrogen receptor status and family history of breast cancer.ConclusionsWe confirmed the previously reported inverse association of genetically predicted BMI with breast cancer risk, and showed a positive association of genetically predicted fasting insulin and 2-h glucose and an inverse association of WHRadj BMI with breast cancer risk. Our study suggests that genetically determined obesity and glucose/insulin-related traits have an important role in the aetiology of breast cancer.

Published
2019

8. Discovery of Novel Macrocyclic MERTK/AXL Dual Inhibitors

Author

Kong, Deyu, primary, Tian, Qiang, additional, Chen, Zhilong, additional, Zheng, Hongchao, additional, Stashko, Michael A., additional, Yan, Dan, additional, Earp, H. Shelton, additional, Frye, Stephen V., additional, DeRyckere, Deborah, additional, Kireev, Dmitri, additional, Graham, Douglas K., additional, and Wang, Xiaodong, additional

Published
2024
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10. MERTK Inhibition as a Targeted Novel Cancer Therapy.

Author

Tanim, K.M., Holtzhausen, Alisha, Thapa, Aashis, Huelse, Justus M., Graham, Douglas K., and Earp, H. Shelton

Subjects
CANCER treatment, PHOSPHATIDYLSERINES, KINASES, PROTEIN-tyrosine kinases, TYROSINE
Abstract

In this issue honoring the contributions of Greg Lemke, the Earp and Graham lab teams discuss several threads in the discovery, action, signaling, and translational/clinical potential of MERTK, originally called c-mer, a member of the TYRO3, AXL, and MERTK (TAM) family of receptor tyrosine kinases. The 30-year history of the TAM RTK family began slowly as all three members were orphan RTKs without known ligands and/or functions when discovered by three distinct alternate molecular cloning strategies in the pre-genome sequencing era. The pace of understanding their physiologic and pathophysiologic roles has accelerated over the last decade. The activation of ligands bridging externalized phosphatidylserine (PtdSer) has placed these RTKs in a myriad of processes including neurodevelopment, cancer, and autoimmunity. The field is ripe for further advancement and this article hopefully sets the stage for further understanding and therapeutic intervention. Our review will focus on progress made through the collaborations of the Earp and Graham labs over the past 30 years. [ABSTRACT FROM AUTHOR]

Published
2024
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11. The MERTK/FLT3 inhibitor MRX-2843 overcomes resistance-conferring FLT3 mutations in acute myeloid leukemia

Author

Minson, Katherine A, Smith, Catherine C, DeRyckere, Deborah, Libbrecht, Clara, Lee-Sherick, Alisa B, Huey, Madeline G, Lasater, Elisabeth A, Kirkpatrick, Gregory D, Stashko, Michael A, Zhang, Weihe, Jordan, Craig T, Kireev, Dmitri, Wang, Xiaodong, Frye, Stephen V, Earp, H Shelton, Shah, Neil P, and Graham, Douglas K

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Hematology, Pediatric, Orphan Drug, Pediatric Cancer, Cancer, Rare Diseases, Childhood Leukemia, 6.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, 2.1 Biological and endogenous factors, Aetiology, Evaluation of treatments and therapeutic interventions, Biomedical and clinical sciences, Health sciences
Abstract

FMS-like tyrosine kinase 3-targeted (FLT3-targeted) therapies have shown initial promise for the treatment of acute myeloid leukemia (AML) expressing FLT3-activating mutations; however, resistance emerges rapidly. Furthermore, limited options exist for the treatment of FLT3-independent AML, demonstrating the need for novel therapies that reduce toxicity and improve survival. MERTK receptor tyrosine kinase is overexpressed in 80% to 90% of AMLs and contributes to leukemogenesis. Here, we describe MRX-2843, a type 1 small-molecule tyrosine kinase inhibitor that abrogates activation of both MERTK and FLT3 and their downstream effectors. MRX-2843 treatment induces apoptosis and inhibits colony formation in AML cell lines and primary patient samples expressing MERTK and/or FLT3-ITD, with a wide therapeutic window compared with that of normal human cord blood cells. In murine orthotopic xenograft models, once-daily oral therapy prolonged survival 2- to 3-fold over that of vehicle-treated controls. Additionally, MRX-2843 retained activity against quizartinib-resistant FLT3-ITD-mutant proteins with clinically relevant alterations at the D835 or F691 loci and prolonged survival in xenograft models of quizartinib-resistant AML. Together, these observations validate MRX-2843 as a translational agent and support its clinical development for the treatment of AML.

Published
2016

14. FOXA1 and adaptive response determinants to HER2 targeted therapy in TBCRC 036

Author

Angus, Steven P., Stuhlmiller, Timothy J., Mehta, Gaurav, Bevill, Samantha M., Goulet, Daniel R., Olivares-Quintero, J. Felix, East, Michael P., Tanioka, Maki, Zawistowski, Jon S., Singh, Darshan, Sciaky, Noah, Chen, Xin, He, Xiaping, Rashid, Naim U., Chollet-Hinton, Lynn, Fan, Cheng, Soloway, Matthew G., Spears, Patricia A., Jefferys, Stuart, Parker, Joel S., Gallagher, Kristalyn K., Forero-Torres, Andres, Krop, Ian E., Thompson, Alastair M., Murthy, Rashmi, Gatza, Michael L., Perou, Charles M., Earp, H. Shelton, Carey, Lisa A., and Johnson, Gary L.

Published
2021
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15. MERTK activation drives osimertinib resistance in EGFR-mutant non-small cell lung cancer

Author

Yan, Dan, Huelse, Justus M., Kireev, Dmitri, Tan, Zikang, Chen, Luxiao, Goyal, Subir, Wang, Xiaodong, Frye, Stephen V., Behera, Madhusmita, Schneider, Frank, Ramalingam, Suresh S., Owonikoko, Taofeek, Earp, H. Shelton, DeRyckere, Deborah, and Graham, Douglas K.

Subjects
Drug resistance -- Genetic aspects, Lung cancer, Non-small cell -- Genetic aspects -- Drug therapy -- Development and progression, Health care industry
Abstract

Acquired resistance is inevitable in non-small cell lung cancers (NSCLCs) treated with osimertinib (OSI), and the mechanisms are not well defined. The MERTK ligand GAS6 promoted downstream oncogenic signaling in EGFR-mutated ([EGFR.sup.MT]) NSCLC cells treated with OSI, suggesting a role for MERTK activation in OSI resistance. Indeed, treatment with MRX-2843, a first-in-class MERTK kinase inhibitor, resensitized GAS6-treated NSCLC cells to OSI. Both GAS6 and EGF stimulated downstream PI3K/AKT and MAPK/ERK signaling in parental cells, but only GAS6 activated these pathways in OSI-resistant (OSIR) derivative cell lines. Functionally, OSIR cells were more sensitive to MRX-2843 than parental cells, suggesting acquired dependence on MERTK signaling. Furthermore, MERTK and/or its ligands were dramatically upregulated in [EGFR.sup.MT] tumors after treatment with OSI in both xenograft models and patient samples, consistent with induction of autocrine/paracrine MERTK activation. Moreover, treatment with MRX-2843 in combination with OSI, but not OSI alone, provided durable suppression of tumor growth in vivo, even after treatment was stopped. These data identify MERTK as a driver of bypass signaling in treatment-naive and [EGFR.sup.MT]-OSIR NSCLC cells and predict that MRX-2843 and OSI combination therapy will provide clinical benefit in patients with [EGFR.sup.MT] NSCLC., Introduction Lung cancer remains a global problem, causing more deaths in both men and women than any other cancer worldwide. Although the 5-year survival rate for lung cancer patients with [...]

Published
2022
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20. Tumor-secreted Prosi inhibits macrophage M1 polarization to reduce antitumor immune response

Author

Ubil, Eric, Caskey, Laura, Holtzhausen, Alisha, Hunter, Debra, Story, Charlotte, and Earp, H. Shelton

Subjects
Macrophages -- Research, Transcription (Genetics) -- Research, Immune response -- Research, Cellular signal transduction -- Research, Health care industry
Abstract

Tyro3, Axl, Mer (TAM) receptor tyrosine kinases reduce inflammatory, innate immune responses. We demonstrate that tumor-secreted protein S (Pros1), a Mer/Tyro3 ligand, decreased macrophage M1 cytokine expression in vitro and in vivo. In contrast, tumor cells with CRISPR-based deletion of Pros1 failed to inhibit M1 polarization. Tumor cell-associated Pros1 action was abrogated in macrophages from Mer- and Tyro3-but not Axl-KO mice. In addition, several other murine and human tumor cell lines suppressed macrophage M1 cytokine expression induced by IFN-[gamma] and LPS. Investigation of the suppressive pathway demonstrated a role for PTP1b complexing with Mer. Substantiating the role of PTP1b, M1 cytokine suppression was also lost in macrophages from PTP1b-KO mice. Mice bearing Pros1-deficient tumors showed increased innate and adaptive immune infiltration, as well as increased median survival. TAM activation can also inhibit TLR-mediated M1 polarization. Treatment with resiquimod, a TLR7/8 agonist, did not improve survival in mice bearing Pros1-secreting tumors but doubled survival for Pros1-deleted tumors. The tumor-derived Pros1 immune suppressive system, like PD-L1, was cytokine responsive, with IFN-[gamma] inducing Pros1 transcription and secretion. Inhibition of Pros1/TAM interaction represents a potential novel strategy to block tumor-derived immune suppression., Introduction Certain cancer cells subvert the immune response by eliciting an environment that favors immunologic tolerance. This immune-privileged status is achieved by mimicking existing homeostatic processes that mitigate immune responses, [...]

Published
2018
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21. Supplemental Figure Legends from TAM Family Receptor Kinase Inhibition Reverses MDSC-Mediated Suppression and Augments Anti–PD-1 Therapy in Melanoma

Author

Holtzhausen, Alisha, primary, Harris, William, primary, Ubil, Eric, primary, Hunter, Debra M., primary, Zhao, Jichen, primary, Zhang, Yuewei, primary, Zhang, Dehui, primary, Liu, Qingyang, primary, Wang, Xiaodong, primary, Graham, Douglas K., primary, Frye, Stephen V., primary, and Earp, H. Shelton, primary

Published
2023
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22. Supplementary Figures from TAM Family Receptor Kinase Inhibition Reverses MDSC-Mediated Suppression and Augments Anti–PD-1 Therapy in Melanoma

Author

Holtzhausen, Alisha, primary, Harris, William, primary, Ubil, Eric, primary, Hunter, Debra M., primary, Zhao, Jichen, primary, Zhang, Yuewei, primary, Zhang, Dehui, primary, Liu, Qingyang, primary, Wang, Xiaodong, primary, Graham, Douglas K., primary, Frye, Stephen V., primary, and Earp, H. Shelton, primary

Published
2023
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24. Supplemental Materials and Methods from MERTK Mediates Intrinsic and Adaptive Resistance to AXL-targeting Agents

Author

McDaniel, Nellie K., primary, Cummings, Christopher T., primary, Iida, Mari, primary, Hülse, Justus, primary, Pearson, Hannah E., primary, Vasileiadi, Eleana, primary, Parker, Rebecca E., primary, Orbuch, Rachel A., primary, Ondracek, Olivia J., primary, Welke, Noah B., primary, Kang, Grace H., primary, Davies, Kurtis D., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, Harari, Paul M., primary, Kimple, Randall J., primary, DeRyckere, Deborah, primary, Graham, Douglas K., primary, and Wheeler, Deric L., primary

Published
2023
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25. Data from MERTK Mediates Intrinsic and Adaptive Resistance to AXL-targeting Agents

Author

McDaniel, Nellie K., primary, Cummings, Christopher T., primary, Iida, Mari, primary, Hülse, Justus, primary, Pearson, Hannah E., primary, Vasileiadi, Eleana, primary, Parker, Rebecca E., primary, Orbuch, Rachel A., primary, Ondracek, Olivia J., primary, Welke, Noah B., primary, Kang, Grace H., primary, Davies, Kurtis D., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, Harari, Paul M., primary, Kimple, Randall J., primary, DeRyckere, Deborah, primary, Graham, Douglas K., primary, and Wheeler, Deric L., primary

Published
2023
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26. Supplementary Figure 3 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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27. Supplementary Figure 2 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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28. Supplementary Figure 4 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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29. Supplemental Figure 5 from Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma

Author

Sinik, Lenka, primary, Minson, Katherine A., primary, Tentler, John J., primary, Carrico, Jacqueline, primary, Bagby, Stacey M., primary, Robinson, William A., primary, Kami, Rotem, primary, Burstyn-Cohen, Tal, primary, Eckhardt, S. Gail, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, DeRyckere, Deborah, primary, and Graham, Douglas K., primary

Published
2023
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30. Supplementary Figure 1 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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32. Figure S4 from MERTK Mediates Intrinsic and Adaptive Resistance to AXL-targeting Agents

Author

McDaniel, Nellie K., primary, Cummings, Christopher T., primary, Iida, Mari, primary, Hülse, Justus, primary, Pearson, Hannah E., primary, Vasileiadi, Eleana, primary, Parker, Rebecca E., primary, Orbuch, Rachel A., primary, Ondracek, Olivia J., primary, Welke, Noah B., primary, Kang, Grace H., primary, Davies, Kurtis D., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, Harari, Paul M., primary, Kimple, Randall J., primary, DeRyckere, Deborah, primary, Graham, Douglas K., primary, and Wheeler, Deric L., primary

Published
2023
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33. Data from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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34. Data from Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma

Author

Sinik, Lenka, primary, Minson, Katherine A., primary, Tentler, John J., primary, Carrico, Jacqueline, primary, Bagby, Stacey M., primary, Robinson, William A., primary, Kami, Rotem, primary, Burstyn-Cohen, Tal, primary, Eckhardt, S. Gail, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, DeRyckere, Deborah, primary, and Graham, Douglas K., primary

Published
2023
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35. Supplemental Figure 2 from Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma

Author

Sinik, Lenka, primary, Minson, Katherine A., primary, Tentler, John J., primary, Carrico, Jacqueline, primary, Bagby, Stacey M., primary, Robinson, William A., primary, Kami, Rotem, primary, Burstyn-Cohen, Tal, primary, Eckhardt, S. Gail, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, DeRyckere, Deborah, primary, and Graham, Douglas K., primary

Published
2023
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38. Supplemental Figure 4 from Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma

Author

Sinik, Lenka, primary, Minson, Katherine A., primary, Tentler, John J., primary, Carrico, Jacqueline, primary, Bagby, Stacey M., primary, Robinson, William A., primary, Kami, Rotem, primary, Burstyn-Cohen, Tal, primary, Eckhardt, S. Gail, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, DeRyckere, Deborah, primary, and Graham, Douglas K., primary

Published
2023
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39. Supplemental Figure 1 from Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma

Author

Sinik, Lenka, primary, Minson, Katherine A., primary, Tentler, John J., primary, Carrico, Jacqueline, primary, Bagby, Stacey M., primary, Robinson, William A., primary, Kami, Rotem, primary, Burstyn-Cohen, Tal, primary, Eckhardt, S. Gail, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, DeRyckere, Deborah, primary, and Graham, Douglas K., primary

Published
2023
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40. Supplementary Figure 5 from UNC569, a Novel Small-Molecule Mer Inhibitor with Efficacy against Acute Lymphoblastic Leukemia In Vitro and In Vivo

Author

Christoph, Sandra, primary, DeRyckere, Deborah, primary, Schlegel, Jennifer, primary, Frazer, J. Kimble, primary, Batchelor, Lance A., primary, Trakhimets, Alesia Y., primary, Sather, Susan, primary, Hunter, Debra M., primary, Cummings, Christopher T., primary, Liu, Jing, primary, Yang, Chao, primary, Kireev, Dmitri, primary, Simpson, Catherine, primary, Norris-Drouin, Jacqueline, primary, Hull-Ryde, Emily A., primary, Janzen, William P., primary, Johnson, Gary L., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
Full Text
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42. Supplemental Figure 3 from Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma

Author

Sinik, Lenka, primary, Minson, Katherine A., primary, Tentler, John J., primary, Carrico, Jacqueline, primary, Bagby, Stacey M., primary, Robinson, William A., primary, Kami, Rotem, primary, Burstyn-Cohen, Tal, primary, Eckhardt, S. Gail, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, DeRyckere, Deborah, primary, and Graham, Douglas K., primary

Published
2023
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43. Table S1 from MERTK Mediates Intrinsic and Adaptive Resistance to AXL-targeting Agents

Author

McDaniel, Nellie K., primary, Cummings, Christopher T., primary, Iida, Mari, primary, Hülse, Justus, primary, Pearson, Hannah E., primary, Vasileiadi, Eleana, primary, Parker, Rebecca E., primary, Orbuch, Rachel A., primary, Ondracek, Olivia J., primary, Welke, Noah B., primary, Kang, Grace H., primary, Davies, Kurtis D., primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, Harari, Paul M., primary, Kimple, Randall J., primary, DeRyckere, Deborah, primary, Graham, Douglas K., primary, and Wheeler, Deric L., primary

Published
2023
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44. Supplemental Figure 7 from Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma

Author

Sinik, Lenka, primary, Minson, Katherine A., primary, Tentler, John J., primary, Carrico, Jacqueline, primary, Bagby, Stacey M., primary, Robinson, William A., primary, Kami, Rotem, primary, Burstyn-Cohen, Tal, primary, Eckhardt, S. Gail, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, DeRyckere, Deborah, primary, and Graham, Douglas K., primary

Published
2023
Full Text
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46. Supplemental Figure 6 from Inhibition of MERTK Promotes Suppression of Tumor Growth in BRAF Mutant and BRAF Wild-Type Melanoma

Author

Sinik, Lenka, primary, Minson, Katherine A., primary, Tentler, John J., primary, Carrico, Jacqueline, primary, Bagby, Stacey M., primary, Robinson, William A., primary, Kami, Rotem, primary, Burstyn-Cohen, Tal, primary, Eckhardt, S. Gail, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, DeRyckere, Deborah, primary, and Graham, Douglas K., primary

Published
2023
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47. Supplementary Data from Identification of Clonal Hematopoiesis Mutations in Solid Tumor Patients Undergoing Unpaired Next-Generation Sequencing Assays

Author

Coombs, Catherine C., primary, Gillis, Nancy K., primary, Tan, Xianming, primary, Berg, Jonathan S., primary, Ball, Markus, primary, Balasis, Maria E., primary, Montgomery, Nathan D., primary, Bolton, Kelly L., primary, Parker, Joel S., primary, Mesa, Tania E., primary, Yoder, Sean J., primary, Hayward, Michele C., primary, Patel, Nirali M., primary, Richards, Kristy L., primary, Walko, Christine M., primary, Knepper, Todd C., primary, Soper, John T., primary, Weiss, Jared, primary, Grilley-Olson, Juneko E., primary, Kim, William Y., primary, Earp, H. Shelton, primary, Levine, Ross L., primary, Papaemmanuil, Elli, primary, Zehir, Ahmet, primary, Hayes, D. Neil, primary, and Padron, Eric, primary

Published
2023
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48. Supplemental Figures from UNC2025, a MERTK Small-Molecule Inhibitor, Is Therapeutically Effective Alone and in Combination with Methotrexate in Leukemia Models

Author

DeRyckere, Deborah, primary, Lee-Sherick, Alisa B., primary, Huey, Madeline G., primary, Hill, Amanda A., primary, Tyner, Jeffrey W., primary, Jacobsen, Kristen M., primary, Page, Lauren S., primary, Kirkpatrick, Gregory G., primary, Eryildiz, Fatma, primary, Montgomery, Stephanie A., primary, Zhang, Weihe, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
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49. Supplemental Tables from UNC2025, a MERTK Small-Molecule Inhibitor, Is Therapeutically Effective Alone and in Combination with Methotrexate in Leukemia Models

Author

DeRyckere, Deborah, primary, Lee-Sherick, Alisa B., primary, Huey, Madeline G., primary, Hill, Amanda A., primary, Tyner, Jeffrey W., primary, Jacobsen, Kristen M., primary, Page, Lauren S., primary, Kirkpatrick, Gregory G., primary, Eryildiz, Fatma, primary, Montgomery, Stephanie A., primary, Zhang, Weihe, primary, Wang, Xiaodong, primary, Frye, Stephen V., primary, Earp, H. Shelton, primary, and Graham, Douglas K., primary

Published
2023
Full Text
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