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Your search keyword '"Hunter, Zachary R"' showing total 14 results
Start Over Author "Hunter, Zachary R" Journal blood advances
14 results on '"Hunter, Zachary R"'

3. Identification of robust predictors for ibrutinib response by multi-omics in MYD88 mutated Waldenstrom Macroglobulinemia

Author

Richardson, Kris, primary, Castillo, Jorge J., additional, Sarosiek, Shayna, additional, Branagan, Andrew R, additional, Flynn, Catherine, additional, Meid, Kirsten E., additional, Gutine, Joshua, additional, Liu, Xia, additional, Kofides, Amanda, additional, Liu, Shirong, additional, Wolf, Julie L, additional, Kacena, Katherine Amy, additional, Patterson, Christopher J, additional, Guerrera, Maria Luisa, additional, Tsakmaklis, Nicholas, additional, Treon, Steven P., additional, and Hunter, Zachary R, additional

Published
2024
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4. Human MYD88L265P is insufficient by itself to drive neoplastic transformation in mature mouse B cells

Author

Sewastianik, Tomasz, Guerrera, Maria Luisa, Adler, Keith, Dennis, Peter S., Wright, Kyle, Shanmugam, Vignesh, Huang, Ying, Tanton, Helen, Jiang, Meng, Kofides, Amanda, Demos, Maria G., Dalgarno, Audrey, Patel, Neil A., Nag, Anwesha, Pinkus, Geraldine S., Yang, Guang, Hunter, Zachary R., Jarolim, Petr, Munshi, Nikhil C., Treon, Steven P., and Carrasco, Ruben D.

Published
2019
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6. Identification of robust predictors for ibrutinib response by multiomics in MYD88-mutated Waldenström macroglobulinemia

Author

Richardson, Kris, Castillo, Jorge J., Sarosiek, Shayna R., Branagan, Andrew R., Flynn, Catherine A., Meid, Kirsten, Gustine, Joshua N., Liu, Xia, Kofides, Amanda, Liu, Shirong, Wolf, Julie L., Kacena, Katherine A., Patterson, Christopher J., Guerrera, Maria Luisa, Tsakmaklis, Nicholas, Treon, Steven P., and Hunter, Zachary R.

Published
2024
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7. A new role for the SRC family kinase HCK as a driver of SYK activation in MYD88 mutated lymphomas

Author

Munshi, Manit, primary, Liu, Xia, additional, Kofides, Amanda, additional, Tsakmaklis, Nickolas, additional, Guerrera, Maria Luisa, additional, Hunter, Zachary R., additional, Palomba, M. Lia, additional, Argyropoulos, Kimon V., additional, Patterson, Christopher J., additional, Canning, Alexa G., additional, Meid, Kirsten, additional, Gustine, Joshua, additional, Branagan, Andrew R., additional, Flynn, Catherine A., additional, Sarosiek, Shayna, additional, Castillo, Jorge J., additional, Wang, Jinhua, additional, Buhrlage, Sara J., additional, Gray, Nathanael S., additional, Munshi, Nikhil C., additional, Anderson, Kenneth C., additional, Treon, Steven P., additional, and Yang, Guang, additional

Published
2022
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8. Comparative genomics of CXCR4MUT and CXCR4WT single cells in Waldenström’s macroglobulinemia

Author

Jiménez, Cristina, primary, Xu, Lian, additional, Tsakmaklis, Nickolas, additional, Demos, Maria G., additional, Kofides, Amanda, additional, Chan, Gloria G., additional, Guerrera, Maria Luisa, additional, Chen, Jiaji G., additional, Liu, Xia, additional, Munshi, Manit, additional, Patterson, Christopher J., additional, Yang, Guang, additional, Castillo, Jorge J., additional, Treon, Steven P., additional, and Hunter, Zachary R., additional

Published
2020
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9. CXCR4 S338X clonality is an important determinant of ibrutinib outcomes in patients with Waldenström macroglobulinemia

Author

Gustine, Joshua N., primary, Xu, Lian, additional, Tsakmaklis, Nicholas, additional, Demos, Maria G., additional, Kofides, Amanda, additional, Chen, Jiaji G., additional, Liu, Xia, additional, Munshi, Manit, additional, Guerrera, Maria Luisa, additional, Chan, Gloria G., additional, Patterson, Christopher J., additional, Keezer, Andrew, additional, Meid, Kirsten, additional, Dubeau, Toni, additional, Yang, Guang, additional, Hunter, Zachary R., additional, Treon, Steven P., additional, and Castillo, Jorge J., additional

Published
2019
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10. Insights into the genomic landscape of MYD88 wild-type Waldenström macroglobulinemia

Author

Hunter, Zachary R., primary, Xu, Lian, additional, Tsakmaklis, Nickolas, additional, Demos, Maria G., additional, Kofides, Amanda, additional, Jimenez, Cristina, additional, Chan, Gloria G., additional, Chen, Jiaji, additional, Liu, Xia, additional, Munshi, Manit, additional, Gustine, Joshua, additional, Meid, Kirsten, additional, Patterson, Christopher J., additional, Yang, Guang, additional, Dubeau, Toni, additional, Samur, Mehmet K., additional, Castillo, Jorge J., additional, Anderson, Kenneth C., additional, Munshi, Nikhil C., additional, and Treon, Steven P., additional

Published
2018
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11. Comparative genomics of CXCR4MUTand CXCR4WTsingle cells in Waldenström's macroglobulinemia

Author

Jiménez, Cristina, Xu, Lian, Tsakmaklis, Nickolas, Demos, Maria G., Kofides, Amanda, Chan, Gloria G., Guerrera, Maria Luisa, Chen, Jiaji G., Liu, Xia, Munshi, Manit, Patterson, Christopher J., Yang, Guang, Castillo, Jorge J., Treon, Steven P., and Hunter, Zachary R.

Abstract

•Single-cell whole-genome amplification can be used to interrogate the genomic architecture of Waldenström's macroglobulinemia.•The mutational signature of CXCR4MUTcells may be associated with alterations in DNA repairing genes and tumor suppressors.

Published
2020
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12. Human MYD88L265Pis insufficient by itself to drive neoplastic transformation in mature mouse B cells

Author

Sewastianik, Tomasz, Guerrera, Maria Luisa, Adler, Keith, Dennis, Peter S., Wright, Kyle, Shanmugam, Vignesh, Huang, Ying, Tanton, Helen, Jiang, Meng, Kofides, Amanda, Demos, Maria G., Dalgarno, Audrey, Patel, Neil A., Nag, Anwesha, Pinkus, Geraldine S., Yang, Guang, Hunter, Zachary R., Jarolim, Petr, Munshi, Nikhil C., Treon, Steven P., and Carrasco, Ruben D.

Abstract

MYD88L265Pis the most common mutation in lymphoplasmacytic lymphoma/Waldenström macroglobulinemia (LPL/WM) and one of the most frequent in poor-prognosis subtypes of diffuse large B-cell lymphoma (DLBCL). Although inhibition of the mutated MYD88 pathway has an adverse impact on LPL/WM and DLBCL cell survival, its role in lymphoma initiation remains to be clarified. We show that in mice, human MYD88L265Ppromotes development of a non-clonal, low-grade B-cell lymphoproliferative disorder with several clinicopathologic features that resemble human LPL/WM, including expansion of lymphoplasmacytoid cells, increased serum immunoglobulin M (IgM) concentration, rouleaux formation, increased number of mast cells in the bone marrow, and proinflammatory signaling that progresses sporadically to clonal, high-grade DLBCL. Murine findings regarding differences in the pattern of MYD88 staining and immune infiltrates in the bone marrows of MYD88wild-type (MYD88WT) and MYD88L265Pmice are recapitulated in the human setting, which provides insight into LPL/WM pathogenesis. Furthermore, histologic transformation to DLBCL is associated with acquisition of secondary genetic lesions frequently seen in de novo human DLBCL as well as LPL/WM-transformed cases. These findings indicate that, although the MYD88L265Pmutation might be indispensable for the LPL/WM phenotype, it is insufficient by itself to drive malignant transformation in B cells and relies on other, potentially targetable cooperating genetic events for full development of lymphoma.

Published
2019
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13. CXCR4S338Xclonality is an important determinant of ibrutinib outcomes in patients with Waldenström macroglobulinemia

Author

Gustine, Joshua N., Xu, Lian, Tsakmaklis, Nicholas, Demos, Maria G., Kofides, Amanda, Chen, Jiaji G., Liu, Xia, Munshi, Manit, Guerrera, Maria Luisa, Chan, Gloria G., Patterson, Christopher J., Keezer, Andrew, Meid, Kirsten, Dubeau, Toni, Yang, Guang, Hunter, Zachary R., Treon, Steven P., and Castillo, Jorge J.

Abstract

•CXCR4S338Xclonality ≥25% is associated with lower very good partial response and shorter progression-free survival to ibrutinib.•CXCR4S338Xclonality assessment represents a novel biomarker to predict outcomes to ibrutinib in Waldenström macroglobulinemia patients.

Published
2019
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14. Predictors of response and survival in a large cohort of 319 Waldenström macroglobulinemia patients treated with ibrutinib monotherapy

Author

Castillo, Jorge J., Sarosiek, Shayna R., Gustine, Joshua N., Flynn, Catherine A., Leventoff, Carly R., White, Timothy P., Meid, Kirsten, Guerrera, Maria L., Kofides, Amanda, Liu, Xia, Munshi, Manit, Tsakmaklis, Nicholas, Hunter, Zachary R., Patterson, Christopher J., Branagan, Andrew R., and Treon, Steven P.

Abstract

Bruton tyrosine kinase (BTK) inhibitors are the only FDA-approved treatments for Waldenström macroglobulinemia (WM). Factors prognostic of survival and predictive of response to BTK inhibitors remained to be clarified. We evaluated 319 patients with WM to identify predictive and prognostic factors on ibrutinib monotherapy. Logistic and Cox proportional-hazard regression models were fitted for response and survival. Multiple imputation analyses were used to address bias associated with missing data. Major (partial response or better) and deep responses (very good partial response or better) were attained in 78% and 28% of patients. CXCR4mutations were associated with lower odds of major (OR 0.2, 95% CI 0.1-0.5; p<0.001) and deep response (OR 0.3, 95% CI 0.2-0.6; p=0.001). CXCR4mutations (HR 2.0, 95% CI 1.2-3.4; p=0.01) and platelet count 100 K/uL or less (HR 2.5, 95% CI 1.3-4.9; p=0.007) were associated with worse progression-free survival (PFS). We proposed a scoring system using these two factors. The median PFS for patients with zero, one and two risk factors were not reached, 5 years and 3 years (p<0.001). Patients with two risk factors had HR 2.2 (95% CI 1.3-3.8; p=0.004) compared with one factor, and patients with one factor had HR 2.3 (95% CI 1.1-5.1; p=0.03) compared with zero factors. Age 65 years or older was the only factor associated with overall survival (HR 3.2, 95% CI 1.4-7.0; p=0.005). Multiple imputation analyses did not alter our results. Our study confirms the predictive and prognostic value of CXCR4mutations in patients with WM treated with ibrutinib monotherapy.

Published
2021
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