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Targeting the leukemia-stroma interaction in acute myeloid leukemia: rationale and latest evidence.

Therapeutic advances in hematology

Rashidi A, DiPersio JF.
PMID: 26834953
Ther Adv Hematol. 2016 Feb;7(1):40-51. doi: 10.1177/2040620715619307.

The concept of 'niche' has become a focus of attention in hematologic malignancies including acute myeloid leukemia (AML). Similar to normal hematopoietic stem cells, AML cells interact both anatomically and functionally with the stroma within the marrow microenvironment. These...

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Rashidi A, DiPersio JF. Targeting the leukemia-stroma interaction in acute myeloid leukemia: rationale and latest evidence. Ther Adv Hematol. 2016;7(1):40-51doi: 10.1177/2040620715619307.
Rashidi, A., & DiPersio, J. F. (2016). Targeting the leukemia-stroma interaction in acute myeloid leukemia: rationale and latest evidence. Therapeutic advances in hematology, 7(1), 40-51. https://doi.org/10.1177/2040620715619307
Rashidi, Armin, and DiPersio, John F. "Targeting the leukemia-stroma interaction in acute myeloid leukemia: rationale and latest evidence." Therapeutic advances in hematology vol. 7,1 (2016): 40-51. doi: https://doi.org/10.1177/2040620715619307
Rashidi A, DiPersio JF. Targeting the leukemia-stroma interaction in acute myeloid leukemia: rationale and latest evidence. Ther Adv Hematol. 2016 Feb;7(1):40-51. doi: 10.1177/2040620715619307. PMID: 26834953; PMCID: PMC4713889.
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Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival.

Scientific reports

Hathi D, Chanswangphuwana C, Cho N, Fontana F, Maji D, Ritchey J, O'Neal J, Ghai A, Duncan K, Akers WJ, Fiala M, Vij R, DiPersio JF, Rettig M, Shokeen M.
PMID: 34996933
Sci Rep. 2022 Jan 07;12(1):30. doi: 10.1038/s41598-021-03748-0.

Multiple myeloma (MM) is a cancer of bone marrow (BM) plasma cells, which is increasingly treatable but still incurable. In 90% of MM patients, severe osteolysis results from pathological interactions between MM cells and the bone microenvironment. Delineating specific...

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Hathi D, Chanswangphuwana C, Cho N, et al. Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Sci Rep. 2022;12(1):30doi: 10.1038/s41598-021-03748-0.
Hathi, D., Chanswangphuwana, C., Cho, N., Fontana, F., Maji, D., Ritchey, J., O'Neal, J., Ghai, A., Duncan, K., Akers, W. J., Fiala, M., Vij, R., DiPersio, J. F., Rettig, M., & Shokeen, M. (2022). Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Scientific reports, 12(1), 30. https://doi.org/10.1038/s41598-021-03748-0
Hathi, Deep, et al. "Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival." Scientific reports vol. 12,1 (2022): 30. doi: https://doi.org/10.1038/s41598-021-03748-0
Hathi D, Chanswangphuwana C, Cho N, Fontana F, Maji D, Ritchey J, O'Neal J, Ghai A, Duncan K, Akers WJ, Fiala M, Vij R, DiPersio JF, Rettig M, Shokeen M. Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Sci Rep. 2022 Jan 07;12(1):30. doi: 10.1038/s41598-021-03748-0. PMID: 34996933; PMCID: PMC8741970.
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Systemic IL-15 promotes allogeneic cell rejection in patients treated with natural killer cell adoptive therapy.

Blood

Berrien-Elliott MM, Becker-Hapak M, Cashen AF, Jacobs MT, Wong P, Foster M, McClain E, Desai S, Pence P, Cooley S, Brunstein CG, Gao F, Abboud CN, Uy GL, Westervelt P, Jacoby MA, Pusic I, Stockerl-Goldstein K, Schroeder MA, DiPersio JF, Soon-Shiong P, Miller JS, Fehniger TA.
PMID: 34797911
Blood. 2021 Nov 19; doi: 10.1182/blood.2021011532. Epub 2021 Nov 19.

NK cells are a promising alternative to T cells for cancer immunotherapy. Adoptive therapies with allogeneic, cytokine-activated NK cells are being investigated in clinical trials. However, the optimal cytokine support after adoptive transfer to promote NK cell expansion, and...

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Berrien-Elliott MM, Becker-Hapak M, Cashen AF, et al. Systemic IL-15 promotes allogeneic cell rejection in patients treated with natural killer cell adoptive therapy. Blood. 2021;doi: 10.1182/blood.2021011532.
Berrien-Elliott, M. M., Becker-Hapak, M., Cashen, A. F., Jacobs, M. T., Wong, P., Foster, M., McClain, E., Desai, S., Pence, P., Cooley, S., Brunstein, C. G., Gao, F., Abboud, C. N., Uy, G. L., Westervelt, P., Jacoby, M. A., Pusic, I., Stockerl-Goldstein, K., Schroeder, M. A., DiPersio, J. F., Soon-Shiong, P., Miller, J. S., & Fehniger, T. A. (2021). Systemic IL-15 promotes allogeneic cell rejection in patients treated with natural killer cell adoptive therapy. Blood, . https://doi.org/10.1182/blood.2021011532
Berrien-Elliott, Melissa M, et al. "Systemic IL-15 promotes allogeneic cell rejection in patients treated with natural killer cell adoptive therapy." Blood vol. (2021). doi: https://doi.org/10.1182/blood.2021011532
Berrien-Elliott MM, Becker-Hapak M, Cashen AF, Jacobs MT, Wong P, Foster M, McClain E, Desai S, Pence P, Cooley S, Brunstein CG, Gao F, Abboud CN, Uy GL, Westervelt P, Jacoby MA, Pusic I, Stockerl-Goldstein K, Schroeder MA, DiPersio JF, Soon-Shiong P, Miller JS, Fehniger TA. Systemic IL-15 promotes allogeneic cell rejection in patients treated with natural killer cell adoptive therapy. Blood. 2021 Nov 19; doi: 10.1182/blood.2021011532. Epub 2021 Nov 19. PMID: 34797911.
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Immunotherapy for T-Cell ALL and T-Cell NHL.

Clinical lymphoma, myeloma & leukemia

DiPersio JF, Staser K, Cooper M.
PMID: 32862870
Clin Lymphoma Myeloma Leuk. 2020 Sep;20:S56-S58. doi: 10.1016/S2152-2650(20)30462-6.

No abstract available.

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DiPersio JF, Staser K, Cooper M. Immunotherapy for T-Cell ALL and T-Cell NHL. Clin Lymphoma Myeloma Leuk. 2020;20:S56-S58doi: 10.1016/S2152-2650(20)30462-6.
DiPersio, J. F., Staser, K., & Cooper, M. (2020). Immunotherapy for T-Cell ALL and T-Cell NHL. Clinical lymphoma, myeloma & leukemia, 20S56-S58. https://doi.org/10.1016/S2152-2650(20)30462-6
DiPersio, John F, et al. "Immunotherapy for T-Cell ALL and T-Cell NHL." Clinical lymphoma, myeloma & leukemia vol. 20 (2020): S56-S58. doi: https://doi.org/10.1016/S2152-2650(20)30462-6
DiPersio JF, Staser K, Cooper M. Immunotherapy for T-Cell ALL and T-Cell NHL. Clin Lymphoma Myeloma Leuk. 2020 Sep;20:S56-S58. doi: 10.1016/S2152-2650(20)30462-6. PMID: 32862870.
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Integrin Regulation of CAF Differentiation and Function.

Cancers

DiPersio CM, Van De Water L.
PMID: 31137641
Cancers (Basel). 2019 May 24;11(5). doi: 10.3390/cancers11050715.

Extensive remodeling of the extracellular matrix, together with paracrine communication between tumor cells and stromal cells, contribute to an "activated" tumor microenvironment that supports malignant growth and progression. These stromal cells include inflammatory cells, endothelial cells, and cancer-associated fibroblasts...

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DiPersio CM, Van De Water L. Integrin Regulation of CAF Differentiation and Function. Cancers (Basel). 2019;11(5)doi: 10.3390/cancers11050715.
DiPersio, C. M., & Van De Water, L. (2019). Integrin Regulation of CAF Differentiation and Function. Cancers, 11(5), . https://doi.org/10.3390/cancers11050715
DiPersio, C Michael, and Van De Water, Livingston. "Integrin Regulation of CAF Differentiation and Function." Cancers vol. 11,5 (2019). doi: https://doi.org/10.3390/cancers11050715
DiPersio CM, Van De Water L. Integrin Regulation of CAF Differentiation and Function. Cancers (Basel). 2019 May 24;11(5). doi: 10.3390/cancers11050715. PMID: 31137641; PMCID: PMC6563118.
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Targeting CXCR4 in AML and ALL.

Frontiers in oncology

Cancilla D, Rettig MP, DiPersio JF.
PMID: 33014834
Front Oncol. 2020 Sep 04;10:1672. doi: 10.3389/fonc.2020.01672. eCollection 2020.

The interaction of acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) blasts with the bone marrow microenvironment regulates self-renewal, growth signaling, as well as chemotherapy resistance. The chemokine receptor, CXC receptor 4 (CXCR4), with its ligand chemokine ligand...

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Cancilla D, Rettig MP, DiPersio JF. Targeting CXCR4 in AML and ALL. Front Oncol. 2020;10:1672doi: 10.3389/fonc.2020.01672.
Cancilla, D., Rettig, M. P., & DiPersio, J. F. (2020). Targeting CXCR4 in AML and ALL. Frontiers in oncology, 101672. https://doi.org/10.3389/fonc.2020.01672
Cancilla, Daniel, et al. "Targeting CXCR4 in AML and ALL." Frontiers in oncology vol. 10 (2020): 1672. doi: https://doi.org/10.3389/fonc.2020.01672
Cancilla D, Rettig MP, DiPersio JF. Targeting CXCR4 in AML and ALL. Front Oncol. 2020 Sep 04;10:1672. doi: 10.3389/fonc.2020.01672. eCollection 2020. PMID: 33014834; PMCID: PMC7499473.
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Epidermal Integrin α3β1 Regulates Tumor-Derived Proteases BMP-1, Matrix Metalloprotease-9, and Matrix Metalloprotease-3.

JID innovations

Longmate WM, Miskin RP, Van De Water L, DiPersio CM.
PMID: 34909716
JID Innov. 2021 Apr 30;1(2):100017. doi: 10.1016/j.xjidi.2021.100017. eCollection 2021 Jun.

As the major cell surface receptors for the extracellular matrix, integrins regulate adhesion and migration and have been shown to drive tumor growth and progression. Previous studies showed that mice lacking integrin α3β1 in the epidermis fail to form...

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Longmate WM, Miskin RP, Van De Water L, et al. Epidermal Integrin α3β1 Regulates Tumor-Derived Proteases BMP-1, Matrix Metalloprotease-9, and Matrix Metalloprotease-3. JID Innov. 2021;1(2):100017doi: 10.1016/j.xjidi.2021.100017.
Longmate, W. M., Miskin, R. P., Van De Water, L., & DiPersio, C. M. (2021). Epidermal Integrin α3β1 Regulates Tumor-Derived Proteases BMP-1, Matrix Metalloprotease-9, and Matrix Metalloprotease-3. JID innovations, 1(2), 100017. https://doi.org/10.1016/j.xjidi.2021.100017
Longmate, Whitney M, et al. "Epidermal Integrin α3β1 Regulates Tumor-Derived Proteases BMP-1, Matrix Metalloprotease-9, and Matrix Metalloprotease-3." JID innovations vol. 1,2 (2021): 100017. doi: https://doi.org/10.1016/j.xjidi.2021.100017
Longmate WM, Miskin RP, Van De Water L, DiPersio CM. Epidermal Integrin α3β1 Regulates Tumor-Derived Proteases BMP-1, Matrix Metalloprotease-9, and Matrix Metalloprotease-3. JID Innov. 2021 Apr 30;1(2):100017. doi: 10.1016/j.xjidi.2021.100017. eCollection 2021 Jun. PMID: 34909716; PMCID: PMC8659409.
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A pilot study of 3D tissue-engineered bone marrow culture as a tool to predict patient response to therapy in multiple myeloma.

Scientific reports

Alhallak K, Jeske A, de la Puente P, Sun J, Fiala M, Azab F, Muz B, Sahin I, Vij R, DiPersio JF, Azab AK.
PMID: 34588522
Sci Rep. 2021 Sep 29;11(1):19343. doi: 10.1038/s41598-021-98760-9.

Cancer patients undergo detrimental toxicities and ineffective treatments especially in the relapsed setting, due to failed treatment attempts. The development of a tool that predicts the clinical response of individual patients to therapy is greatly desired. We have developed...

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Alhallak K, Jeske A, de la Puente P, et al. A pilot study of 3D tissue-engineered bone marrow culture as a tool to predict patient response to therapy in multiple myeloma. Sci Rep. 2021;11(1):19343doi: 10.1038/s41598-021-98760-9.
Alhallak, K., Jeske, A., de la Puente, P., Sun, J., Fiala, M., Azab, F., Muz, B., Sahin, I., Vij, R., DiPersio, J. F., & Azab, A. K. (2021). A pilot study of 3D tissue-engineered bone marrow culture as a tool to predict patient response to therapy in multiple myeloma. Scientific reports, 11(1), 19343. https://doi.org/10.1038/s41598-021-98760-9
Alhallak, Kinan, et al. "A pilot study of 3D tissue-engineered bone marrow culture as a tool to predict patient response to therapy in multiple myeloma." Scientific reports vol. 11,1 (2021): 19343. doi: https://doi.org/10.1038/s41598-021-98760-9
Alhallak K, Jeske A, de la Puente P, Sun J, Fiala M, Azab F, Muz B, Sahin I, Vij R, DiPersio JF, Azab AK. A pilot study of 3D tissue-engineered bone marrow culture as a tool to predict patient response to therapy in multiple myeloma. Sci Rep. 2021 Sep 29;11(1):19343. doi: 10.1038/s41598-021-98760-9. PMID: 34588522; PMCID: PMC8481555.
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Liposomal phytohemagglutinin: In vivo T-cell activator as a novel pan-cancer immunotherapy.

Journal of cellular and molecular medicine

Alhallak K, Sun J, Muz B, Jeske A, O'Neal J, Ritchey JK, Achilefu S, DiPersio JF, Azab AK.
PMID: 35014164
J Cell Mol Med. 2022 Jan 11; doi: 10.1111/jcmm.16885. Epub 2022 Jan 11.

Immunotherapy is an attractive approach for treating cancer. T-cell engagers (TCEs) are a type of immunotherapy that are highly efficacious; however, they are challenged by weak T-cell activation and short persistence. Therefore, alternative solutions to induce greater activation and...

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Alhallak K, Sun J, Muz B, et al. Liposomal phytohemagglutinin: In vivo T-cell activator as a novel pan-cancer immunotherapy. J Cell Mol Med. 2022;doi: 10.1111/jcmm.16885.
Alhallak, K., Sun, J., Muz, B., Jeske, A., O'Neal, J., Ritchey, J. K., Achilefu, S., DiPersio, J. F., & Azab, A. K. (2022). Liposomal phytohemagglutinin: In vivo T-cell activator as a novel pan-cancer immunotherapy. Journal of cellular and molecular medicine, . https://doi.org/10.1111/jcmm.16885
Alhallak, Kinan, et al. "Liposomal phytohemagglutinin: In vivo T-cell activator as a novel pan-cancer immunotherapy." Journal of cellular and molecular medicine vol. (2022). doi: https://doi.org/10.1111/jcmm.16885
Alhallak K, Sun J, Muz B, Jeske A, O'Neal J, Ritchey JK, Achilefu S, DiPersio JF, Azab AK. Liposomal phytohemagglutinin: In vivo T-cell activator as a novel pan-cancer immunotherapy. J Cell Mol Med. 2022 Jan 11; doi: 10.1111/jcmm.16885. Epub 2022 Jan 11. PMID: 35014164.
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Author Correction: Comprehensive characterization of 536 patient-derived xenograft models prioritizes candidates for targeted treatment.

Nature communications

Sun H, Cao S, Mashl RJ, Mo CK, Zaccaria S, Wendl MC, Davies SR, Bailey MH, Primeau TM, Hoog J, Mudd JL, Dean DA, Patidar R, Chen L, Wyczalkowski MA, Jayasinghe RG, Rodrigues FM, Terekhanova NV, Li Y, Lim KH, Wang-Gillam A, Van Tine BA, Ma CX, Aft R, Fuh KC, Schwarz JK, Zevallos JP, Puram SV, Dipersio JF, Davis-Dusenbery B, Ellis MJ, Lewis MT, Davies MA, Herlyn M, Fang B, Roth JA, Welm AL, Welm BE, Meric-Bernstam F, Chen F, Fields RC, Li S, Govindan R, Doroshow JH, Moscow JA, Evrard YA, Chuang JH, Raphael BJ, Ding L.
PMID: 34996889
Nat Commun. 2022 Jan 07;13(1):294. doi: 10.1038/s41467-021-27678-7.

No abstract available.

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Sun H, Cao S, Mashl RJ, et al. Author Correction: Comprehensive characterization of 536 patient-derived xenograft models prioritizes candidates for targeted treatment. Nat Commun. 2022;13(1):294doi: 10.1038/s41467-021-27678-7.
Sun, H., Cao, S., Mashl, R. J., Mo, C. K., Zaccaria, S., Wendl, M. C., Davies, S. R., Bailey, M. H., Primeau, T. M., Hoog, J., Mudd, J. L., Dean, D. A., Patidar, R., Chen, L., Wyczalkowski, M. A., Jayasinghe, R. G., Rodrigues, F. M., Terekhanova, N. V., Li, Y., Lim, K. H., Wang-Gillam, A., Van Tine, B. A., Ma, C. X., Aft, R., Fuh, K. C., Schwarz, J. K., Zevallos, J. P., Puram, S. V., Dipersio, J. F., Davis-Dusenbery, B., Ellis, M. J., Lewis, M. T., Davies, M. A., Herlyn, M., Fang, B., Roth, J. A., Welm, A. L., Welm, B. E., Meric-Bernstam, F., Chen, F., Fields, R. C., Li, S., Govindan, R., Doroshow, J. H., Moscow, J. A., Evrard, Y. A., Chuang, J. H., Raphael, B. J., & Ding, L. (2022). Author Correction: Comprehensive characterization of 536 patient-derived xenograft models prioritizes candidates for targeted treatment. Nature communications, 13(1), 294. https://doi.org/10.1038/s41467-021-27678-7
Sun, Hua, et al. "Author Correction: Comprehensive characterization of 536 patient-derived xenograft models prioritizes candidates for targeted treatment." Nature communications vol. 13,1 (2022): 294. doi: https://doi.org/10.1038/s41467-021-27678-7
Sun H, Cao S, Mashl RJ, Mo CK, Zaccaria S, Wendl MC, Davies SR, Bailey MH, Primeau TM, Hoog J, Mudd JL, Dean DA, Patidar R, Chen L, Wyczalkowski MA, Jayasinghe RG, Rodrigues FM, Terekhanova NV, Li Y, Lim KH, Wang-Gillam A, Van Tine BA, Ma CX, Aft R, Fuh KC, Schwarz JK, Zevallos JP, Puram SV, Dipersio JF, Davis-Dusenbery B, Ellis MJ, Lewis MT, Davies MA, Herlyn M, Fang B, Roth JA, Welm AL, Welm BE, Meric-Bernstam F, Chen F, Fields RC, Li S, Govindan R, Doroshow JH, Moscow JA, Evrard YA, Chuang JH, Raphael BJ, Ding L. Author Correction: Comprehensive characterization of 536 patient-derived xenograft models prioritizes candidates for targeted treatment. Nat Commun. 2022 Jan 07;13(1):294. doi: 10.1038/s41467-021-27678-7. PMID: 34996889.
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Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival.

Scientific reports

Hathi D, Chanswangphuwana C, Cho N, Fontana F, Maji D, Ritchey J, O'Neal J, Ghai A, Duncan K, Akers WJ, Fiala M, Vij R, DiPersio JF, Rettig M, Shokeen M.
PMID: 34996933
Sci Rep. 2022 Jan 07;12(1):30. doi: 10.1038/s41598-021-03748-0.

Multiple myeloma (MM) is a cancer of bone marrow (BM) plasma cells, which is increasingly treatable but still incurable. In 90% of MM patients, severe osteolysis results from pathological interactions between MM cells and the bone microenvironment. Delineating specific...

Cite
Hathi D, Chanswangphuwana C, Cho N, et al. Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Sci Rep. 2022;12(1):30doi: 10.1038/s41598-021-03748-0.
Hathi, D., Chanswangphuwana, C., Cho, N., Fontana, F., Maji, D., Ritchey, J., O'Neal, J., Ghai, A., Duncan, K., Akers, W. J., Fiala, M., Vij, R., DiPersio, J. F., Rettig, M., & Shokeen, M. (2022). Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Scientific reports, 12(1), 30. https://doi.org/10.1038/s41598-021-03748-0
Hathi, Deep, et al. "Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival." Scientific reports vol. 12,1 (2022): 30. doi: https://doi.org/10.1038/s41598-021-03748-0
Hathi D, Chanswangphuwana C, Cho N, Fontana F, Maji D, Ritchey J, O'Neal J, Ghai A, Duncan K, Akers WJ, Fiala M, Vij R, DiPersio JF, Rettig M, Shokeen M. Ablation of VLA4 in multiple myeloma cells redirects tumor spread and prolongs survival. Sci Rep. 2022 Jan 07;12(1):30. doi: 10.1038/s41598-021-03748-0. PMID: 34996933; PMCID: PMC8741970.
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Baricitinib prevents GvHD by increasing Tregs via JAK3 and treats established GvHD by promoting intestinal tissue repair via EGFR.

Leukemia

Kim S, Ashami K, Lim S, Staser K, Vij K, Santhanam S, Ritchey J, Peterson S, Gao F, Ciorba MA, Cooper ML, DiPersio JF, Choi J.
PMID: 34304247
Leukemia. 2022 Jan;36(1):292-295. doi: 10.1038/s41375-021-01360-9. Epub 2021 Jul 24.

No abstract available.

Cite
Kim S, Ashami K, Lim S, et al. Baricitinib prevents GvHD by increasing Tregs via JAK3 and treats established GvHD by promoting intestinal tissue repair via EGFR. Leukemia. 2021;36(1):292-295doi: 10.1038/s41375-021-01360-9.
Kim, S., Ashami, K., Lim, S., Staser, K., Vij, K., Santhanam, S., Ritchey, J., Peterson, S., Gao, F., Ciorba, M. A., Cooper, M. L., DiPersio, J. F., & Choi, J. (2022). Baricitinib prevents GvHD by increasing Tregs via JAK3 and treats established GvHD by promoting intestinal tissue repair via EGFR. Leukemia, 36(1), 292-295. https://doi.org/10.1038/s41375-021-01360-9
Kim, Sena, et al. "Baricitinib prevents GvHD by increasing Tregs via JAK3 and treats established GvHD by promoting intestinal tissue repair via EGFR." Leukemia vol. 36,1 (2022): 292-295. doi: https://doi.org/10.1038/s41375-021-01360-9
Kim S, Ashami K, Lim S, Staser K, Vij K, Santhanam S, Ritchey J, Peterson S, Gao F, Ciorba MA, Cooper ML, DiPersio JF, Choi J. Baricitinib prevents GvHD by increasing Tregs via JAK3 and treats established GvHD by promoting intestinal tissue repair via EGFR. Leukemia. 2022 Jan;36(1):292-295. doi: 10.1038/s41375-021-01360-9. Epub 2021 Jul 24. PMID: 34304247; PMCID: PMC8732299.
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