If you made any changes in Pure, your changes will be visible here soon.

Personal profile

Research Interests

Research in the Crispino laboratory is focused on investigating the regulatory mechanisms governing normal and malignant blood cell development, with an emphasis on understanding the growth of erythroid cells (red blood cells) and megakaryocytes (platelet-producing cells). In addition, the group has a major interest in learning how changes in normal essential regulatory molecules lead to human blood diseases, including acute leukemias and myeloproliferative neoplasms (MPNs). The lab seeks to make seminal basic science discoveries while simultaneously translating these discoveries in ways that will benefit patients with hematologic malignancies.

Education/Academic qualification

PhD, MIT

… → 1996

Research interests

  • Blood Cancer (leukemia and lymphomas)
  • Gene Regulation
  • Molecular Biology
  • Blood and Bleeding Disorders (anemia, clotting, etc.)

Fingerprint Dive into the research topics where John D Crispino is active. These topic labels come from the works of this person. Together they form a unique fingerprint.

  • 28 Similar Profiles
Megakaryocytes Medicine & Life Sciences
Leukemia, Megakaryoblastic, Acute Medicine & Life Sciences
Down Syndrome Medicine & Life Sciences
Primary Myelofibrosis Medicine & Life Sciences
Mutation Medicine & Life Sciences
Leukemia Medicine & Life Sciences
Neoplasms Medicine & Life Sciences
Hematopoiesis Medicine & Life Sciences

Network Recent external collaboration on country level. Dive into details by clicking on the dots.

Grants 2006 2024

Chromatin Assembly and Disassembly
Leukemia
Stem Cells
Genes
Down Syndrome
Myeloid Progenitor Cells
Acute Myeloid Leukemia
Myeloid Cells
Down Syndrome
Genes
Neoplasms
Essential Thrombocythemia
Polycythemia Vera
Primary Myelofibrosis
Clustered Regularly Interspaced Short Palindromic Repeats
Neoplasms
Medicine
Research
Population

Research Output 1991 2019

1 Citation (Scopus)

Activation of JAK/STAT signaling in megakaryocytes sustains myeloproliferation in vivo

Woods, B., Chen, W., Chiu, S., Marinaccio, C., Fu, C., Gu, L., Bulic, M., Yang, Q., Zouak, A., Jia, S., Suraneni, P. K., Xu, K., Levine, R. L., Crispino, J. D. & Wen, Q., Oct 1 2019, In : Clinical Cancer Research. 25, 19, p. 5901-5912 12 p.

Research output: Contribution to journalArticle

Megakaryocytes
Erythropoiesis
Neoplasms
Primary Myelofibrosis
Maintenance

AKT activation is a feature of CALR mutant myeloproliferative neoplasms

Fu, C., Wen, Q., Marinaccio, C., Ling, T., Chen, W., Bulic, M., Lasho, T., Tefferi, A., Crispino, J. D. & Xu, K., Jan 1 2019, In : Leukemia. 33, 1, p. 271-274 4 p.

Research output: Contribution to journalArticle

Neoplasms
5 Citations (Scopus)

An activating mutation of the NSD2 histone methyltransferase drives oncogenic reprogramming in acute lymphocytic leukemia

Swaroop, A., Oyer, J. A., Will, C. M., Huang, X., Yu, W., Troche, C., Bulic, M., Durham, B. H., Wen, Q., Crispino, J. D., MacKerell, A. D., Bennett, R. L., Kelleher, N. L. & Licht, J. D., Jan 31 2019, In : Oncogene. 38, 5, p. 671-686 16 p.

Research output: Contribution to journalArticle

Precursor Cell Lymphoblastic Leukemia-Lymphoma
Mutation
Histones
Methylation
Lysine
4 Citations (Scopus)

Aurora kinase A inhibition provides clinical benefit, normalizes megakaryocytes, and reduces bone marrow fibrosis in patients with myelofibrosis: A phase I trial

Gangat, N., Marinaccio, C., Swords, R., Watts, J. M., Gurbuxani, S., Rademaker, A., Fought, A. J., Frankfurt, O., Altman, J. K., Wen, Q. J., Farnoud, N., Famulare, C. A., Patel, A., Tapia, R., Vallapureddy, R. R., Barath, S., Graf, A., Handlogten, A., Zblewski, D., Patnaik, M. M. & 14 others, Al-Kali, A., Dinh, Y. T., Prahl, K. E., Patel, S., Nobrega, J. C., Tejera, D., Thomassen, A., Gao, J., Ji, P., Rampal, R. K., Giles, F. J., Tefferi, A., Stein, B. & Crispino, J. D., Aug 15 2019, In : Clinical Cancer Research. 25, 16, p. 4898-4906 9 p.

Research output: Contribution to journalArticle

Aurora Kinase A
Primary Myelofibrosis
Megakaryocytes
Fibrosis
Splenomegaly

Erratum: Mechanisms of Progression of Myeloid Preleukemia to Transformed Myeloid Leukemia in Children with Down Syndrome (Cancer Cell (2019) 36(2) (123–138.e10), (S1535610819302983), (10.1016/j.ccell.2019.06.007))

Labuhn, M., Perkins, K., Matzk, S., Varghese, L., Garnett, C., Papaemmanuil, E., Metzner, M., Kennedy, A., Amstislavskiy, V., Risch, T., Bhayadia, R., Samulowski, D., Hernandez, D. C., Stoilova, B., Iotchkova, V., Oppermann, U., Scheer, C., Yoshida, K., Schwarzer, A., Taub, J. W. & 14 others, Crispino, J. D., Weiss, M. J., Hayashi, Y., Taga, T., Ito, E., Ogawa, S., Reinhardt, D., Yaspo, M. L., Campbell, P. J., Roberts, I., Constantinescu, S. N., Vyas, P., Heckl, D. & Klusmann, J. H., Sep 16 2019, In : Cancer Cell. 36, 3, 1 p.

Research output: Contribution to journalComment/debate

Open Access
Preleukemia
Myeloid Leukemia
Down Syndrome
Names
Neoplasms