Constitutive Ras signaling and Ink4a/Arf inactivation cooperate during the development of B-ALL in mice-Reference-Cited by-同舟云学术

Constitutive Ras signaling and Ink4a/Arf inactivation cooperate during the development of B-ALL in mice

Published:2017-11-21 Issue:25 Volume:1 Page:2361-2374
ISSN:2473-9529
Container-title:Blood Advances
language:en
Short-container-title:

Author:

Sewastianik Tomasz¹²,Jiang Meng¹³,Sukhdeo Kumar⁴⁵,Patel Sanjay S.⁶,Roberts Kathryn⁷,Kang Yue¹,Alduaij Ahmad⁸,Dennis Peter S.¹,Lawney Brian⁹,Liu Ruiyang¹,Song Zeyuan¹,Xiong Jessie¹⁰,Zhang Yunyu¹¹,Lemieux Madeleine E.¹²,Pinkus Geraldine S.⁶,Rich Jeremy N.⁴,Weinstock David M.¹¹,Mullighan Charles G.⁷,Sharpless Norman E.¹⁰,Carrasco Ruben D.¹⁶

Affiliation:

1. Department of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, MA;

2. Department of Experimental Hematology, Institute of Hematology and Transfusion Medicine, Warsaw, Poland;

3. Department of Surgical Oncology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China;

4. Department of Stem Cell Biology and Regenerative Medicine, Cleveland Clinic, Cleveland, OH;

5. Department of Pathology, Case Western Reserve University, Cleveland, OH;

6. Department of Pathology, Brigham & Women’s Hospital, Boston, MA;

7. Department of Pathology, St. Jude Children’s Research Hospital, Memphis, TN;

8. Pathology and Laboratory Medicine Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, United Arab Emirates;

9. Center for Computational Cancer Biology, Dana-Farber Cancer Institute, Boston, MA;

10. Lineberger Comprehensive Cancer Center, School of Medicine, University of North Carolina, Chapel Hill, NC;

11. Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA; and

12. Bioinfo, Plantagenet, ON, Canada

Abstract

Key Points Ras pathway activation cooperates with Ink4a/Arf locus deletion in B cells to induce a fully penetrant lymphoma/leukemia phenotype in mice. These tumors resemble high-risk subtypes of human B-ALL, providing a convenient and highly reproducible model of refractory B-ALL.

Publisher

American Society of Hematology

Subject

Hematology

Link

http://ashpublications.org/bloodadvances/article-pdf/1/25/2361/879286/advances012211.pdf

Reference71 articles.

1. Where do we stand in the treatment of relapsed acute lymphoblastic leukemia?;Raetz,2012

2. Adolescents and young adults with acute lymphoblastic leukemia;Stock,2010

3. Genomic profiling of high-risk acute lymphoblastic leukemia;Collins-Underwood;Leukemia,2010

4. Genomics in acute lymphoblastic leukaemia: insights and treatment implications;Roberts;Nat Rev Clin Oncol,2015

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