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2. CTX110 Allogeneic CRISPR-Cas9-Engineered CAR T Cells in Patients (Pts) with Relapsed or Refractory (R/R) Large B-Cell Lymphoma (LBCL): Results from the Phase 1 Dose Escalation Carbon Study

Author

McGuirk, Joseph P., primary, Tam, Constantine S., additional, Kröger, Nicolaus, additional, Riedell, Peter A., additional, Murthy, Hemant S., additional, Ho, Phoebe Joy, additional, Maakaron, Joseph E., additional, Waller, Edmund K., additional, Awan, Farrukh T., additional, Shaughnessy, Paul J., additional, Ghobadi, Armin, additional, Bishop, Michael R., additional, Alfonso-Pierola, Ana, additional, Dickinson, Michael, additional, Ramakrishnan Geethakumari, Praveen, additional, Ross, Ainsley, additional, Stevens, William, additional, Xu, Huansheng, additional, Ma, Anna, additional, Cohen, Sarah Beaussant, additional, Maziarz, Richard T., additional, and Bachier, Carlos, additional

Published
2022
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4. How I treat warts, hypogammaglobulinemia, infections, and myelokathexis syndrome

Author

Badolato, Raffaele, Donadieu, Jean, Dotta, Laura, and Beaussant Cohen, Sarah

Subjects
0301 basic medicine, Neutropenia, Primary Immunodeficiency Diseases, Immunology, Infections, Biochemistry, CXCR4, Hypogammaglobulinemia, 03 medical and health sciences, 0302 clinical medicine, Agammaglobulinemia, hemic and lymphatic diseases, medicine, Humans, Preschool, Child, Congenital Neutropenia, Myelokathexis, Bronchiectasis, business.industry, Immunologic Deficiency Syndromes, Autosomal dominant trait, Cell Biology, Hematology, medicine.disease, Biomarkers, Child, Preschool, Disease Progression, Female, Infection, Phenotype, Treatment Outcome, Warts, 030104 developmental biology, 030220 oncology & carcinogenesis, business, WHIM syndrome
Abstract

Warts, hypogammaglobulinemia, infections, and myelokathexis (WHIM) syndrome is a genetic disease characterized by neutropenia, lymphopenia, susceptibility to infections, and myelokathexis, which describes degenerative changes of mature neutrophils and hyperplasia of bone marrow myeloid cells. Some patients present with hypogammaglobulinemia and/or refractory warts of skin and genitalia. Congenital cardiac defects constitute uncommon manifestations of the disease. The disorder, which is inherited as an autosomal dominant trait, is caused by heterozygous mutations of the chemokine receptor CXCR4. These mutations lead to an increased sensitivity of neutrophils and lymphocytes to the unique ligand CXCL12 and to an increased accumulation of mature neutrophils in the bone marrow. Despite greatly improved knowledge of the disease, therapeutic choices are insufficient to prevent some of the disease outcomes, such as development of bronchiectasis, anogenital dysplasia, or invasive cancer. The available therapeutic measures aimed at preventing the risk for infection in WHIM patients are discussed. We critically evaluate the diagnostic criteria of WHIM syndrome, particularly when WHIM syndrome should be suspected in patients with congenital neutropenia and lymphopenia despite the absence of hypogammaglobulinemia and/or warts. Finally, we discuss recent results of trials evaluating plerixafor, a selective antagonist of CXCR4, as a mechanism-oriented strategy for treatment of WHIM patients.

Published
2017
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6. PKC412 Inhibits the ZNF198-FGFR1 Fusion Tyrosine Kinase and Is Efficacious in Treatment of t(8;13)(p11;q12) Associated Stem Cell Myeloproliferative Disease.

Author

Chen, Jing, primary, DeAngelo, Daniel J., additional, Kutok, Jeffery L., additional, Williams, Ifor R., additional, Lee, Benjamin H., additional, Wadleigh, Martha, additional, Duclos, Nicole, additional, Cohen, Sarah, additional, Adelsperger, Jennifer, additional, Okabe, Rachel, additional, Coburn, Allison, additional, Galinsky, Ilene, additional, Huntly, Brian J.P., additional, Cohen, Pamela, additional, Meyer, Thomas, additional, Fabbro, Doriano, additional, Banerji, Lolita, additional, Griffin, James D., additional, Xiao, Sheng, additional, Fletcher, Jonathan A., additional, Stone, Richard M., additional, and Gilliland, D. Gary, additional

Published
2004
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8. PKC412 Effectively Inhibits Constitutively Activated FGFR3 Mutants in Murine Leukemia Models and t(4;14) Myeloma Cell Lines.

Author

Chen, Jing, primary, Lee, Benjamin H., primary, Williams, Ifor R., primary, Kutok, Jeffery L., primary, Duclos, Nicole, primary, Cohen, Sarah, primary, Adelsperger, Jennifer, primary, Okabe, Rachel, primary, Coburn, Allison, primary, Moore, Sandra, primary, Huntly, Brian J.P., primary, Mitsiades, Constantine S., primary, Anderson, Kenneth C., primary, Griffin, James D., primary, Fabbro, Doriano, primary, and Gilliland, D. Gary, primary

Published
2004
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9. Oncogenic K-rascooperates with PML-RARα to induce an acute promyelocytic leukemia-like disease

Author

Chan, Iris T., Kutok, Jeffery L., Williams, Ifor R., Cohen, Sarah, Moore, Sandra, Shigematsu, Hirokazu, Ley, Timothy J., Akashi, Koichi, Le Beau, Michelle M., and Gilliland, D. Gary

Abstract

Most patients with acute promyelocytic leukemia (APL) express PML-RARα, the fusion product of t(15;17)(q22;q11.2). Transgenic mice expressing PML-RARα develop APL with long latency, low penetrance, and acquired cytogenetic abnormalities. Based on observations that 4% to 10% of APL patients harbor oncogenic rasmutations, we coexpressed oncogenic K-rasfrom its endogenous promoter with PML-RARα to generate a short-latency, highly penetrant mouse model of APL. The APL disease was characterized by splenomegaly, leukocytosis, extramedullary hematopoiesis (EMH) in spleen and liver with an increased proportion of immature myeloperoxidase-expressing myeloid forms; transplantability to secondary recipients; and lack of cytogenetic abnormalities. Bone marrow cells showed enhanced self-renewal in vitro. This model establishes a role for oncogenic ras in leukemia pathogenesis and thus validates the oncogenic RAS signaling pathway as a potential target for therapeutic inhibition in leukemia patients. This mouse model should be useful for investigating signaling pathways that promote self-renewal in APL and for testing the in vivo efficacy of RAS signaling pathway inhibitors in conjunction with other targeted therapies such as ATRA (all transretinoic acid) and arsenic trioxide.

Published
2006
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