The Penn team, in collaboration with Alain Rook, MD, director of the Cutaneous T -
cell Lymphoma Program and a professor of Dermatology, aims to develop a molecular taxonomy for mutations in SS patients.
Not exact matches
A specialist in leukemia,
lymphoma, and blood and marrow transplantation, Dr. Collins leads the Hematologic Malignancies / Blood and Marrow Transplantation
Program and the combined Adult / Pediatric Stem
Cell Transplant
Program at UT Southwestern Medical Center.
We are part of a National Cancer Institute - funded Specialized
Programs of Research Excellence (SPORE) grant and participate in Children's Oncology Group and internal
lymphoma studies within Texas Children's Cancer Center and the
Cell and Gene Therapy
Program.
The histone lysine methyltransferase KMT2D sustains a gene expression
program that represses B
cell lymphoma development
In this Cancer.net video, Sonali M. Smith, MD, director of the
lymphoma program, provides an introduction to bone marrow / stem
cell transplantation.
This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T -
lymphoma cell lines by modulating
cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B -
lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B -
cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T -
cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid
cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression
program.
A combination of complementary immunotherapy drugs brentuximab vedotin (Adcetris ®) and nivolumab (Opdivo ®) destroyed most cancer
cells in 64 percent of patients with recurrent Hodgkin
lymphoma, according to the results of an early - phase clinical trial led by Catherine M. Diefenbach, MD, assistant professor of medicine and director of the Clinical Lymphoma
lymphoma, according to the results of an early - phase clinical trial led by Catherine M. Diefenbach, MD, assistant professor of medicine and director of the Clinical
Lymphoma Lymphoma Program.