Not exact matches
Basically, CAR - T therapy
involves taking a patient's own immune «killer» T -
cells, inserting new genetic code into those
cells which turn them into cancer - hunters that can home in on
malignant B -
cells (another kind of immune
cell), and then pumping these specialized leukemia - busting
cells back into the patient.
By providing a woman's family history of these cancers, including the ages they were diagnosed, the programs calculate a probability that the patient carries a harmful mutation in BRCA1 or BRCA2 (genes
involved in controlling
malignant cell growth).
By manipulating it in vitro, a team of researchers led by Prof. David Mooney at Harvard SEAS have identified a possible mechanism by which normal
cells turn
malignant in mammary epithelial tissues, the tissues frequently
involved in breast cancer.
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.
Cambridge, Mass. — June 16, 2014 — A team of researchers led by David J. Mooney, Robert P. Pinkas Family Professor of Bioengineering at the Harvard School of Engineering and Applied Sciences (SEAS), have identified a possible mechanism by which normal
cells turn
malignant in mammary epithelial tissues, the tissues frequently
involved in breast cancer.
We do not know the precise cause of
malignant cancers of bones in dogs but abnormal bone
cell growth and unusual hormone stimulation may be
involved.
Leukemia is a progressive,
malignant disease that
involves out - of - control growth of white blood
cells (leukocytes) in a dog's blood and bone marrow.