Ibrutinib and Venetoclax — Doubling Down on CLL
Adrian Wiestner, M.D., Ph.D.
This article has no abstract; the first 100 words appear below.
https://www.nejm.org/doi/full/10.1056/NEJMe1904362?query=oncology-hematology
Chronic lymphocytic leukemia (CLL) is a clonal expansion of mature B cells in blood, bone marrow, and lymphoid tissues that usually manifests as a high lymphocyte count in the circulating blood. Cell expansion is driven by constitutive B-cell receptor signaling and sustained by overexpression of the antiapoptotic protein B-cell lymphoma 2 (BCL2) (Fig. 1A).1,2 Microbial and autoantigens have been implicated in activating B-cell receptor signaling in CLL cells. Furthermore, many types of B-cell receptors that are expressed by CLL cells also bind to epitopes within their structural domains, promoting cell-autonomous signaling. B-cell receptor signaling mainly occurs in lymphoid tissues and . . .
Adrian Wiestner, M.D., Ph.D.
This article has no abstract; the first 100 words appear below.
https://www.nejm.org/doi/full/10.1056/NEJMe1904362?query=oncology-hematology
Chronic lymphocytic leukemia (CLL) is a clonal expansion of mature B cells in blood, bone marrow, and lymphoid tissues that usually manifests as a high lymphocyte count in the circulating blood. Cell expansion is driven by constitutive B-cell receptor signaling and sustained by overexpression of the antiapoptotic protein B-cell lymphoma 2 (BCL2) (Fig. 1A).1,2 Microbial and autoantigens have been implicated in activating B-cell receptor signaling in CLL cells. Furthermore, many types of B-cell receptors that are expressed by CLL cells also bind to epitopes within their structural domains, promoting cell-autonomous signaling. B-cell receptor signaling mainly occurs in lymphoid tissues and . . .
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου