Nutlin-3a-targeted p53 signaling induced cytotoxicity preclinically, along with new compounds such as ibrutinib, Prima<sup>Met</sup>, or CP31398 that bypass p53 pathway in WM, paving the path for future treatment-tailored options.<b>Conclusions:</b> Our results highlight the clinical significance of detection of <i>TP5</i>3 alteration in WM to determine the prognosis of WM and guide the treatment choice.<i></i>.
Furthermore, siRNA knockdown of p53 in WM cell line did not influence the PRIMA-1Met-induced apoptotic response whereas silencing of p73 inhibited latter response in WM cells.
We studied mononuclear cells from 100 patients with chronic B-cell leukemias [B-CLL, 90 patients; B-prolymphocytic leukemia (B-PLL), 7; Waldenström's macroglobulinemia (WM), 3] by fluorescence ISH with a genomic p53 DNA probe.
Fourteen patients with various leukemias were examined and two with acute lymphoblastic leukemia and one with Waldenström's macroglobulinemia were identified to have mutations in the coding region of the p53 gene.