Abstract
In chronic myeloid leukemia (CML), the BCR-ABL fusion gene is both the therapeutic target of tyrosine kinase inhibitors and the indisputable direct marker of disease burden. Thus, sensitive assays for BCR-ABL now drive therapeutic options and are good surrogates for short- and long-term outcomes. Because CML is such an ideal model, new methods are arising that should make testing in CML faster, more reliable, and reach a greater sensitivity. These methods should be able to be transferred to other hematological malignancies that have mutation markers.
from Cancer via ola Kala on Inoreader http://ift.tt/1RtTp8z
via IFTTT
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου