Chronic myelogenous leukemia and The Philadelphia chromosome

Introduction and Aim: Chronic myelogenous leukemia (CML), also known as chronic myeloid leukemia, is a myeloproliferative condition marked by increased granulocytic cell proliferation without loss of differentiation potential. CML is responsible for ۱۵–۲۰ percent of all adult leukemias. The Philadelphia chromosome (Ph) is a shortened version of chromosome ۲۲ caused by the reciprocal translocation t(۹;۲۲) (q۳۴;q۱۱), which was initially discovered in a patient with CML in ۱۹۶۰. The goal of this research was to look into the relationship between CML and The Ph. method: The study method is based on the CML articles, which were analyzed by searching scientific databases such as Science Direct, Springer, Google Scholar, PubMed. Results: The results showed a BCR-ABL۱ fusion gene is formed when the proto-oncogene tyrosine-protein kinase (ABL۱) gene on chromosome ۹ is translocated to the breakpoint cluster region (BCR) gene on chromosome ۲۲. BCR-ABL۱ protein isoforms p۲۱۰, p۱۹۰, and p۲۳۰, which have continuously increased tyrosine kinase (TK) activity, are encoded by three BCR-ABL۱ fusion gene hybrids. Downstream signaling pathways are disrupted by these abnormally active kinases, resulting in increased proliferation, differentiation arrest, and resistance to cell death. Conclusion: As a result, the Ph carrying the BCR-ABL۱ fusion gene is the primary initiator of several leukemia phenotypes with varying prognoses. During leukemogenesis, the translocation causes sustained TK activation and genomic instability. Multiple signaling system disorders and genetic abnormalities, in combination with the Ph, are critical for the progression of various kinds of leukemia, including CML.

کلیدواژه ها:

Chronic myeloid leukemia ، Philadelphia chromosome ، BCR-ABL۱