Opinion Article - (2024) Volume 13, Issue 2

Role of Cytogenetics and Chromosomal Variants in CML
Masahiro Hidaka*
 
Department of Biology, Sapporo Hokuyu Hospital, Sapporo, Japan
 
*Correspondence: Masahiro Hidaka, Department of Biology, Sapporo Hokuyu Hospital, Sapporo, Japan, Email:

Received: 04-Jun-2024, Manuscript No. GJBAHS-24-26469; Editor assigned: 07-Jun-2024, Pre QC No. GJBAHS-24-26469 (PQ); Reviewed: 21-Jun-2024, QC No. GJBAHS-24-26469 (QC); Revised: 28-Jun-2024, Manuscript No. GJBAHS-24-26469 (R); Published: 05-Jul-2024, DOI: 10.35248/2319-5584.24.13.222

Description

A rare form of neoplasia, Chronic Myeloid Leukemia (CML) has an annual incidence of 1-2 cases per 100,000 people. CML accounts for 0.5% of all new cases of cancer in the United States and is the most common chronic myeloproliferative neoplasm. This addresses 15% of all leukemia in grown-ups and is more normal in men than ladies (1.3-1.7 contrasted with 1.0). According to estimates provided by the National Institutes of Health (NIH), there will be approximately 1,080 deaths and 8,950 new cases of CML in 2017. CML is most common in people between the ages of 40 and 60, with a mean age of 53, and only 10% of patients are diagnosed when they are younger than 20. The clonal expansion of hematopoietic progenitor cells in CML leads to an increase in the number of granulocytic cells that circulate in the body. Chronic fatigue, anemia, agranulocytosis, and immature granulocytes, as well as the presence of basophils, thrombocytosis, and splenomegaly, are the disease's most defining symptoms.

At the chronic phase of the disease, the first CML treatments significantly improved quality of life. For a long time, the main treatment accessible for patients was hematopoietic undeveloped cells transplantation. The development of cytogenetic research that involved molecular alterations and the Philadelphia chromosome enabled the development of a novel perspective for the treatment of CML, making it more accurate and efficient. The point of this article is a refreshed survey about CML, featuring the significance of cytogenetic examination for checking progress and remedial administration of this disease. CML is traditionally described by the presence of the Ph chromosome (Ph+), saw as in 90% of the patients. CML is referred to as atypical (aCML) and is pathobiologically distinct from conventional CML in the absence of the Ph chromosome (Ph-). There are only 1-2 cases of this type of leukemia for every 100 cases of Ph+ CML. It is anticipated that the rates of survival and survival without progression of the disease will be 80% and 86%, respectively.

Past basic corresponding movement between chromosome 9 and 22, around 5%-10% of CML cases might have variation Ph movements. In addition to chromosomes 9 and 22, these straightforward variants always alter chromosome 22. In 9 to 16 percent of CML patients with a normal karyotype, secondary changes or other complex cryptic chromosomal rearrangements in BCR-ABL1 may be observed. Ph+ cells frequently contain Additional Chromosomal Abnormalities (ACAs), which are categorized as "major" or "minor" route changes. These changes impede the disease's progression and increase in the advanced stage, rising from 30% in AP to 80% in BC. They are connected with unfortunate forecast, with lower pace of cytogenetic reaction rate to treatment with Imatinib Mesylate (IM).

The fact that major-route ACAs have a worse prognosis than minor-route ACAs demonstrates that the impact of cytogenetic alterations is dependent on the type of ACA, not the percentage at which these alterations occur. Trisomy 8, isochromosome 17 q, and the second Ph chromosome are the abnormalities that are found in advanced CML with major-route ACA the most frequently. Shorter overall survival and progression-free survival are linked to them. These patients have a poor clinical outcome and a low rate of response to Tyrosine Kinase Inhibitor (TKI) treatment. Since the presence of these abnormalities during treatment reflects genetic instability and, as a result, a negative response to the drug, this information may assist the physician in selecting alternative therapeutic options, despite the fact that it is not entirely clear.

Citation: Hidaka M (2024) Role of Cytogenetics and Chromosomal Variants in CML. Glob J Agric Health Sci. 13.222.

Copyright: © 2024 Hidaka M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.