mostafa kamandi

and 1 more

IntroductionChronic Myeloid Leukemia (CML) is a clonal disorder of hematopoietic stem cells, characterized by the presence of a specific chromosomal translocation, t(9;22)(q34;q11), which generates the so-called Philadelphia chromosome (Ph), denoted as 22q–. This cytogenetic abnormality results in the fusion of the ABL1 gene on chromosome 9 with the BCR gene on chromosome 22, producing the BCR–ABL1 fusion gene. The resulting fusion protein exhibits constitutive tyrosine kinase activity, driving uncontrolled cell proliferation. While the molecular basis and downstream signaling pathways of CML are well elucidated, the initial events that trigger this translocation remain unclear. (1) Chronic Lymphocytic Leukemia (CLL) is defined by the clonal expansion and progressive accumulation of mature B lymphocytes, most of which express the CD5 antigen. These cells infiltrate the peripheral blood, bone marrow, lymphatic tissues, and spleen. The initiating leukemogenic event is thought to occur at the level of multipotent hematopoietic stem cells with self-renewal capacity, although the precise pathogenesis remains an area of active investigation. (2) Chronic Lymphocytic Leukemia (CLL) is the most prevalent form of leukemia in adults across Western countries. Its incidence is comparable between Europe and the United States, estimated at approximately 4 to 6 cases per 100,000 individuals annually. In 2014, around 15,720 new cases were projected in the U.S., alongside over 12,000 new diagnoses within Europe. The likelihood of developing CLL increases substantially with age, with over 70% of patients diagnosed at 65 years or older. (3)However, coexistence of CML and CLL in a single patient is exceedingly rare, and there are few documented cases of this in the medical literature, with only a limited number of cases reported in the medical literature. Documented presentations include both sequential diagnoses, where one malignancy follows the other, and synchronous onset, in which both entities are identified at the same time. (4) In most of the documented cases, CML has been diagnosed either following or preceding a diagnosis of CLL. Simultaneous presentation of both malignancies is exceptionally uncommon. The underlying pathogenesis of this rare co-occurrence remains poorly understood. It is still under debate whether CML and CLL in such cases originate from a common hematopoietic progenitor cell or represent independent clonal proliferations arising through separate oncogenic events. (5)In this Study, we present the case of a 79-year-old male who was concurrently diagnosed with CLL and CML, highlighting the clinical presentation, diagnostic workup, and therapeutic approach. This case underscores the importance of comprehensive evaluation in patients presenting with atypical hematological findings and contributes to the limited body of knowledge on the co-existence of CLL and CML.

Mostafa Kamandi

and 7 more

Background: Adult T-cell leukemia (ATL) is one of the most important hematological malignancies caused by the HTLV-I virus. The disease has a poor prognosis due to the low median survival of the patients. Aim: Given the need for effective therapeutic interventions, this study aimed to investigate the efficacy of Hyper-CVAD and As/IFN/AZT regimens and compare their performance. Methods and Results: This study is a randomized clinical trial conducted on individuals recently diagnosed with acute ATL. Individuals who tested positive in a HTLV-I serological test based on ELISA and/or PCR were randomly assigned to receive treatment with either Hyper-CVAD or As/IFN/AZT using block randomization. The drug regimens were administered for 60 days, and patients underwent follow-up assessments. Overall, 29 individuals were enrolled in the trial. No significant differences were found in gender distribution, LDH levels, and lymphocyte counts between the two groups (P-value>0.05). The treatment response rates for the Hyper-CVAD and As/IFN/AZT regimens were 46.67% and 35.71%, respectively, with no significant differences between the two groups (P-value >0.05). Survival analysis revealed a significant difference in survival between the two groups, favoring those under the Hyper-CVAD regimen (P-value<0.05). The predominant toxicities were hematological toxicities; one patient in the Hyper-CVAD group experienced Grade 3 toxicity, while three patients in the As/IFN/AZT group experienced Grade 3 toxicity. Conclusion: The results of this study suggest no significant differences in efficacy between the Hyper-CVAD and As/IFN/AZT regimens. Additionally, higher toxicity rates were observed in the As/IFN/AZT regimen. Further investigations into frontline treatments and the timing of the As/IFN/AZT regimen in future studies may provide valuable insights in this regard. Clinical Trial Registration: IRCT20210703051770N1.