Chronic lymphocytic leukemia (CLL) and acute lymphoblastic leukemia (ALL) are blood cancers that affect lymphocytes and can be diagnosed by flow cytometry. Flow cytometry is a laboratory technique that analyzes cell properties, including cell surface markers such as cluster of differentiation 19 (CD19).
The main objective of this study was to explore the correlation of the number of CD19-positive cells with other CD antigens in patients with CLL and ALL.
After receiving ethical approval (Approval No. 5S/401), blood was collected from participants who had been diagnosed by a physician. Then the collected blood was prepared for flow cytometry analysis according to the protocol by staining with fluorescent antibodies.
The results of the current study showed that sex and different age groups had no statistical influence on the number of CD19-positive cells in the patients evaluated. The generated models did not reveal an association with the number of CD19-positive cells in patients with CLL and ALL. In patients with CLL, the number of cells expressing CD5, CD20, CD23, and CD200 was significantly and positively related with the number of CD19-positive cells. In patients with ALL, the number of cells expressing CD79 and CD99 was significantly and positively correlated with the number of CD19-positive cells. This comparison study also found that in patients with CLL, the number of CD19-positive cells was significantly higher than the number of cells expressing CD20, CD23, and CD200. In patents with ALL, there was a significantly higher number of CD19-positive cells than CD34-positive and CD79-positive cells.
In patients with CLL, there was a strong positive correlation between the number of CD19-positive cells and the number of cells expressing CD5, CD20, CD23, and CD200. Additionally, in patients with ALL, there was a positive correlation of CD79 and CD99 with the number of CD19-positive cells.
© 2024 The Authors.

Metabolic flexibility allows cells to adapt to various environments and limits the efficacy of metabolic drugs. Therapeutic targeting of cancer metabolism relies on defining limiting requirements and vulnerabilities in the highly dynamic metabolic network. Here, we characterize the metabolic reprogramming and identify cancer-specific metabolic vulnerabilities in response to the pharmacological inhibition of mitochondrial complex I. Our work reveals the adaptation mechanism in malignant lymphocytes providing resistance against the biguanides phenformin and metformin by transcriptionally reprogramming glucose metabolism. Metabolic adaptation to complex I inhibition is mediated by mitochondrial reactive oxygen species (mROS) serving as a mitochondrial stress signal activating hypoxia-inducible factor-1a (HIF-1a). Inhibition of the mROS/HIF-1a axis through antioxidants or direct suppression of HIF-1a selectively disrupts metabolic adaptation and survival during complex I dysfunction in malignant lymphocytes. Our results identify HIF-1a signaling as a critical factor in resistance against biguanide-induced mitochondrial dysfunction, allowing selective targeting of metabolic pathways in leukemia and lymphoma.
Published by Elsevier Inc.

Primary plasma cell leukemia (pPCL) is an uncommon form of plasma cell dyscrasia, and the most aggressive of the human monoclonal gammopathies. The t(11;14)(q13;q32) rearrangement is the most common alteration in pPCL, promoting cyclin D1 (CCND1) gene overexpression caused by its juxtaposition with the immunoglobulin heavy locus chromosome region. The myeloma overexpressed (MYEOV) gene maps very close to the CCND1 gene on chromosome 11, but its overexpression is rarely observed in multiple myeloma. The present study describes a case of pPCL with t(11;14) characterized by a breakpoint on der(11), unlike the one usually observed. Droplet digital polymerase chain reaction analysis revealed overexpression of CCND1 and MYEOV. To the best of our knowledge, MYEOV gene overexpression has never been previously described in pPCL.