White blood cells (WBCs) are the cells of immune system, protecting against infective diseases and invasion of viruses and bacteria. Their aberrant number, both abnormal increase and decrease, is a sign of an ongoing pathology, a precise evaluation of their number is of the utmost importance as the first step of assessing a potential disease. In blood cell microscopic images, since red blood cells and platelets are similar in color with WBCs, and WBCs are partially adhesive, WBC segmentation for counting is often not resulting in a good performance. Therefore, in this work, a color space transformation is proposed to filter out red blood cells and platelets, which is transforming the blood cell microscopic images of patients with acute lymphoblastic leukemia from RGB color space to HSV to detect and extract WBCs. For precisely segmenting adhesive WBCs in extraction results, we set cell border to the third class, in addition to foreground and background. A weighted cross-entropy loss function based on class weight and distance transformation weight enhanced U-Net to learn cell border features. Our results showed that the method proposed in this paper for WBC segmentation using the data set ALL_IDB1 could achieve an accuracy of 97.92%.

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Multiple myeloma is the second most commonly diagnosed hematologic malignancy. As an incurable disease, the molecular mechanisms underlying its many aspects remain unclear. Intracellular calcium ion is an essential signaling molecule that modulates malignant cell behavior, and abnormal regulation of cellular calcium homeostasis may promote cancer cell survival and induce drug resistance. Transient receptor potential (TRP) cation channels are a superfamily of non-selective Ca 2+ -permeable channels that regulate intracellular calcium signaling and are involved in the regulation of various characteristics of cancer cells. Emerging evidence shows a close connection between TRP channels and multiple myeloma. This review summarizes the roles of TRP channels in multiple myeloma progression, metastasis, bone destruction, and drug resistance. TRPV1 and TRPV2 orchestrate the progression of multiple myeloma, while TRPM7 promotes myeloma cell dissemination and spreading. TRPV2 and TRPV4, that activate osteoclasts, contribute to the development of osteolytic bone disease caused by multiple myeloma. Both TRPV1 inhibition and TRPV2 activation synergize with bortezomib in the chemotherapy of multiple myeloma, and TRPC1 can determine the responsiveness of multiple myeloma to MTI-101, a cyclic beta-hairpin peptide.Antagonizing TRPA1 can alleviate bortezomib-induced painful peripheral neuropathy. Future studies in this field may identify certain TRP channels as markers or therapeutic targets for predicting the prognosis, preventing progression, and improving drug responsiveness in patients with multiple myeloma.