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Yingmei Wu,1,2,* Junhui Zheng,1,2,* Yanhua Yan,1,2 Jiduo Liu,3 Yingchun Zhou3 1Guangzhou University of Chinese Medicine, Guangzhou, 510000, People’s Republic of China; 2Lingnan Medical Research Center, Guangzhou University of Chinese Medicine, Guangzhou, 510000, People’s Republic of China; 3Department of Clinical Laboratory, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, 510000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yingchun Zhou; Jiduo LiuDepartment of Clinical Laboratory, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, 510000, People’s Republic of ChinaEmail yingchunbaby@126.com; 13668996592@163.comBackground: Gelsolin (GSN) is the most widely expressed actin-severing protein in humans, which could regulate cell morphology, differentiation, movement and apoptosis. This study aims to explore the GSN as a prognostic biomarker of stomach adenocarcinoma (STAD).Methods: In this study, we used several online databases to comprehensively analyze the role of GSN in STAD. Oncomine and HPA databases were used to explore the GSN expression in various cancer, especially in gastric cancer. Then, UALCAN database was used to evaluate the relationship between GSN expression and promoter methylation in clinical characteristics. Finally, we used TIMER to analyze the correlation between GSN expression and immune infiltrates in gastric cancer.Results: GSN was down-regulated in gastric cancer, and decreased expression of GSN was related to worse survival. The GSN expression was significantly related to tumor purity in STAD and significantly correlated with infiltrating level of various immune cells, especially the dendritic cells.Conclusion: Our study proposes that GSN can be served as the biomarker of disease and neoantigen for STAD treatment, which can improve the deficiency of disease-specific targeted therapies currently exist.Keywords: gelsolin, gastric cancer, prognosis, immune cell infiltration

Lineage switch is very rare in blastic crisis of chronic myeloid leukemia (CML-BC). Here, we report a case of CML-BC in which the blast lineage switched from myeloid to B-lymphoid. A 35-year-old male was initially admitted to our hospital because of abdominal distention for over a year and dizziness for one week. Prior to presentation at our hospital, he visited a local hospital because of abdominal distention where his white blood cell count and bone marrow (BM) smear indicated CML. Results from peripheral blood (PB) counts, bone marrow analysis, immunophenotyping by flow cytometry, and the detection of the Philadelphia chromosome were consistent with a diagnosis of myeloid blast crisis from CML. The patient received chemotherapy with imatinib for induction, which diminished the number of blasts. However, after three months, the blasts were increased in the PB and BM. The BM study and immunophenotyping by flow cytometry revealed B-lymphoblastic leukemia. In accordance with his first admission, a chromosome study revealed a karyotype of 46, XY, t(9; 22)(q34; q11) in all 20 cells analyzed, and B-lymphoblastic transformation from CML was diagnosed. Despite three months of treatment with DVCP (daunorubicin, vincristine, cyclophosphamide and prednisone) chemotherapy in combination with dasatinib, the patient did not achieve complete remission. The patient decided to stop treatment and was discharged from the hospital for financial reasons. This case implicates the Philadelphia chromosome with p210 BCR-ABL1 fusion proteins as a key molecule in CML-BC. Further research is needed to assess the frequency, treatment, and prognosis of CML-BC patients with lineage switch.