Background 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.
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.
Hemophagocytic lymphohistiocytosis (HLH) is a rare hyperinflammatory syndrome characterized by fever, pancytopenia and splenomegaly. The underlying hemophagocytosis occurs primarily in the bone marrow, liver and lymph nodes. Multiple microbiological agents, including cytomegalovirus, Epstein-Barr virus and Mycobacterium tuberculosis, have been implicated in the pathogenesis of HLH. The present study presents a case of HLH associated with Leuconostoc pseudomesenteroides infection treated successfully with clindamycin. A 33-year-old man presented with recurrent episodes of fever and diarrhea. Upon initial treatment at another hospital (the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China), blood chemistry analysis demonstrated moderate anemia (hemoglobin 88 g/l; reference range, 120.0–160.0), elevated ferritin (1,068.47 mg/l; reference range, 21.81–274.66), total bilirubin (392.4 mmol/l; reference range, 5.1–28.0), conjugated bilirubin (335.7 mmol/l; reference range, 0–10.0), and γ-glutamyl transpeptidase (150 U/l; reference range, 10–60). The patient was treated with antibiotics for suspected pneumonia and cholecystitis, but new symptoms (including diarrhea and inflammatory colitis) started to emerge. The patient was subsequently treated with ganciclovir (5 mg/kg/day for 1 month), but body temperature increased to 41.0°C. Upon transferring to our hospital, the patient had severe anemia (hemoglobin, 39 g/l; red blood cell, 1.61×1012/l; reference range, 4.0–5.5×1012/l). Jaundice was apparent: Total bilirubin, 299.5 mmol/l; conjugated bilirubin, 215.7 mmol/l. The patient was treated with clindamycin (150 mg, taken orally every 12 h for 1 week) and supportive care that included parenteral nutrition. Symptoms rapidly dissipated after the treatment. Blood chemistry analysis 5 days after the first dose of clindamycin revealed substantial improvement in anemia and jaundice. The patient requested discharge for financial reasons, but continued treatment (details not available) at a local hospital (Pengpai Memorial Hospital, Shanwei, China). Upon a visit to our hospital 8 months later, the patient has no notable complaints, with the exception of moderate anemia. The present case suggests that HLH may be associated with L. pseudomesenteroides infection.
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