thymosin and Brain-Neoplasms

Thymosin beta15 is a small actin-binding protein upregulated in highly metastatic rat prostate cancer cells, relative to low metastatic cells. We have previously established an important role for thymosin beta15 as a diagnostic marker in human prostate cancer, with potential as a prognostic indicator. We here review the data supporting increased thymosin beta15 expression in other cancer types, including breast, brain, and lung. Human NB thymosin beta is a beta-thymosin originally found in neuroblastoma. New data demonstrate that NB thymosin beta represents the human homolog of rat thymosin beta15; thus we suggest classification as human thymosin beta15. In addition to the previously described gene, thymosin beta15a, we report the discovery of a new isoform of human thymosin beta15, thymosin beta15b, which is transcribed from an independent gene on human chromosome X. The gene structure of thymosin beta15a and beta15b is conserved and the isoforms show 87% identity across the nucleotide sequence. Across the coding sequence the nucleotide differences are silent, resulting in identical proteins. Other thymosin family members have recently been shown to exert potent clinical effects. The functional data available for thymosin beta15, combined with the tumor expression pattern, suggest that thymosin beta15 may play an important role in tumor development and progression in addition to its value as a biomarker in prostate cancer.

Topics: Amino Acid Sequence; Animals; Brain Neoplasms; Breast Neoplasms; Endometrial Neoplasms; Female; Head and Neck Neoplasms; Humans; Male; Molecular Sequence Data; Prostatic Neoplasms; Protein Isoforms; Rats; RNA, Messenger; Sequence Alignment; Sequence Homology, Amino Acid; Thymosin

From June 1979 through April 1982, we treated 35 patients with limited small cell carcinoma on an intensive chemo-radio-immunotherapy regimen, consisting of induction with cyclophosphamide, doxorubicin, and vincristine, alternately cycled with VP-16 and cisplatin. Patients were stratified by performance status and randomized to thymosin, fraction V, or no thymosin. Induction was followed by consolidation, consisting of prophylactic whole-brain radiotherapy and multifield radiotherapy to the primary and mediastinum with cyclophosphamide and vincristine. Patients who were complete responders (CRs) postconsolidation resumed maintenance immediately. Patients were followed from 1 to 3.8 years (median, 2.2 years) at the time of analysis. After induction, 35% (12/34) had become CRs; after consolidation radiotherapy, an additional 10/34 became CRs for a total CR rate of 65% (22/34). There were only 9/34 local failures (26%), of which all but one were impatients who had not become CRs. A prolonged median survival (21 months) has been obtained in patients with limited small cell carcinoma of lung treated with an intensive combined modality regimen. At 1 year, survival is 83%; at 2 years, 46%. There is a 33% long-term survival (greater than 3 years). There is no difference in survival or recurrence rate between patients treated with or without thymosin.

Topics: Adult; Aged; Antineoplastic Combined Chemotherapy Protocols; Brain Neoplasms; Carcinoma, Small Cell; Combined Modality Therapy; Female; Follow-Up Studies; Humans; Lung Neoplasms; Male; Middle Aged; Prognosis; Radiotherapy Dosage; Thymosin; Tomography, X-Ray Computed

Glioma is a highly aggressive form of brain cancer characterized by limited treatment options and poor patient prognosis. In this study, we aimed to elucidate the oncogenic role of thymosin beta-10 (TMSB10) in glioma through comprehensive analyses of patient data from the TCGA and GTEx databases. Our investigation encompassed several key aspects, including the analysis of patients' clinical characteristics, survival analysis, in vitro and in vivo functional experiments, and the exploration of correlations between TMSB10 expression and immune cell infiltration. Our findings revealed a significant upregulation of TMSB10 expression in glioma tissues compared to normal brain tissues, with higher expression levels observed in tumors of advanced histological grades. Moreover, we observed positive correlations between TMSB10 expression and patient age, while no significant association with gender was detected. Additionally, TMSB10 exhibited marked elevation in gliomas with wild-type IDH and noncodeletion of 1p/19q. Survival analysis indicated that high TMSB10 expression was significantly associated with worse overall survival, disease-specific survival, and progression-free survival in glioma patients. Functionally, knockdown of TMSB10 in glioma cells resulted in reduced cellular growth rates and impaired tumor growth in xenograft models. Furthermore, our study revealed intriguing correlations between TMSB10 expression and immune cell infiltration within the tumor microenvironment. Specifically, TMSB10 showed negative associations with plasmacytoid dendritic cells (pDC) and

Topics: Brain Neoplasms; Clinical Relevance; Glioma; Humans; Prognosis; Survival Analysis; Thymosin; Tumor Microenvironment

Topics: Brain Neoplasms; Glioma; Glycoproteins; Hemodynamics; Humans; Immunity, Cellular; Lymphocytes; Skin Tests; T-Lymphocytes; Thymosin