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A11, a S100 calcium-binding protein, has been identified as the oncogene of most tumors. To determine the expression of S100A11, this analysis used public records from The Cancer Genome Atlas and the Genotype-Tissue Expression database. For Gene set variation analysis of S100A11, the R package "GSVA" was used. To further investigate the connection between S100A11 and TME, the R package "ESTIMATE" was used. The Genomics of Drug Sensitivity in Cancer database was used to investigate the effect of S100A11 on anticancer drug kinetics. In addition, S100A11 expression in pan-cancer was highly related to the majority of immunosuppressive cells, such as tumor-associated macrophages, tumor-associated fibroblasts, and Treg cells. In addition, the regulation of S100A11 expression made cancer patients with cancer-resistant to the administration of the majority anticancer drugs, such as sorafenib, difficult to treat. Patients with cancer resistant to sorafenib therapy were unable to tolerate S100A11 expression after regulation.
Source link: https://europepmc.org/article/MED/36605485
The two key variables in NMIBC's pathophysiology are age and sex, with age and sex as the two main variables. Here, we explore a significant knowledge gap in the role of BCG-induced rise of a B cell population called, u2018atypical B cells u2019 in the context of age and sex. We first looked at whether pre-BCG TLSs associates had an immediate reaction to BCG. The discovery of immune related proteins in pre-BCG TLSs in tumors from both BCG responders and non-responders in both BCG responders and non-responders, according to spatial proteomic profiling of 49 immune function and phenotype-associated proteins. ABCs are injected to the bladder mucosa following repeated BCG instillations in the induction phase and dampen local anti-tumor immunity in patients who are classified as non-responders by BCG. We hypothesized that ABCs are recruited to the bladder mucosa. We investigated the role of B cells in aging mice using the N-butyl-N-nitrosamine carcinogen-induced murine model. Local and systemic immune responses to Bladder's post-BCG therapy were characterized as either B cell depletion or B cell depletion. BCG treatment in combination with B-cell depletion resulted in distinct bladder immune microenvironment states and systemic immune profiles. This research shows that ABCs play a key role in disease progression, and that B cell-infiltrate pre-BCG therapy TA-TLSs reflects a systemically exhausted B cell functional state in patients classified as BCG non-responders. The findings from this research provide the first evidence indicating the role of B cells/ABCs in BCG responses and may help with future translation to the development of pharmaceuticals along the B cell exhaustion axis.
Source link: https://europepmc.org/article/PPR/PPR590600
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