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Currently, the main treatment for familial adenomatous polyposis (FAP) is surgery, however, surgery is far from ideal as there are many complications such as uncontrollable bowel movements, pouch inflammation, anastomotic stricture, and secondary fibroids. Therefore, it is necessary to further expand the understanding of FAP and develop new treatments for FAP. The immune microenvironment including immune cells and cytokines, plays an important role in FAP and the progression of FAP to adenocarcinoma, thus it may be a promising treatment for FAP. In the current review, we summarized the recent progress in the immune microenvironment of FAP.

Triple-negative breast cancer (TNBC) is one of the most aggressive subtypes of breast cancer with poorest clinical outcomes. Patients of childbearing age have a higher probability of TNBC diagnosis, with more demands on maintenance and restoration of physical and psychosocial function. This study aimed to design effective and comprehensive nomograms to predict survival in these patients.

We used the SEER database to identify patients with TNBC aged between 18 and 45 and randomly classified these patients into a training (n=2,296) and a validation (n=2,297) cohort. Nomograms for estimating overall survival (OS) and breast cancer-specific survival (BCSS) were generated based on multivariate Cox proportional hazards models and competing-risk models in the training cohort. anti-PD-L1 antibody The performances of the nomograms were quantified in the validation cohort using calibration curves, time-dependent receiver operating characteristic (ROC) curves and Harrell's concordance index (C-index).

A total of 4,593 TNBC patients of childbearing age were enrolled. Four prognostic factors for OS and six for BCSS were identified and incorporated to construct nomograms. In the validation cohort, calibration curves showed excellent agreement between nomogram-predicted and actual survival data. The nomograms also achieved relatively high Harrell's C-indexes and areas under the time-dependent ROC curves for estimating OS and BCSS in both training and validation cohorts.

Independent prognostic factors were identified, and used to develop nomograms to predict OS and BCSS in childbearing-age patients with TNBC. These models could enable individualized risk estimation and risk-adapted treatment for these patients.

Independent prognostic factors were identified, and used to develop nomograms to predict OS and BCSS in childbearing-age patients with TNBC. These models could enable individualized risk estimation and risk-adapted treatment for these patients.Rapid proliferation of cancer cells is enabled by favoring aerobic glycolysis over mitochondrial oxidative phosphorylation (OXPHOS). P32 (C1QBP/gC1qR) is essential for mitochondrial protein translation and thus indispensable for OXPHOS activity. It is ubiquitously expressed and directed to the mitochondrial matrix in almost all cell types with an excessive up-regulation of p32 expression reported for tumor tissues. We recently demonstrated high levels of non-mitochondrial p32 to be associated with high-grade colorectal carcinoma. Mutations in human p32 are likely to disrupt proper mitochondrial function giving rise to various diseases including cancer. Hence, we aimed to investigate the impact of the most common single nucleotide polymorphism (SNP) rs56014026 in the coding sequence of p32 on tumor cell metabolism. In silico homology modeling of the resulting p.Thr130Met mutated p32 revealed that the single amino acid substitution potentially induces a strong conformational change in the protein, mainly affecting the mitochondrial targeting sequence (MTS). In vitro experiments confirmed an impaired mitochondrial import of mutated p32-T130M, resulting in reduced OXPHOS activity and a shift towards a low metabolic phenotype. Overexpression of p32-T130M maintained terminal differentiation of a goblet cell-like colorectal cancer cell line compared to p32-wt without affecting cell proliferation. Sanger sequencing of tumor samples from 128 CRC patients identified the heterozygous SNP rs56014026 in two well-differentiated, low proliferating adenocarcinomas, supporting our in vitro data. Together, the SNP rs56014026 reduces metabolic activity and proliferation while promoting differentiation in tumor cells.The immune response plays a critical role in gastric cancer (GC) development, metastasis, and treatment. A better understanding of the tumor-immune system interactions in gastric cancer may provide promising diagnostic, prognostic, and therapeutic biomarkers for patients with this disease. In the present study, we aimed to identify a prognostic signature of GC through a comprehensive bioinformatics analysis on the tumor-immune interactions as well as the molecular characteristics. We firstly identified two immunophenotypes and immunological characteristics by employing multiple algorithms, such as the single sample Gene Sets Enrichment Analysis and Cell type Identification By Estimating Relative Subsets of RNA Transcripts. Next, we developed a six-immune-gene signature as a promising independent prognostic biomarker for GC using Lasso Cox regression and verified it via the external validation set and systematically correlated the immune signature with GC clinicopathologic features and genomic characteristics. Finally, a nomogram was successfully constructed based on the immune signature and clinical characteristics and showed a high potential for GC prognosis prediction. This study may shed light on the treatment strategies for GC patients from the perspective of immunology.Cancer initiation, progression, and metastasis leverage many regulatory agents, such as signaling molecules, transcription factors, and regulatory RNA molecules. Among these, regulatory non-coding RNAs have emerged as molecules that control multiple cancer types and their pathologic properties. The human microRNA-211 (MIR211) is one such molecule, which affects several cancer types, including melanoma, glioblastoma, lung adenocarcinomas, breast, ovarian, prostate, and colorectal carcinoma. Previous studies suggested that in certain tumors MIR211 acts as a tumor suppressor while in others it behaves as an oncogenic regulator. Here we summarize the known molecular genetic mechanisms that regulate MIR211 gene expression and molecular pathways that are in turn controlled by MIR211 itself. We discuss how cellular and epigenetic contexts modulate the biological effects of MIR211, which exhibit pleiotropic effects. For example, up-regulation of MIR211 expression down-regulates Warburg effect in melanoma tumor cells associated with an inhibition of the growth of human melanoma cells in vitro, and yet these conditions robustly increase tumor growth in xenografted mice.