Oncotarget最新文献

Background: Breast cancer is a type of cancer that can affect both males and females, but it is widespread among women. Blood types may be associated with breast cancer, as many studies have reported on this relationship but rarely described it. The primary objective of our research is to summarize and analyze the available evidence to produce comprehensive and accurate information that can be used to make evidence-based decisions.

Methods: Researchers searched for studies on breast cancer patients and ABO blood groups across four major databases: PubMed, Scopus, Web of Science, and Google. The outcomes of the studies were presented as a relative risk and odds ratio with a 95% confidence interval.

Results: Twenty-nine case-control studies with 13029 breast cancer patients. Blood type A was the most common blood type among patients. For blood type A, there was an association with breast cancer (OR = 1.18, 95% CI: 1.03-1.36). Blood types B, AB, and Rh factor showed no significant association with breast cancer (OR = 0.97, 95% CI: 0.86-1.11, OR = 1.05, 95% CI: 0.89-1.25, and OR = 1.14, 95% CI: 0.81-1.60 respectively) in compare to blood type A.

Conclusions: This study highlights the potential of blood type A as a risk factor for breast cancer compared to blood type O. This relationship was insignificant for blood types B, AB, or Rh. Further studies are needed to understand the mechanisms behind the blood type and breast cancer correlation.

N6-methyladenosine (m6A), one of the most prominent and reversible internal modifications of eukaryotic RNAs, has emerged as a critical regulator of gene expression in various cancers including oral squamous cell carcinoma (OSCC), wherein it shapes the tumor-specific epitranscriptomic gene-regulatory networks. METTL3, the primary m6A RNA methyltransferase, is significantly upregulated in OSCC cells leading to increased global m6A levels. Interestingly, METTL3 positively regulates miRNA biogenesis by modulating the processing of primary miRNAs in a m6A-dependent manner. We identified miR-146a-5p, an oncogenic miRNA as one of the METTL3-regulated miRNAs in OSCC. METTL3-depletion or inhibition of its catalytic activity leads to a reduction of miR-146a-5p and an appreciable accumulation of primary miR-146a in OSCC cells. Functional assays examining the effects of miR-146a-5p inhibition or overexpression confirm its oncogenic role in OSCC pathophysiology. Further, SMAD4, a central transducer in TGF-β signaling, was identified as a miR-146a-5p target. In OSCC cells, SMAD4-depletion exacerbates the oncogenic traits, whereas its overexpression exerts the opposite effect. Additionally, METTL3-depletion dysregulates SMAD4-regulated genes suggesting its potential involvement in SMAD4-dependent TGF-β signaling. Taken together, we report that METTL3, an oncogene regulates the expression of SMAD4, a tumor-suppressor via miR-146a-5p, thus unveiling a novel regulatory axis of METTL3/miR-146a-5p/SMAD4 in OSCC, which can potentially have therapeutic implications.

Host immunosurveillance is an important factor in the progression of high-grade squamous intraepithelial lesions (HSIL) into high-risk human papillomavirus (HR-HPV)-related squamous cell carcinoma. Immune escape by forkhead box protein P3 (FOXP3+) immunoregulatory T cells and the programmed death-ligand 1 (PD1/PD-L1) axis, mechanisms best described in the context of invasive neoplasms, may play a role in the evolution of pre-malignant lesions. This morphological study aimed to characterize the inflammatory response and expression of FOXP3 and PD-L1 in anal, vulvar, and penile HSILs and compare them with those in low-grade SILs co-infected with HR-HPV (LSIL_HR). The study group comprised 157 samples from 95 male and 55 female patients (median age = 35.5 years), including 122 HSILs and 35 LSILs_HR. Dense inflammatory infiltrates and high counts of FOXP3⁺ cells were significantly more frequent in patients with HSILs than in those with LSILs_HR (p = 0.04 and 0.02, respectively). HSILs also exhibited higher PD-L1 expression (p_adj < 0.01 and < 0.01 for the SP142 and 22C3 clones, respectively), based on the Poisson generalized linear model. In addition, concordant higher PD-L1 expression was observed in cases with a greater number of FOXP3+ cells (p < 0.05). Our findings indicate a putative role of transcriptionally active HR-HPV in evoking an inflammatory response and immune evasion in the early phases of carcinogenesis in a subset of non-cervical anogenital HSILs.

The polymorphic genes PTGS1 and PTGS2 encode cyclooxygenases COX-1 and COX-2, respectively. Overexpression of these cyclooxygenases is linked to inflammation and neoplasms. This study investigated the potential association between the single nucleotide polymorphism (SNP) -842A>G (rs10306114) of the PTGS1 gene and SNP-765G>C (rs20417) of the PTGS2 gene with prostate cancer (PCa) and benign prostate hyperplasia (BPH). Blood leucocyte DNA from 56 healthy individuals, 61 individuals with PCa, and 51 individuals with BPH were genotyped using the PCR-RFLP method. Associations were inferred by calculating odds ratios (OR) and relative risks (RR) of genotype distributions and allele frequencies. The genotypes for both SNPs were in Hardy-Weinberg equilibrium for all groups. No significant association was observed between the A or G alleles or the AA, AG, or GG genotypes of the SNP-842A>G of the PTGS1 gene and prostatic diseases. However, the C allele of SNP-765G>C of the PTGS2 gene was significantly associated with an increased risk of BPH (OR = 2.30, p-value = 0.01). Differences in the ratios of GG/GC and GG/(GC+CC) genotypes also suggested a potential association between the C allele and PCa (p-value <0.1), and the combined affected (PCa+BPH) group (p-value <0.04). The small sample size and sampling from one ethnic group are limitations of this study.

Recent advances in deep learning models have transformed medical imaging analysis, particularly in radiology. This editorial outlines how uncertainty quantification through embedding-based approaches enhances diagnostic accuracy and reliability in hepatobiliary imaging, with a specific focus on oncological conditions and early detection of precancerous lesions. We explore modern architectures like the Anisotropic Hybrid Network (AHUNet), which leverages both 2D imaging and 3D volumetric data through innovative convolutional approaches. We consider the implications for quality assurance in radiological practice and discuss recent clinical applications.