Autophagy is no longer considered merely a cellular recycling mechanism but rather a critical regulator of metabolic adaptation, immune homeostasis, and stress responses. In cancer, its dual function enables context-dependent effects, acting as a tumor-suppressive mechanism during early carcinogenesis while supporting tumor survival and therapeutic resistance in established malignancies. Among stress-response pathways, autophagy occupies a central position at the interface of cellular metabolism, immune regulation, and microbial sensing. Dysregulated autophagy has been implicated in metabolic reprogramming, immune evasion, tumor progression, and resistance to anticancer therapies [1]. The intratumoral microbiome is increasingly recognized as a potential functional component of the tumor microenvironment (TME). Tumor-resident microorganisms and their metabolites can influence tumor biology, immune activity, and therapeutic responses, rather than acting merely as passive bystanders [2,3]. Importantly, microbial communities can engage in dynamic crosstalk with host signaling and metabolic pathways, including autophagy, while autophagy itself contributes to the regulation of host–microbe interactions and immune responses. The biological consequences of this bidirectional interplay are likely to depend on the microbial composition, cancer type, disease stage, and characteristics of the surrounding TME [4]. Oral squamous cell carcinoma (OSCC) provides a useful model for studying this interaction because it develops in a microbiota-rich environment where epithelial cells, immune cells, and microorganisms continuously interact. Increasing evidence indicates that oral microorganisms can directly influence tumor behavior through inflammatory signaling, immune modulation, and alteration of host cellular pathways. Importantly, recent experimental studies have provided direct evidence linking specific oral microorganisms to autophagy in oral cancer. Porphyromonas gingivalis has been shown to promote OSCC progression by modulating autophagy [5], while outer membrane vesicles derived from Fusobacterium nucleatum activate autophagic flux and promote oral cancer invasion and metastasis [6]. Together, these findings suggest that microbial signals can actively shape autophagic responses in oral cancer. These observations raise a broader question: do individual microorganisms exert isolated effects on autophagy, or does the intratumoral microbial ecosystem collectively shape autophagic plasticity within OSCC? Although specific microorganism–autophagy interactions have now been demonstrated, the broader relationship between the intratumoral microbiome and autophagy remains poorly defined. We propose that the intratumoral microbiome may function as an upstream regulator of autophagic plasticity, with the potential to influence tumor adaptation, immune escape, and therapeutic responsiveness. In this context, alterations in microbial composition or microbial-derived metabolites could potentially reprogram autophagic activity and modify the response of tumor cells to anticancer therapies. This concept also suggests a potential therapeutic opportunity. Rather than targeting autophagy or the tumor-associated microbiome independently, future approaches could explore whether manipulation of the intratumoral microbiome can be used to reprogram autophagy and restore therapeutic sensitivity. Such strategies may include targeted modulation of microbial communities or their metabolites, potentially in combination with agents that regulate autophagic activity. Future studies should therefore investigate the microbiome–autophagy axis at the level of microbial composition, microbial metabolites, host signaling pathways, and treatment response. Establishing the causal relationships within this axis could provide a new conceptual framework for precision therapeutic strategies in OSCC.

BACKGROUND HER2 overexpression marks out a biologically aggressive targetable subset of breast cancer accounting for 15–20% of cases in Western series Data from Iraq are limited and Karbala Province has not been studied before MATERIALS AND METHODS We reviewed 99 women with confirmed invasive breast cancer at a single Karbala centre grouped into four age bands (28–39 40–49 50–59 60–69 years) HER2 was scored 0 1+ 2+ or 3+ by immunohistochemistry (IHC) using the 2013 ASCOCAP guideline We tested associations with age and histological type using chisquare tests and multivariable logistic regression (HER2 3+ as the dependent variable) reporting odds ratios (OR) and 95% confidence intervals (CI) RESULTS The 40–49year band was largest (333%) Invasive ductal carcinoma was the most common type (566%) followed by locally advanced disease (162%) invasive lobular carcinoma (121%) metastatic carcinoma (81%) and triplenegative breast cancer (71%) Fortyseven tumours (475%) were HER2negative (IHC 0); of the rest 13 (131%) scored 1+ 13 (131%) scored 2+ (equivocal) and 26 (263%) scored 3+ meeting strict ASCOCAP positivity criteria HER2 score was not linked to age (χ² = 782 p = 025) but histology varied significantly with age (χ² = 524 p < 0001) No variable independently predicted HER2 3+ positivity (IDC vs other: OR 175 95% CI 068–452 p = 024) CONCLUSIONS Over half of this cohort showed detectable HER2 expression and the strict HER2positivity rate (263%) is higher than the global benchmark in line with other Arab cohorts Reflex FISH was not available onsite to confirm equivocal (2+) cases pointing to a need for expanded confirmatory testing Histology but not age alone varied meaningfully across age groups which should inform diagnostic planning

Background: Cancer remains a major global health problem, with 20 million newly diagnosed cases and an estimated 9.7 million cancer deaths in 2022. Cancer cell proliferation is closely related to the dysregulation of cell cycle progression, which is mainly mediated by cyclin-dependent kinases (CDKs). In this study, neoflavonoids are investigated as novel therapeutic agents that target CDK4, a key regulator of cell cycle transition from G1 to S phase. Method: We performed a pan-cancer analysis of CDK expression using several state-of-the-art databases and found high CDK4 levels in many cancers, and in several cancers higher CDK4 levels were associated with poorer patient survival. Molecular docking studies were performed on 26 neoflavonoid compounds to determine their binding affinity at the ATP binding site of CDK4 to the known inhibitors aemaciclib and flavopiridol. Results: We found that several neoflavonoids bind with similar affinities to these established inhibitors and thus may be effective CDK4 inhibitors. Conclusion: This research shows the therapeutic potential of neoflavonoids in the treatment of cancer and suggests that more preclinical studies are needed to confirm their effectiveness and clarify their mechanisms of action.

Africa contribute significantly in the global burden of breast cancer. Crucial efforts have been made to understand the landscape of breast cancer in sub-Saharan Africa (SSA). This article specifically examine the the existing evidence to better understand the risk factors that shape the epidemiology of breast cancer within the SSA region. This article sets off by discussing the epidemiology of breast cancer in SSA, with emphasis on how disparities occur in the region. The article explored the incidence rate across various countries in SSA. The article explored the various risk factors associated with breast cancer in SSA including genetic factors, relevant biomarkers, hormonal factors, reproductive factors, and some disparities in treatments amongst others. Genetics mutations in BRCA1 and BRCA2 genes were discussed, buttressing how they contribute to the occurrence of breast cancer in the region. Certain biomarkers were also identified as risk factors of breast cancer and deserving of mention is the kaiso biomarker. Hormonal and reproductive factors such as age, breastfeeding time, family history, and body hormones such as estrogen and progesterone amongst others were identified as common risk factors of breast cancer in SSA. The poor treatment strategies and regimens in breast cancer care in SSA is also associated with breast cancer outcome, leading to an overall impact on the epidemiology of breast cancer in SSA. Evidence-based recommendations were also made to improve breast cancer care in SSA. Recommended techniques to addressing breast cancer care rely on genetic insights primarily aimed at informing a technologically-inclined future progress and research.  

Introduction:Breast cancer is the most common invasive cancer among women worldwide. While advancements in early diagnosis and treatment have improved survival rates, many breast cancer patients experience persistent sleep disturbances, anxiety, and stress, which negatively impact their quality of life. Pharmacological treatments for sleep disorders pose risks such as dependency and side effects, making non-pharmacological interventions like mindfulness-based interventions (MBIs) increasingly relevant. This systematic review evaluates the effectiveness of MBIs, particularly Mindfulness-Based Stress Reduction (MBSR) and Mindfulness-Based Cognitive Therapy (MBCT), in improving sleep quality and reducing psychological distress in breast cancer patients. Methods:Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a comprehensive search was conducted across databases including PubMed, Web of Science (WOS), Scopus, Cochrane Library, SID, Irandoc, and Noormags. Studies published up to November 5, 2024, were screened using Medical Subject Headings (MeSH) terms and Boolean operators. Eligible studies included randomized controlled trials (RCTs) and quasi-experimental studies investigating MBIs' effects on sleep and psychological health in breast cancer patients. Data extraction and quality assessment were performed using the Joanna Briggs Institute (JBI) checklist. Results:Out of 207 initially identified studies, eight met the inclusion criteria. MBIs significantly improved sleep quality by reducing insomnia severity, sleep latency, and nighttime awakenings while enhancing sleep efficiency. Additionally, MBIs led to substantial reductions in anxiety and depression scores. Some studies reported improvements in emotional resilience and psychological well-being. However, variations in intervention duration, follow-up periods, and study designs influenced result consistency. Discussion:The findings indicate that MBIs effectively enhance sleep quality and reduce psychological distress in breast cancer patients. Compared to pharmacological treatments, MBIs provide a safer, non-invasive alternative. The benefits are attributed to mindfulness-induced stress reduction and emotional regulation. Despite promising outcomes, variations in methodologies and limited long-term evaluations warrant further research. Conclusion:MBIs are a valuable complementary approach to conventional breast cancer care, addressing sleep and psychological challenges. Further large-scale, high-quality RCTs are needed to confirm long-term efficacy and establish standardized protocols.

Prostate cancer (PCa) is the second most prevalent malignancy and a leading cause of cancer-related mortality in males worldwide. Despite advancements in therapeutic strategies, such as radical prostatectomy, radiotherapy, androgen deprivation therapy (ADT), and chemotherapy, treatment outcomes for metastatic castration-resistant PCa (mCRPC) remain suboptimal. The androgen receptor (AR) and its downstream signaling pathways play a critical role in PCa progression, with genetic aberrations, including AR amplification, TP53 and PTEN deletions, and MYC oncogene activation contributing to disease advancement. Although prostate-specific antigen (PSA)-based screening is widely used, its limitations in improving survival rates highlight the urgent need for more reliable biomarkers. Emerging evidence indicates that non-coding RNAs (ncRNAs), including long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs), act as key regulators of gene expression, influencing PCa cell proliferation, apoptosis, invasion, and metastasis. Their differential expression across various stages of PCa underscores their potential as prognostic and diagnostic biomarkers as well as therapeutic targets. This review summarizes recent advancements in ncRNA research in PCa, providing insights into their mechanistic roles, clinical applications, and future directions in precision oncology