Cancer immunotherapy is a type of treatment that harnesses the power of the immune systems of patients to target cancer cells with better precision compared to traditional chemotherapy. Several lines of treatment have been approved by the US Food and Drug Administration (FDA) and have led to remarkable success in the treatment of solid tumors, such as melanoma and small-cell lung cancer. These immunotherapies include checkpoint inhibitors, cytokines, and vaccines, while the chimeric antigen receptor (CAR) T-cell treatment has shown better responses in hematological malignancies. Despite these breakthrough achievements, the response to treatment has been variable among patients, and only a small percentage of cancer patients gained from this treatment, depending on the histological type of tumor and other host factors. Cancer cells develop mechanisms to avoid interacting with immune cells in these circumstances, which has an adverse effect on how effectively they react to therapy. These mechanisms arise either due to intrinsic factors within cancer cells or due other cells within the tumor microenvironment (TME). When this scenario is used in a therapeutic setting, the term “resistance to immunotherapy” is applied; “primary resistance” denotes a failure to respond to treatment from the start, and “secondary resistance” denotes a relapse following the initial response to immunotherapy. Here, we provide a thorough summary of the internal and external mechanisms underlying tumor resistance to immunotherapy. Furthermore, a variety of immunotherapies are briefly discussed, along with recent developments that have been employed to prevent relapses following treatment, with a focus on upcoming initiatives to improve the efficacy of immunotherapy for cancer patients.

Triple-negative breast cancer (TNBC) is a highly aggressive malignancy with pronounced immunogenicity, exhibiting rapid proliferation and immune cell infiltration into the tumor microenvironment. TNBC’s heterogeneity poses challenges to immunological treatments, inducing resistance mechanisms in the tumor microenvironment. Therapeutic modalities, including immune checkpoint inhibitors (ICIs) targeting PD-1, PD-L1, and CTLA-4, are explored in preclinical and clinical trials. Promising results emerge from combining ICIs with anti-TGF-β and VISTA, hindering TNBC tumor growth. TNBC cells employ complex evasion strategies involving interactions with stromal and immune cells, suppressing immune recognition through various cytokines, chemokines, and metabolites. The recent focus on unraveling humoral and cellular components aims to disrupt cancer crosstalk within the tumor microenvironment. This review identifies TNBC’s latest resistance mechanisms, exploring potential targets for clinical trials to overcome immune checkpoint resistance and enhance patient survival rates.

Aim: Recent studies show that human microbiomes play a significant role in the development of endometrial carcinoma, which is a common gynecological cancer affecting women of reproductive age. This review provides an extensive analysis of how the microbiome interacts with endometrial carcinoma while focusing on its impact on disease progression and potential therapeutic advancements. Methods: Extensive literature research was conducted to examine how microbial dysbiosis affects endometrial cancer development. The research analyzed both animal model studies and clinical cohort data to assess how microbiome composition influences cancer risk and progression alongside treatment outcomes. The research explored possible microbiome interventions alongside the translational challenges they present. Results: New research findings demonstrate that microbial imbalance contributes to endometrial cancer development through chronic inflammatory processes and estrogen metabolism changes while affecting immune system behavior in the tumor microenvironment. Scientists are exploring unique microbial patterns to serve as biomarkers for detecting diseases and predicting treatment outcomes. Microbiome‐targeted strategies, including probiotics and diet changes, demonstrate the potential to enhance treatment results for individuals receiving immunotherapy and chemotherapy. Conclusions: This review examines the detailed interactions between the microbiome and endometrial carcinoma and outlines their importance in developing predictive models and innovative treatments. We explore both the obstacles faced in applying microbiome research to clinical settings and potential research paths that could speed up the integration of microbiome‐based therapies into patient healthcare.

The clinical practicum for biomedical science students aims to provide graduates with the knowledge and skills required to work in diagnostic laboratory settings. This study examines graduates’ perspectives on content, teachers and clinical training and their satisfaction rates based on the skills gained during training. The study was conducted on females who graduated from Qatar University between 2015 and 2020. We used a previously validated questionnaire called CPAT-QU. Telephonic interviews were conducted and were analyzed using SPSS. The results showed a high satisfaction rate, of 80%, for the content and organization of the clinical training. The participants’ main concerns included the evaluation criteria, as 8.7% were not satisfied. The students suggested increasing the length of the training in order to obtain experience that was more practical. The students’ satisfaction with the teachers was 70% in terms of their attitude, command of knowledge and ability to convey knowledge. In total, 69.5% of the graduates claimed that their instructors were interested in teaching and 4.4% claimed their instructors conveyed disinterest in teaching. The Qatar University graduates were satisfied with the content of their clinical training. However, they reported some gaps in this training. Identifying these gaps will help in restructuring clinical training to improve student experience.

The skin acts as a primary barrier against environmental insults and maintains homeostasis. Injury initiates a wound healing cascade of hemostasis, inflammation, proliferation, and remodeling. In chronic wounds, persistent microbial colonization and inflammation disrupt this process, with bacterial virulence factors acting as key drivers. While the microbiome’s role in chronic wounds is recognized, the effects of individual virulence factors on acute repair remain unclear. Therefore, this study investigated the differential effects of virulence factors derived from five skin-associated bacterial species on acute wound healing dynamics. In this context, virulence factors from Pseudomonas aeruginosa, Staphylococcus aureus, Streptococcus pyogenes, Lactobacillus plantarum, and Enterococcus faecalis were tested on HDF-n cell viability and wound closure, with multiplex ELISA used to assess inflammatory mediator secretion and underlying mechanisms. Overall, virulence factors were generally well tolerated across concentrations (0.05–16 µg/mL) and time points (24, 48 h), with cell viability >80%, except for S. aureus, which reduced viability to ~70% at higher concentrations by 48 h. Wound healing responses varied markedly: S. aureus significantly impaired closure in a dose-dependent manner (~10% closure at 16 µg/µL, 48 h), and E. faecalis similarly delayed repair. In contrast, factors from P. aeruginosa, S. pyogenes, and L. plantarum showed neutral or mildly pro-healing effects. Notably, co-treatment with S. pyogenes partially rescued impairment caused by S. aureus and E. faecalis. Collectively, these findings highlight that bacterial virulence factors have variable impacts on acute wound healing. These findings suggest potential therapeutic applications through targeted modulation or combinations of bacterial factors.