Oncolytic viruses (OVs) are emerging as potential treatment options for cancer. Natural and genetically engineered viruses exhibit various antitumor mechanisms. OVs act by direct cytolysis, the potentiation of the immune system through antigen release, and the activation of inflammatory responses or indirectly by interference with different types of elements in the tumor microenvironment, modification of energy metabolism in tumor cells, and antiangiogenic action. The action of OVs is pleiotropic, and they show varied interactions with the host and tumor cells. An important impediment in oncolytic virotherapy is the journey of the virus into the tumor cells and the possibility of its binding to different biological and nonbiological vectors. OVs have been demonstrated to eliminate cancer cells that are resistant to standard treatments in many clinical trials for various cancers (melanoma, lung, and hepatic); however, there are several elements of resistance to the action of viruses per se. Therefore, it is necessary to evaluate the combination of OVs with other standard treatment modalities, such as chemotherapy, immunotherapy, targeted therapies, and cellular therapies, to increase the response rate. This review provides a comprehensive update on OVs, their use in oncolytic virotherapy, and the future prospects of this therapy alongside the standard therapies currently used in cancer treatment.

Background: The prognostic value of Immunoscore was evaluated in Stage II/III colon cancer (CC) patients, but it remains unclear in Stage I/II, and in early-stage subgroups at risk. An international Society for Immunotherapy of Cancer (SITC) study evaluated the pre-defined consensus Immunoscore in tumors from 1885 AJCC/UICC-TNM Stage I/II CC patients from Canada/USA (Cohort 1) and Europe/Asia (Cohort 2). METHODS: Digital-pathology is used to quantify the densities of CD3+ and CD8+ T-lymphocyte in the center of tumor (CT) and the invasive margin (IM). The time to recurrence (TTR) was the primary endpoint. Secondary endpoints were disease-free survival (DFS), overall survival (OS), prognosis in Stage I, Stage II, Stage II-high-risk, and microsatellite-stable (MSS) patients. RESULTS: High-Immunoscore presented with the lowest risk of recurrence in both cohorts. In Stage I/II, recurrence-free rates at 5 years were 78.4% (95%-CI, 74.4–82.6), 88.1% (95%-CI, 85.7–90.4), 93.4% (95%-CI, 91.1–95.8) in low, intermediate and high Immunoscore, respectively (HR (Hi vs. Lo) = 0.27 (95%-CI, 0.18–0.41); p < 0.0001). In Cox multivariable analysis, the association of Immunoscore to outcome was independent (TTR: HR (Hi vs. Lo) = 0.29, (95%-CI, 0.17–0.50); p < 0.0001) of the patient’s gender, T-stage, sidedness, and microsatellite instability-status (MSI). A significant association of Immunoscore with survival was found for Stage II, high-risk Stage II, T4N0 and MSS patients. The Immunoscore also showed significant association with TTR in Stage-I (HR (Hi vs. Lo) = 0.07 (95%-CI, 0.01–0.61); P = 0.016). The Immunoscore had the strongest (69.5%) contribution χ² for influencing survival. Patients with a high Immunoscore had prolonged TTR in T4N0 tumors even for patients not receiving chemotherapy, and the Immunoscore remained the only significant parameter in multivariable analysis. CONCLUSION: In early CC, low Immunoscore reliably identifies patients at risk of relapse for whom a more intensive surveillance program or adjuvant treatment should be considered.

Cervical cancer ranks third among malignant diseases of the female reproductive system and progressively develops through a series of pathological changes known as cervical intraepithelial neoplasia (CIN). Despite being extremely aggressive and causing increased mortality, the main treatment options include surgery or a combination of chemotherapy and radiotherapy, often based on cisplatin-based chemotherapy and external beam radiotherapy or brachytherapy. Cervical dysplasia is an abnormal growth of cells on the surface of the cervix that could lead to cervical cancer. CIN most commonly occurs at the squamocolumnar junction of the cervix, a transitional zone between the squamous epithelium of the vagina and the columnar epithelium of the endocervix. The primary cause of CIN is chronic infection of the cervix with Human Papillomavirus (HPV). Oxidative stress (OS) and chronic inflammation are associated with HPV-induced cervical dysplasia. Reactive oxygen species (ROS) facilitate the progression of CIN through DNA damage, immune evasion, and cellular mutations. Thus, the inflammatory environment, characterized by increased expression of proinflammatory cytokines, contributes to epithelial transformation. Given these mechanisms, antioxidants, including vitamins A, C, D, E, polyphenols, and carotenoids, are being investigated for their potential as adjunctive therapies in CIN management. This review aims to provide a comprehensive analysis of the influence of oxidative stress, antioxidants, and inflammation on cervical cancer.

Natural compounds have garnered increasing interest as potential antitumor agents due to their multifaceted biological activities and relatively low toxicity profiles. This review focuses on three well-studied natural molecules: rhein, curcumin, and resveratrol, analyzing and comparing their antitumor potential across a variety of cancer models. For each compound, we present an integrated perspective encompassing natural sources, physicochemical properties, pharmacological and pharmacokinetic characteristics, and the latest in vitro and in vivo evidence of anticancer activity. Special attention is given to the molecular mechanisms underlying their antitumor effects, including the modulation of cell cycle regulators, induction of apoptosis, inhibition of metastasis and angiogenesis, and regulation of key signaling pathways such as NF-κB, PI3K/Akt/mTOR, STAT3, and MAPKs. Although numerous studies highlighted their therapeutic promise, significant barriers remain—particularly related to poor solubility and limited bioavailability—which have hindered clinical translation, especially in the case of rhein. Advances in nanotechnology-based drug delivery systems offer promising solutions to these limitations, enabling improved targeting and enhanced efficacy. This review underscores the need for continued preclinical and clinical investigations to fully elucidate the therapeutic value of these compounds and support their integration into modern oncological treatment strategies.

Branched-chain amino acids (BCAAs), comprising leucine (Leu), isoleucine (Ile), and valine (Val), are essential nutrients vital for protein synthesis and metabolic regulation via specialized signaling networks. Their association with cardiovascular diseases (CVDs) has become a focal point of scientific debate, with emerging evidence suggesting both beneficial and detrimental roles. This review aims to dissect the multifaceted relationship between BCAAs and cardiovascular health, exploring the molecular mechanisms and clinical implications. Elevated BCAA levels have also been linked to insulin resistance (IR), type 2 diabetes mellitus (T2DM), inflammation, and dyslipidemia, which are well-established risk factors for CVD. Central to these processes are key pathways such as mammalian target of rapamycin (mTOR) signaling, nuclear factor kappa-light-chain-enhancer of activate B cells (NF-κB)-mediated inflammation, and oxidative stress. Additionally, the interplay between BCAA metabolism and gut microbiota, particularly the production of metabolites like trimethylamine-N-oxide (TMAO), adds another layer of complexity. Contrarily, some studies propose that BCAAs may have cardioprotective effects under certain conditions, contributing to muscle maintenance and metabolic health. This review critically evaluates the evidence, addressing the biological basis and signal transduction mechanism, and also discusses the potential for BCAAs to act as biomarkers versus active mediators of cardiovascular pathology. By presenting a balanced analysis, this review seeks to clarify the contentious roles of BCAAs in CVD, providing a foundation for future research and therapeutic strategies required because of the rising prevalence, incidence, and total burden of CVDs.

Kounis syndrome (KS) is a rare condition where hypersensitivity reactions trigger coronary vasospasm, destabilization of atherosclerotic plaques, or stent thrombosis, posing diagnostic and therapeutic challenges due to its overlap with acute coronary syndrome (ACS) and the absence of specific guidelines. This study reviews cases of KS from the Institute of Cardiovascular Disease to highlight clinical presentations, triggers, and treatment strategies. We analyzed four cases of KS treated at our institution between 2019 and 2024. Detailed clinical histories, laboratory findings, imaging studies, and treatment plans were reviewed. Patients were classified by KS subtype based on coronary anatomy and pathophysiological mechanisms. Management strategies were tailored to each subtype, combining myocardial revascularization, antiplatelet therapy, and treatment for allergic reactions. The series included two cases of Type I KS in patients with structurally normal coronary arteries and two cases of Type II KS involving pre-existing atherosclerosis. No Type III KS was observed. Triggers included insect stings, antibiotics, iodinated contrast agents, and anesthetics. Coronary angiography confirmed the diagnosis in all cases. Treatments included percutaneous coronary interventions, dual antiplatelet therapy, and prophylactic antihistamines or corticosteroids. All patients experienced favorable outcomes, although diagnostic delays were noted in cases with atypical presentations. KS remains underdiagnosed, especially in emergency settings where it mimics ACS. Early recognition and multidisciplinary management involving allergology and cardiology are crucial. Future research should focus on safer diagnostic tools, understanding the pathophysiology, and developing evidence-based preventive strategies. Increasing the awareness of KS and its inclusion in ACS differentials are essential to improving patient outcomes and preventing recurrences.