Gastric cancer (GC) continues to be a significant global contributor to cancer-related mortality, primarily due to late-stage diagnoses, tumor heterogeneity, and the frequent emergence of therapeutic resistance. Despite advancements in surgical techniques, chemotherapy, targeted therapies, and immunotherapy, long-term survival rates remain unsatisfactory, underscoring the need for innovative, molecularly driven approaches. SiRNA has emerged as a promising gene-silencing tool capable of selectively downregulating oncogenic drivers and pathways associated with resistance via RNA interference. Preclinical studies using GC models demonstrate promising biological activity following siRNA-mediated suppression of various molecular targets - including CD44v6, Rac1, and ZNRD1-leading to reduced cell proliferation, inhibited migration and invasion, enhanced apoptosis, and increased chemosensitivity. However, the successful translation of siRNA-based strategies into clinical practice is fundamentally reliant on the development of efficient and safe delivery systems. Recent advancements in nanotechnology have enabled the development of multifunctional nanocarriers, including lipid-based nanoparticles, peptide-based systems, chitosanderived platforms, exosome-mimetic vesicles, layer-by-layer architectures, and stimuli-responsive theranostic nanoparticles. These engineered platforms are designed to enhance siRNA stability, improve tumor targeting, facilitate intracellular trafficking, and promote endosomal escape while minimizing off-target effects and immune activation. Preclinical findings suggest significant biological potential; however, additional research is required to address issues concerning biodistribution, safety, scalability, and regulatory standardization before clinical application. Overall, siRNA-based strategies may play a crucial role in the future development of precision-oriented therapeutic frameworks in GC research. Importantly, this review emphasizes the integration of molecular target selection with delivery system design in a GC-specific context. By systematically linking validated siRNA targets with corresponding nanocarrier strategies, this work provides a more application-oriented and translationally relevant perspective that is not typically addressed in conventional RNA interference or nanocarrier-focused reviews.

Recently, the identification of minimal residual disease (MRD), also known as measurable residual disease, has seen significant advances driven by the evolving technological landscape in this field. Initially based on raw morphology, the field has since evolved to incorporate karyotyping, cytogenetics, flow cytometry, and other sensitive methods. This updated review discusses key technical considerations for successful MRD detection. We explore the correlation between the results obtained by flow cytometry and molecular genetic techniques.

Respiratory motion is a concern in radiotherapy of most sites, including breast cancer. Conventional radiation treatment planning routinely increases the margins around breast target volumes to account for motion. However, few studies have quantified the actual extent of respiratory motion during free breathing. A review of publicly available four-dimensional computed tomography (4D CT) video data was conducted to estimate the preponderance of breast respiratory motion. Selected videos were those containing sequences displaying movement of the breast/chest wall. Images were visually categorized as showing minimal motion if movements were estimated as ≤ 3 mm, moderate if about 5 mm, and substantial if about 10 mm or more. Respiratory motion of the breast/chest wall was minimal in 22 of the 38 cases (57.9%), moderate in 12 cases (31.6%), and substantial in 4 cases (10.5%). In line with emerging surface-guided data, this video review shows the frequent observation of minimal respiratory motion of the breast/chest wall. These findings question whether routine respiratory-motion-based target expansion is necessary in all patients.

Adenosquamous carcinoma and pure squamous cell carcinoma (SCC) of the rectum are extremely rare malignancies, accounting for approximately 0.15% of all colorectal cancers. Increasing attention has been paid to tumor phenotypic plasticity in the context of intensive anticancer therapy. We report the case of a 45-year-old patient with locally advanced rectal adenocarcinoma (cT4bN2M0) who underwent total neoadjuvant therapy consisting of XELOX chemotherapy combined with pelvic radiotherapy. Baseline biopsy samples from multiple tumor areas showed moderately differentiated adenocarcinoma with an intestinal immunophenotype. After treatment, the resected tumor showed complete loss of intestinal differentiation markers (CK20, CDX2) and the emergence of a squamous immunophenotype with positive expression of p40 and p63. Histologically, the tumor was composed exclusively of poorly differentiated SCC. PCR analysis detected HPV16 DNA in the SCC component. Strong, diffuse p16INK4a expression was observed in both the primary adenocarcinoma and the post-treatment tumor. These findings indicate a marked therapy-associated phenotypic shift in tumor differentiation. However, the underlying biological mechanism remains uncertain. Possible explanations include therapy-associated tumor plasticity, clonal selection of a pre-existing squamous subclone, or an initially unrecognized mixed tumor phenotype. This case highlights the importance of careful pathological reassessment after neoadjuvant therapy in rectal cancer and illustrates the complexity of interpreting phenotypic changes in treated tumors. The potential role of HPV in such processes remains hypothetical and requires further investigation.

Thiazole and thiazolidinone derivatives constitute an important class of heterocyclic compounds, widely investigated in modern medicinal chemistry for their diverse biological activities and significant potential for structural modification. Particular attention has focused on their anticancer properties and the design of multifunctional hybrid molecules with improved pharmacological profiles. This review summarizes recent advances in the synthesis and biological evaluation of functionally substituted condensed and non-condensed thiazole/thiazolidinone derivatives with anticancer activity. Available literature demonstrates that many of these compounds exhibit pronounced cytotoxic and pro-apoptotic effects across various tumor models. Their biological activity is associated with interactions with multiple molecular targets, including PPARγ receptors, integrins, PI3K/mtOR signaling pathways, histone deacetylases, matrix metalloproteina- ses, StAt3, and Pim-kinases. These multitarget mechanisms highlight the potential of these heterocyclic scaffolds for developing innovative anticancer agents. Analysis of structure-activity relationships has revealed promising directions for further optimization of the lead compounds. Overall, thiazole and thiazolidinone derivatives remain attractive plat- forms for the rational design of new anticancer drugs with improved selectivity and reduced toxicity.

Cancer metastasis, the process by which cancer cells spread from the primary tumor to distant sites, remains the leading cause of cancer-related deaths. Th s complex process involves a series of steps, including cell detachment, migration, invasion, survival in the circulatory system, extravasation, and colonization of new tissues. A fundamental characteristic of cancer cells is their altered metabolism, often exhibiting increased glucose uptake and a preference for glycolysis even in the presence of oxygen, a phenomenon known as the Warburg effect. Th s metabolic shift provides cancer cells with a rapid source of adenosine triphosphate (AtP) and essential biosynthetic intermediates, supporting their rapid growth and proliferation. While early concepts attributed the Warburg effect to mitochon- drial dysfunction, it is now recognized that mitochondria in cancer cells often remain functionally active, including oxidative phosphorylation, and critically regulate tumor progression. Notably, metastatic cells frequently depend on mitochondrial activity, refl cting metabolic plasticity that supports dissemination. Thus, targeting glycolysis-mito- chondria crosstalk may represent a promising antimetastatic therapeutic strategy. Th s review aims to elucidate the mechanisms by which inhibitors of glycolysis and OXPhOS impact cancer cell migration, invasion, and metastasis, and to explore their potential therapeutic applications.