The early detection of cutaneous melanoma is critical to survival outcomes. Because less than one half of melanomas in the United States are diagnosed by dermatologists, the ABCD (asymmetry, border irregularity, color variation, diameter >6 mm) acronym, created 40 years ago with the later addition of "E" for evolution (ABCDE), was developed for nondermatologist health care professionals and the public to simplify and enhance the diagnosis of early melanoma. It continues to be the global, naked-eye, nondevice-assisted standard for initial triage of pigmented lesions. This clinical review discusses the changing clinical diagnostic landscape and examines the currently available first-line and second-line detection modalities for melanoma. It also provides updates to the first-line triage approach and discusses the challenges of regulatory agency oversight for the safe and effective use of current and emerging skin cancer detection technologies. It is critical that health care professionals globally have knowledge of these technologies to enhance their diagnosis of melanoma.

Breast carcinoma remains a major global health burden requiring innovative diagnostic and therapeutic strategies. Exosomal miRNAs have emerged as key factors in breast carcinoma that influence tumor progression, metastasis and treatment resistance. Recent studies have elucidated their mechanisms of action, including their roles in regulating oncogenic and tumor‑suppressive pathways, modulating the tumor microenvironment and promoting chemo‑resistance. Advances in miRNA‑based therapies such as miRNA mimics and inhibitors have shown promise in combination treatments, enhancing their therapeutic efficacy. Furthermore, exosomal miRNAs play a role in breast carcinoma calcification, offering novel insights into tumor progression. Unlike previous reviews that focus on a single function or therapeutic potential of miRNAs, the present review systematically integrated the multilevel role of exosomal miRNAs in breast cancer from the two dimensions of oncogenicity and tumor inhibition and the regulatory mechanism of breast carcinoma calcification and proposes that the exosomal miRNA calcification axis may be a key link connecting tumor metabolism and pathological calcification. Despite the potential of miRNAs, challenges remain in optimizing exosome isolation techniques and standardizing miRNA detection methods for clinical applications. Future research should focus on refining miRNA‑based liquid biopsies, developing delivery systems that target exosomes to enhance therapeutic efficacy and early detection strategies and ultimately improving patient survival and quality of life. The present review comprehensively explored the roles of exosomal miRNAs and highlighted their importance in breast carcinoma research. The present review illustrated the potential of exosomal miRNAs as non‑invasive biomarkers and therapeutic targets in precision medicine.

Mitochondria are central to cellular metabolic reprogramming, and their energy metabolism pathways are indispensable for T‑cell activation, proliferation and differentiation. Mitochondrial metabolic reprogramming enhances T‑cell activity and antitumor function. Mitochondrial dynamics, including fusion, fission and transfer, regulate T‑cell tumor immune function by modulating the number, morphology and distribution of mitochondria, which is vital for the antitumor effects of T cells. The release of mitochondrial DNA can activate multiple innate immune signaling pathways, such as cyclic GMP‑AMP synthase‑stimulator of interferon genes, Toll‑like receptor 9, and NOD‑, LRR‑, and pyrin domain‑containing protein 3, serving a complex regulatory role in shaping the tumor immunosuppressive microenvironment and T‑cell antitumor immune responses. Notably, mitochondrial dysfunction is a major driver of tumor initiation and progression. T‑cell mitochondrial metabolic reprogramming, dynamic changes and mitochondrial DNA release all affect the antitumor immunity of tumor‑infiltrating T cells. The present review focuses on the relationship between mitochondria and T‑cell antitumor immune responses, exploring the core role of mitochondria in T‑cell tumor immunity from multiple aspects, including mitochondrial energy metabolism, mitochondrial dynamics and mitochondrial DNA. In addition, the present review examines state‑of‑the‑art research on antitumor therapies targeting mitochondria from multiple perspectives, with the aim of providing a reference for developing mitochondria‑targeted antitumor immunotherapy strategies.

Circulating tumor cells (CTCs) are shed from the primary tumor into the peripheral bloodstream, where they play crucial roles in tumor metastasis and recurrence. As a cornerstone of liquid biopsy, CTCs hold significant potential for early tumor diagnosis, therapeutic response monitoring, and prognosis. However, the rarity and heterogeneity of CTCs pose considerable challenges for their isolation and enrichment. Additionally, their predictive usefulness in tumor immunotherapy remains relatively limited. The present review summarizes recent advancements in CTC isolation and detection technologies, explores their clinical applications in immunotherapy, and discusses current challenges alongside potential strategies for improvement. The integration of these technologies into clinical practice could pave the way for more personalized and precise cancer treatment strategies in the future.

DNA replication stress and energy homeostasis are critical yet underexplored pathways in prostate cancer (PCa). Identifying PCa prognostic biomarkers associated with these pathways are essential for advancing diagnostics and treatment. The present study aimed to analyze transcriptomic and clinical data from public datasets to identify DNA replication stress and energy homeostasis‑related genes associated with PCa. Biomarkers were assessed using reverse transcription‑quantitative (RT‑q) PCR, western blotting and consistent expression trends across datasets. Survival analyses evaluated the effect of biomarkers on clinical outcomes, while immune microenvironment changes and immunotherapy responses were evaluated. Mutation and drug sensitivity analyses explored genetic variations and chemotherapy efficacy. Functional assays, including cell proliferation, migration, RT‑qPCR and western blotting, confirmed biomarker roles in PCa progression. RecQ mediated genome instability 1 (RMI1) was identified as a novel biomarker, consistently upregulated in PCa tissues across datasets and experiments (P<0.05). High RMI1 expression was associated with worse survival outcomes, advanced clinical stages, immune escape and TP53 mutations. Enrichment analysis linked RMI1 to cell cycle, DNA replication and metabolic pathways. Functional assays revealed that RMI1 knockdown inhibited PCa cell proliferation and migration, suggesting its role in tumor progression. Additionally, high RMI1 expression was associated with resistance to certain chemotherapeutic agents, such as irinotecan. These results underscored RMI1 as a promising prognostic biomarker and a potential therapeutic target for the management of PCa. In conclusion, the present study identified RMI1 as a biomarker for the detection of PCa and may promote cancer cell progression by promoting proliferation and migration.

Adrenocortical carcinoma (ACC) is a rare adrenal cortex cancer (0.7-2.0 cases per million) with high malignancy and poor prognosis (5-year survival <40%). Early detection is difficult due to adrenal location, and effective treatments are lacking, highlighting the need for prognostic biomarkers and therapeutic targets. Anillin actin-binding protein (ANLN), a key regulator of cytokinesis, is overexpressed in many cancers compared with normal tissues and is associated with poor prognosis and advanced stage. However, the clinicopathological significance of ANLN in ACC remains unclear.

ANLN mRNA expression and survival in patients with ACC [normal (n=128), stage I (n=9), stage II (n=37), stage III (n=16), stage IV (n=15)] were analyzed from TCGA database by using the UALCAN and GEPIA platforms, assessing ANLN mRNA expression across disease stages and its correlation with patient survival.

ANLN was found to be significantly increased in stage IV ACC tissues compared with stage I, II and III ACC tissues (p<0.05). Furthermore, increased expression was significantly correlated with poor patient prognosis (p<0.005).

ANLN may be a prognostic biomarker for patients with ACC and may play a role in tumor biology. Further studies are needed to determine whether ANLN is clinically useful as a prognostic factor in the treatment of ACC and to clarify its involvement in the mechanism of malignant progression of ACC.

Pancreatic cancer has a poor prognosis, with a 5-year survival rate of only 9%. Thus, there is an urgent need to develop effective cancer therapeutics for this disease. It is expected that nucleic acid therapeutics will be a next-generation cancer treatment. We previously reported that MIRTX - a complementary strand of miR-29b-1-5p (the passenger sequence of miR-29b) - exerts strong anti-tumor effects in colorectal cancer cells. Here we investigated the anti-tumor effects of MIRTX, compared to those of the guide sequence of miR-29b (miR-29b-3p), in pancreatic cancer cells.

We evaluated how treatment with MIRTX and miR-29b-3p affected cell proliferation, cell cycle, apoptosis, and invasion in pancreatic cancer cell lines (Panc-1, SUIT-2, and BxPC-3). We also performed RNA-seq and in silico analyses to explore novel target genes of MIRTX.

Compared to miR-29b-3p, MIRTX strongly suppressed cell proliferation and invasion, delayed cell cycle progression, and induced apoptosis in pancreatic cancer cells. RNA-seq and in silico prediction identified the genes encoding cyclin A2, cyclin B2, and NCAPD3 as potential candidate targets of MIRTX.

MIRTX is a potential therapeutic miRNA in pancreatic cancer cells.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, characterized by aggressive progression, profound chemoresistance and unique metabolic adaptations such as elevated autophagy. Although the splicing factor SF3B4 has been reported to function as an oncogene in other malignancies, its role in PDAC remains unclear. This study aimed to elucidate the functional and mechanistic significance of SF3B4 in PDAC.

SF3B4 expression in PDAC was analyzed using patient datasets and experimental models. Functional assays including cell proliferation, colony formation, migration, and autophagy analyses were performed in PDAC cells. Reactive oxygen species (ROS) levels were evaluated. Sensitivity to 5-fluorouracil (5-FU) and apoptotic responses were also evaluated.

SF3B4 acts as a tumor suppressor in PDAC by inhibiting autophagy, a process that this cancer uniquely depends on for survival. SF3B4 overexpression inhibited proliferation, colony formation and migration of PDAC cells. Mechanistically, SF3B4 suppressed autophagic flux, resulting in increased ROS accumulation and subsequent inhibition of tumorigenic phenotypes. Treatment with the antioxidant N-acetylcysteine (NAC) rescued the tumor suppressive effects of SF3B4 overexpression. Moreover, SF3B4 overexpression sensitized PDAC cells to 5-FU, accompanied by enhanced apoptotic responses.

SF3B4 is a context-dependent splicing factor that functions as a tumor suppressor in PDAC by regulating autophagy and redox homeostasis. Targeting the SF3B4-autophagy-ROS axis may represent a promising strategy to suppress PDAC progression and overcome chemoresistance.

In recent studies, circ_0060055, a newly identified circRNA with implications in oncology, was examined for its expression levels in pancreatic cancer cells versus normal pancreatic tissue, utilizing RT-qPCR. This circRNA was evaluated for its effects on cellular functions, including invasion, migration, proliferation, tube formation, vascular leakiness and apoptosis through a series of functional assays, both inhibitory and promotional. Moreover, investigations extended to in vivo studies. Findings suggest a strong association between circ_0060055 and enhanced cellular proliferation, migration, and invasion capabilities, alongside a notable reduction in apoptosis. Alterations in the expression levels of proteins that regulate apoptosis have been observed, characterized by elevated levels of the anti-apoptotic protein Bcl-2 and diminished levels of the pro-apoptotic protein Bax. Additionally, through dual luciferase reporter assays and further qRT-PCR analyses, miR-1298-5p was identified as a direct interactor with circ_0060055, which in turn modulates miR-1298-5p levels, thereby acting as a molecular sponge. The findings highlight the critical influence of circ_0060055 on the progression of pancreatic cancer by regulating essential apoptotic proteins, suggesting it could serve as a potential therapeutic target for pancreatic cancer.

Breast cancer is a significant global health issue, with resistance to doxorubicin (DOX) posing a major challenge to effective treatment. SUMOylation, a post-translational modification process, is linked to cancer progression and therapy resistance. PIAS4, a SUMO E3 ligase involved in maintaining genome stability and stress response, may play a role in these mechanisms. However, its function in breast cancer progression and DOX resistance remains uncertain. This study investigates the potential role of PIAS4 in mediating DOX resistance in breast cancer.

Naked mole-rats (NMRs) are cancer-resistant rodents with improved genome maintenance, yet the role of SUMOylation in this trait remains unclear. SUMOylation machinery gene expression levels are investigated using qPCR in NMR tissue in comparison with carcinogenic breast cancer (MCF-7) cell line. Functional studies are performed in MCF-7 cells overexpressing PIAS4 to demonstrate effects on proliferation, invasion, drug sensitivity, and protein expression in the presence and absence of DOX treatment. While most SUMOylation genes were expressed at low levels in NMR intestinal tissues, PIAS4 showed higher expression compared to MCF-7 cells. PIAS4 overexpression in MCF-7 cells significantly decreases colony formation, invasiveness, and resistance to DOX. Western blot analysis showed downregulated Bcl-2 protein levels after DOX treatment, indicating a potential role in apoptosis evasion.

PIAS4 expression level plays a role in breast cancer cell survival, invasiveness, and chemoresistance, partly by altering anti-apoptotic pathways. These findings position PIAS4 as a potential biomarker and therapeutic target for overcoming resistance to anthracycline-based therapies in breast cancer.