BRCA1 is a key player in the homologous recombination DNA repair process. Pathogenic BRCA1 germline mutations confer a high risk of breast and ovarian cancers. Nevertheless, the association between BRCA1 mutations and colorectal cancer (CRC) risk remains unclear. While BRCA1 alterations significantly influence diagnosis and therapeutic decisions in breast and ovarian cancer, including the use of FDA-approved poly (ADP-ribose) polymerase (PARP) inhibitors, their role in CRC management is less established. Here, we present a case of a 57-year-old female diagnosed with CRC and a family history of ovarian and endometrial cancers. All her cancer-affected family members, including herself, were found to carry two germline BRCA1 mutations, including a novel mutation (c.212+2T>G) that has not previously been reported in CRC. The proband exhibited peculiar clinicopathological and molecular features, including a CK7-positive/CK20-negative immunophenotype that mimicked an ovarian origin. The patient received five cycles of nab-paclitaxel plus carboplatin, followed by maintenance therapy with the PARP inhibitor (PARPi) niraparib. This case provides real-world evidence supporting the pathogenicity of the BRCA1 c.212+2T>G mutation and highlights the potential of PARPi therapy in CRC patients harboring BRCA1 mutations. Further, it demonstrates the possibility of a rare immunohistochemical phenotype in CRC cells harboring a deleterious BRCA1 mutation.

Cancer patients experiencing acute complications frequently present to emergency departments, where traditional care often overlooks the psychological distress and self-care challenges accompanying tumor progression and treatment-related crises. This study investigates the effect of problem-oriented nursing intervention on psychological stress and self-care ability in tumor patients requiring emergency care. A total of 160 patients admitted to the emergency department of Tongji Shanxi Hospital from June 2021 to December 2023 for cancer- or treatment-related complications were enrolled. Based on the nursing plan, participants were assigned to a control group receiving routine care (n = 80) or an observation group receiving problem-oriented nursing intervention (n = 80). All participants provided informed consent before enrollment. Anxiety and depression were measured using the Hamilton Anxiety Scale and Hamilton Depression Rating Scale, while social phobia was evaluated using the Social Phobia Inventory. Quality of life was evaluated using the Medical Outcomes Study 36-Item Short-Form Health Survey, and self-management behavior and confidence were assessed using the Chronic Disease Self-Management Scale and Self-Efficacy Scale for Chronic Disease, respectively. The results showed no significant differences in baseline characteristics between the two groups (p>0.05). After intervention, the observation group demonstrated significantly lower anxiety and depression scores, along with reduced fear, avoidance, and physical discomfort, compared with the control group (p<0.05). Furthermore, physical functioning, pain perception, general health, and mental health scores, as well as self-management and self-efficacy, were significantly higher in the observation group (p<0.05) compared to the control group. Problem-oriented nursing intervention significantly reduces psychological stress and enhances self-care ability and quality of life in tumor patients requiring emergency care.

Although DNA damage-inducible transcript 3 (DDIT3) has been identified as a novel gene associated with breast cancer, its clinical significance, biological function, and underlying mechanisms remain unclear. By integrating immunohistochemistry with data from The Cancer Genome Atlas (TCGA), we discovered that elevated levels of DDIT3 Messenger RNA and protein expression are significantly associated with poor prognosis in patients with breast cancer. Functional assays and preliminary mechanistic studies reveal that DDIT3 may promote breast cancer cell proliferation and metastasis, potentially by downregulating activating transcription factor-2.

Lung cancer remains one of the most common malignancies. It is usually categorized into two types: small-cell lung cancer and non-small-cell lung cancer (NSCLC). Among the types of NSCLC, adenocarcinoma is the most common and is more prevalent in women than in men. The current study aims to identify KRAS mutations in a population with metastatic lung cancer. Moreover, the clinical significance of the KRAS mutations was also explored. For this purpose, KRAS status was evaluated by polymerase chain reaction and reverse hybridization. According to the molecular results, mutations were observed at codons 12, 13, 59, 61, 117, and 146. Interestingly, the number of patients with stage II disease was significantly higher, indicating that the type of KRAS alteration may be associated with early disease spread. Thus, these mutations were associated with poor responses to cetuximab and panitumumab, underscoring the important role of KRAS profiling in strategizing treatment modifications. We can also conclude that molecular diagnostics plays its role in everyday clinical practice by complementing precision oncology and improving the outlook for patients with NSCLC.

Viral latency represents a complex and dynamic balance between persistent viral genomes and the host’s immune system, profoundly influencing cellular aging and increasing the risk of cancer through epigenetic reprogramming. This review examines the interconnected mechanisms linking viral latency, epigenetic alterations, and immune system aging, emphasizing their combined contribution to malignancy development. Persistent viral infections, such as those caused by Epstein-Barr virus, human cytomegalovirus, human papillomavirus, and human immunodeficiency virus, disrupt the host’s epigenetic machinery, leading to abnormal DNA methylation, histone modification, and chromatin remodeling. These changes accelerate biological aging and silence tumor suppressor genes, creating cellular environment that favors uncontrolled proliferation. At the same time, chronic immune activation and T-cell exhaustion generate a state of persistent inflammation and immunosuppression that promotes cancer initiation and progression. The review integrates findings from molecular, cellular, and epidemiological studies to highlight key signaling pathways, including nuclear factor kappa B, signal transducer and activator of transcription 3, mechanistic target of rapamycin, and sirtuin pathways, which mediate the interaction between viral persistence and host epigenetic aging. Therapeutic implications are discussed, focusing on the potential use of immune checkpoint inhibitors and biomarker-based precision strategies to counteract virus-associated carcinogenesis. Key research gaps have also been identified, including the need for longitudinal, multi-omic studies to distinguish viral-specific effects from host aging and lifestyle factors. This review provides an integrative framework for understanding how viral latency accelerates biological aging and increases cancer risk, highlighting opportunities for early detection, prevention, and targeted therapeutic interventions.

Cancer stem cells (CSCs) pose a significant challenge in tumor treatment due to their ability to remain quiescent during therapy and thus evade chemo- and radio-therapy. In addition, their ability to initiate tumor formation from a single cell is another essential factor to consider when developing a strategy to eradicate CSCs. Given that developing novel drugs is a time-consuming and costly process, drug repurposing has become an increasingly utilized and appealing alternative in recent research. Drug repurposing involves testing existing medications that have already completed substantial portions of drug development for the treatment of new medical conditions. Artificial intelligence tools can assist in this process. This review presents a series of compounds, initially developed for a wide range of conditions, including antidiabetic, antipsychotic, anti-inflammatory, cholesterol-lowering, and antiparasitic drugs, that can be repurposed as targeted therapies for CSCs. Metformin and doxycycline have also been evaluated in clinical studies targeting CSCs. Furthermore, novel artificial intelligence tools will be vital for predicting the potential of repurposed drugs before in vitro and in vivo testing.

The primary clinical goals of treatment for cancer, other chronic illnesses, and terminal diseases are to manage symptoms and improve the quality of life (QoL). The aim of this study is to investigate the three-way interaction effect of nutritional counselling (NC) and cognitive behavior therapy (CBT) on the QoL of breast cancer patients in south-western Nigeria. This study employed a pre-test-post-test quasi-experimental design with a 3 × 2 × 3 factorial matrix, involving 92 breast cancer patients. The first three levels were CBT, NC, and control, followed by two levels of psychological distress (PD), and three levels of risk of malnutrition (RoM). The instruments used include the European Organisation for Research and Treatment of Cancer QoL Questionnaire (general and breast cancer-specific; α = 0.80), the Hospital Anxiety and Depression Scale (α = 0.83), the Malnutrition Universal Screening Tool (α = 0.81), and the Functional Assessment of Cancer Therapy-Breast for screening. Data were analyzed using analysis of covariance and estimated marginal means at the significance level p < 0.05. There was a significant three-way interaction among treatment, PD, and RoM (F_(4,73) = 3.44, partial η² = 0.16), with the greatest improvement (mean score = 131.52) in participants with low levels of PD and RoM in the NC group. This study underscores the synergistic impact of treatment, PD, and RoM on the QoL of breast cancer patients in south-western Nigeria. Breast cancer patients should be screened for distress and malnutrition risk and have access to appropriate psychological and nutritional care.

Natural killer group 2, member D (NKG2D) ligands are highly expressed in various tumor cells and therefore represent an attractive target for cancer immunotherapy. A bispecific T-cell engager (BiTE) with a fused extracellular domain of NKG2D and an anti-CD3 single-chain fragment variable (scFv) has shown significant anti-tumor potency. To circumvent the manufacturing challenges and short serum half-life of BiTEs, we developed lipid nanoparticle-encapsulated messenger RNA (mRNA) encoding α-CD3-mNKG2D fusion proteins. In vitro functional analysis revealed that the BiTE-encoded mRNA induced T cell activation and cell cytotoxicity against tumor cells. An in vivo study using an A20 lymphoma mouse model showed that BiTE-encoding mRNA significantly inhibited tumor growth. Notably, BiTE constructs without an antibody Fc domain exhibited markedly higher anti-tumor efficacy than BiTE constructs with an Fc fragment. Additionally, we designed a human version of the BiTE mRNA encoding an NKG2D and an anti-CD3 (OKT3) scFv fusion protein. Human BiTE mRNA treatment significantly upregulated CD69 expression on T cells, promoted cytotoxicity against tumor cells in vitro, and suppressed tumor growth in a peripheral blood mononuclear cell-engrafted, tumor-bearing mouse model. Based on these preclinical findings, NKG2D BiTE mRNA holds promise as a potential anti- tumor treatment meriting further clinical development.

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide. Although the coiled-coil domain-containing protein 51 (CCDC51) has been implicated in retinal pathologies, its function in HCC remains poorly defined. Here, we report that reduced CCDC51 expression is associated with favorable clinical outcomes in HCC patients. Bioinformatic analyses revealed significant correlations between CCDC51 levels and multiple tumor characteristics, including immune cell infiltration, the tumor microenvironment, and microsatellite instability status. Notably, multivariate Cox regression and nomogram analyses established CCDC51 as an independent prognostic biomarker for HCC. Pathway enrichment studies further linked elevated CCDC51 expression to dysregulation of RNA transport and Wnt signaling. Functionally, genetic silencing of CCDC51 in HCC cell lines resulted in significant suppression of proliferation, migration, and invasion. Collectively, these findings identify CCDC51 as a novel prognostic marker and a potential therapeutic target in HCC.

Oncolytic virotherapy has emerged as a promising approach to cancer treatment, and mesenchymal stem cells (MSCs) are increasingly recognized as effective carriers to enhance the delivery and efficacy of oncolytic viruses (OVs). This study explores the potential use of MSCs as carriers for OVs in targeted cancer therapy. MSCs are considered ideal delivery vehicles for OVs due to their immunomodulatory properties, inherent tumor-homing ability, and capacity to protect and transport therapeutic agents. Advances in genetic engineering have enhanced the interaction between MSCs and OVs, improving delivery efficiency and therapeutic outcomes in cancer treatment. This study conducted a bibliometric analysis of the 100 most-cited articles on both MSCs and OVs, using data from the Web of Science Core Collection database. It identified major trends, challenges, and research hotspots, highlighting significant progress in preclinical studies while noting ongoing issues related to delivery efficiency, virus modification, and tumor microenvironment optimization. The findings underscore the promise of MSCs as effective delivery systems for Ovs and outline emerging research areas, such as precise delivery methods and clinical applications, alongside current obstacles. As this field advances, it is expected to play a crucial role in the future of cancer immunotherapy.