Introduction: Colorectal cancer (CRC) is a remarkable global health burden, considering its high morbidity and mortality. For both resectable and unresectable colorectal cancer (CRC), chemotherapy is the first-line option. The survival rate was significantly affected by the location of the tumor and the mutation status of the KRAS gene. This study aimed to systematically synthesize current evidence on how primary tumor location and KRAS mutations influence the survival of colorectal cancer patients receiving chemotherapy. Methods: We performed a systematic search of the electronic databases with defined inclusion and exclusion criteria. Independent reviews were performed by two reviewers of the literature that was included. Methodological quality of the studies included was evaluated using the Joanna Briggs Institute (JBI) critical appraisal methods. Information was obtained and qualitatively analyzed. The analysis was performed through a qualitative measure. P-value < 0.05 is considered statistically significant. Results: A total of 11 studies were reviewed. All the studies reviewed reported improved quality of methodology. The qualitative synthesis suggested a trend toward worse survival for patients with right-sided tumors, although some studies reported no statistically significant difference between tumor locations. In contrast, the association between KRAS gene mutations and poorer survival outcomes appeared more consistent across studies. Overall, these findings indicate that KRAS mutations and, to a lesser extent, right-sided tumor location may predict unfavorable outcomes in chemotherapy-treated colorectal cancer patients. Conclusion: KRAS mutations were linked to poorer survival, while right-sided tumor location showed a less consistent but generally unfavorable trend among chemotherapy-treated colorectal cancer patients.

Background: Gastrointestinal cancers including malignancies of the colon, rectum, stomach, pancreas, liver, and esophagus represent a significant global health burden with high morbidity and mortality. Advances in molecular oncology reveal that these cancers arise through complex genetic, epigenetic, microenvironmental, and metastatic processes. Understanding these mechanisms is essential for oncology nurses to support precision medicine and deliver effective, patient-centered care. Methods: This literature review employed a structured thematic analysis to synthesize knowledge on cancer biology concepts relevant to gastrointestinal oncology nursing. Comprehensive database searches (PubMed, CINAHL, Scopus, Google Scholar) targeted publications from 2000 to 2024 addressing genetic mutations, epigenetics, tumor microenvironment, metastasis, and nursing education. Eligible articles were critically reviewed and thematically coded to identify major themes and subthemes with clinical and nursing practice relevance. Results: Three primary themes emerged: (1) Genetic and Epigenetic Alterations, including oncogene activation, tumor suppressor inactivation, microsatellite instability, and DNA methylation; (2) Tumor Microenvironment and Immune Evasion, encompassing stromal barriers, angiogenesis, immune suppression, and intercellular signaling; and (3) Mechanisms of Metastasis, detailing local invasion, epithelial-mesenchymal transition, circulation, colonization, dormancy, and reactivation. Each theme includes nursing roles in patient education, decision-making support, therapy monitoring, and psychosocial care. Conclusion: Integrating cancer biology knowledge into nursing practice is essential for anticipating patient needs, supporting shared decision-making, and managing advanced therapies in gastrointestinal oncology. Nurses must engage in ongoing education and interdisciplinary collaboration to navigate the evolving landscape of precision oncology and improve outcomes and quality of life for patients facing these complex cancers.

Background: Colorectal cancer (CRC) is responsible for nearly 10% of cancer cases and deaths and is emerging as one of the most prominent malignant diseases worldwide. Carcinoembryonic antigen (CEA) is the most widely used serum biomarker for CRC, but its limited sensitivity and specificity highlight the need for additional diagnostic and prognostic markers. The mitochondrial enzyme aldehyde dehydrogenase 1B1 (ALDH1B1) is highly expressed in CRC and cancer stem cells (CSCs), representing a novel biomarker, especially as its overexpression triggers an autoantibody response detectable in a patient’s serum. This study aims to quantify serum concentration of CEA and ALDH1B1 autoantibodies in patients with colorectal cancer (CRC) and to investigate the relationship between them. It further seeks to evaluate their prognostic potential as circulating biomarkers for CRC. The underlying hypothesis proposes that elevated CEA and ALDH1B1 autoantibody levels are positively correlated and collectively reflect the underlying cancer stem cell (CSC) burden. This correlation is assessed through a predictive equation developed in the study, providing a novel, noninvasive indicator of tumor progression and aggressiveness. Method: Blood samples were collected from 75 newly diagnosed CRC patients (stages II–IV) and 25 healthy controls. CEA and ALDH1B1 autoantibodies were measured using ELISA techniques. Statistical analyses include analysis of variance (ANOVA), paired t-tests, Duncan’s test, regression analysis, and receiver operating characteristic (ROC) curve assessments using SPSS software. Results: The findings show significantly higher CEA and ALDH1B1 autoantibody levels in CRC patients compared to the controls, though neither marker varied significantly across tumour stages, emphasising their role as indicators of tumour biology rather than tumour burden. The regression analysis revealed a significant direct relationship between CEA and ALDH1B1 autoantibody levels (β = 0.026, p < 0.001), as CEA explains 87% of the variability in ALDH1B1 autoantibody levels. The ROC analysis indicated a good diagnostic performance for CEA (AUC = 0.88) and a fair performance for ALDH1B1 autoantibodies (AUC = 0.67). Conclusion: The strong predictive relationship between CEA and ALDH1B1 autoantibodies suggests that CEA levels may indirectly reflect CSC activity, potentially guiding personalised treatment strategies targeting both bulk tumours and CSCs.

Objective: This research seeks to assess the relationship between YAP1 expression and histological grading, lymphovascular invasion, and lymph node metastasis in patients with invasive breast cancer in Makassar, a study that has not been previously performed. Methods: A cross-sectional study was carried out on 100 mastectomy samples identified as invasive breast carcinoma at Dr. Wahidin Sudirohosodo Hospital, Makassar, Indonesia. YAP1 expression was assessed through immunohistochemistry and scored according to the immunoreactive score (IRS) method. A statistical evaluation was conducted using Fisher’s exact test. Result: The average age of patients was 50.22 ± 10.20 years. YAP1 expression was positive in every instance, with 72% showing strong expression (+3), 25% exhibiting moderate expression (+2), and 3% demonstrating weak expression (+1). A significant correlation existed between YAP1 expression and histological grade (p=0.001), showing increased expression in grade 3 tumors. Nonetheless, no significant correlation was discovered between YAP1 expression and lymph node metastasis (p=0.912) or lymphovascular invasion (p=0.276). Conclusion: YAP1 expression shows a strong correlation with histological grade in invasive breast cancer, indicating its potential as a biomarker for tumor aggressiveness. Nonetheless, YAP1 expression is not directly linked to lymph node metastasis or lymphovascular invasion.

Genetic biosensors lead to a revolutionary integration of genetic engineering and biosensing techniques, suggesting high precision in molecular diagnostics and personalized medicine. These tools use nucleic acids and proteins to enabling early disease diagnosis, and real-time scanning of biological procedures like cancer. Their high sensitivity, specificity, and adaptability make them promising for clinical applications in spite of challenges in optimization and scalability. This review explores the design principles, technological advancements, and biomedical applications of genetic biosensors, focusing on their potential to improve healthcare through personalized medicine and more progress therapeutic interventions.

Objective: This study assesses the effectiveness of combining Dapagliflozin and etoricoxib in inhibiting cancer cell growth and investigates its effects on the mutant PI3K/Akt/mTOR signaling pathway to understand the underlying mechanisms. Methods: After incubation periods of 24 and 72 hours, HeLa cells and normal human fibroblasts (NHF) were utilized to assess the anticancer efficacy and safety profile of Dapagliflozin, Etoricoxib, their combination, and 5-fluorouracil (5FU). The tested concentrations ranged from 0.1 to 1000 µg/ml. To determine potential synergy and selectivity, the combination index (CI) and the selective toxicity index (SI) were estimated. Additionally, molecular docking simulations were performed to evaluate the binding affinities of Dapagliflozin and Etoricoxib to mutant proteins within the PI3K/Akt/mTOR signaling pathway. Results: The MTT assays showed that a combination of Dapagliflozin and etoricoxib has significant anticancer activity. The mixture effectively inhibits the growth of cervical cancer cells, achieving results similar to 5-fluorouracil (5FU) and outperforming Dapagliflozin or etoricoxib alone. Additionally, the cytotoxic effects of the mixture on normal human fibroblast (NHF) cells were much lower than those seen with 5FU, indicating decreased toxicity. The combined use of Dapagliflozin and etoricoxib exhibited synergistic cytotoxic effects, as indicated by the combination index (CI) score. This drug pair also showed selectivity in targeting cancer cells, as reflected by the selectivity index (SI). The molecular docking results showed that Dapagliflozin and Etoricoxib have affinities for interacting with the mutant PI3K/Akt/mTOR signaling protein. Docking scores for Dapagliflozin binding to these proteins were -8, -6.7, and -7.3 kcal/mol, while those for Etoricoxib were -8, -6.6, and -6.8 kcal/mol, respectively. Conclusion: The findings, supported by established pharmacokinetic and safety data, suggest that combining Dapagliflozin and Etoricoxib may provide a safer and more effective treatment option for cervical conditions, with a possible mechanism involving the PI3K/Akt/mTOR pathway, as predicted by molecular docking.

Background: The most common malignancy in men is prostate cancer. Chronic inflammation and bacterial infections exacerbate insulin resistance in type 2 diabetes (T2D) patients, potentially worsened by chemotherapy in those with prostate cancer. This study investigates the effects of Docetaxel chemotherapy on systemic inflammation, Insulin Resistance, and bacterial resistance in T2D patients with prostate cancer. Methods: Eighty participants (aged 50–75 years) were enrolled in a cross-sectional study and divided into four groups: Group 1 (T2D without cancer, n=40), Group 2 (T2D with prostate cancer, pre-chemotherapy, n=40), Group 3 (Group 2 subset post-two Docetaxel cycles), and Group 4 (Group 2 subset post-five Docetaxel cycles). Serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), procalcitonin (PCT), fasting glucose, fasting insulin, and prostate-specific antigen (PSA) were measured via immunoassays. Insulin resistance was assessed using the Homeostatic Model Assessment (HOMA-IR). Urine samples were analyzed for Escherichia coli isolation and antibiotic resistance via the Kirby-Bauer method. Statistical significance was determined using t-tests (P≤0.05). Results: Group 4 exhibited notably elevated inflammatory markers (PCT, IL-6, TNF-α), fasting glucose, fasting insulin, PSA, and the value of HOMA-IR compared to Groups 1–3 (P≤0.01). E. coli isolation rates increased from 67.5% (Group 2) to 80% (Group 4, P=0.20), with antibiotic resistance rising, notably for Amikacin (17.5% to 35%, P=0.08) and Nitrofurantoin (25% to 30%, P=0.61), though these differences were not statistically significant. Multidrug-resistant (MDR) and extensively drug-resistant (XDR) isolates also increased slightly post-chemotherapy. Conclusion: Docetaxel chemotherapy in T2D prostate cancer patients is associated with heightened systemic inflammation, insulin resistance, and bacterial resistance, underscoring the need for integrated therapeutic strategies to mitigate these effects.

Background: Leucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5), also known as GPR49, is a Wnt signaling target that plays an important role in colorectal carcinogenesis and is often associated with poor prognosis in patients with colorectal cancer. Aim of this study was to assess the influence of LGR5 expression and its relationship with overall survival (OS) in colorectal cancer. Material and methods: This retrospective study assessed LGR5 expression via immunohistochemistry (IHC) in 30 archival colorectal cancer tissue samples from patients resected between 2019-2020 in Makassar, Indonesia. The association between LGR5 expression levels (high vs. low) and overall survival (OS) was analyzed. Result: Research results were obtained from 30 samples. Overall, 8 patients with high LGR5 expression and 22 patients with low LGR5 were reported. Among the total number of patients enrolled, 22 patients had an OS of 3 years and 8 patients had an OS of 5 years. Statistical analysis showed that there was no association between LGR5 expression and the clinical profile of colorectal cancer patients (p-value > 0.05). A statistically significant association between OS and both tumor stage and histopathological grading (p-value <0.001 and 0.016, respectively) was found. However, no statistically significant association between OS and LGR5 expression was observed (p-value 0.418). Conclusion: LGR5 expression was not associate with either OS and or clinical characteristics of CRC patients in Makassar, Indonesia. However, there was a tendency for low LGR5 expression to be associated with improved OS, although this finding was not statistically significant. Both tumor stage and histopathological grading were associated with OS.

Objective: Multifunctional hydrogels represent a promising strategy for localized and sustained drug delivery in cancer and chronic disease management. C. inophyllum, a medicinal plant with known bioactive properties, was explored in this study for its potential integration into a chitosan-polyvinyl alcohol (Cs-PVA) hydrogel system to enhance therapeutic efficacy. Methods: The Cs-PVA hydrogel was synthesized using a freeze-thaw technique and loaded with C. inophyllum extract. Structural and chemical characterizations were performed using Fourier-transform infrared spectroscopy (FTIR) and scanning electron microscopy (SEM), confirming the incorporation and uniform dispersion of phytochemicals. In vitro cytotoxicity was assessed against HT-29 colon cells using the MTT assay. Antioxidant activity was evaluated using the DPPH assay, while anti-inflammatory potential was determined through protein denaturation inhibition. Drug release kinetics were analyzed over a 24-hour period, and α-amylase inhibition assays were performed to determine antidiabetic potential. Results: FTIR and SEM analyses confirmed successful integration of the extract within the hydrogel matrix. The hydrogel exhibited concentration-dependent cytotoxicity, with an IC₅₀ of 17 µg/mL, alongside visible apoptotic morphology in HT-29 cells. Antioxidant and anti-inflammatory activities showed 72.4% and 67.8% inhibition at 75 µg/mL, comparable to ascorbic acid and diclofenac, respectively. The hydrogel achieved nearly 100% drug release within 24 hours. Antidiabetic activity was demonstrated by 67.1% α-amylase inhibition at 50 µg/mL, close to metformin’s 79.3%. Conclusion: The C. inophyllum-loaded Cs-PVA hydrogel shows strong potential as a biodegradable, multifunctional therapeutic platform, offering cytotoxic, antioxidant, anti-inflammatory, and antidiabetic effects for future cancer and chronic disease treatments.

Background: Breast and cervical cancers represents major public health challenges globally, with considerable impact on women’s health in India. Early detection through screening plays a critical role in improving survival rates and treatment outcomes. Understanding the knowledge, attitudes, and practices surrounding cancer screening is essential to develop effective, targeted interventions that can improve uptake and reduce the burden of these diseases. This study aims to explore these factors among women in Chennai, including both those diagnosed with cancer and non-cancer participants. Methods: This qualitative KAP study, conducted between October 2021 and May 2022, involved 189 purposively sampled women (with and without breast/cervical cancer) across five tertiary care institutions in Chennai. Thirteen Focus Group Discussions (FGDs) were conducted to assess participants’ knowledge of cancer and screening, explore their attitudes toward prevention and early detection, and document their screening practices. Audio recordings were transcribed and analyzed using descriptive content analysis. Results: The findings revealed a generally low level of awareness, widespread misconceptions, and a diminished perception of personal risk, contributing to negative attitudes toward screening. However, screening behaviors were positively influenced by strong social support from peers and family, as well as by trusted media sources indicating these factors may help overcome some attitudinal barriers. Conclusion: Despite limited awareness and prevailing misconceptions, leveraging social support networks and accessible media presents a key opportunity for improving screening uptake. Public health initiatives should focus on strengthening knowledge, correcting misconceptions, and utilizing existing social and communication networks to enhance women’s participation in cancer screening programs.