Colorectal cancer (CRC) is the second most prevalent type of cancer among males and the third among females. CRC recurrence and poor prognosis may be related to the prevalence of chemotherapy-resistant cancer stem cells (CSCs). Recent studies have indicated the role of doublecortin-like kinase 1 (DCLK1) protein as a marker of CSC in CRC. This review focuses on the role of DCLK1 in CRC. Long-lived DCLK1-positive tuft cells can function as cancer-initiating cells. Numerous studies have shown DCLK1 overexpression to be significantly correlated with the stage of disease, the presence of metastasis and poor survival rate. DCLK1 may also be used to identify patients at high risk and those with chemotherapy-resistant tumors. DCLK1-specific drugs are examined as potential cancer treatments.

Introduction: Glaucoma is a leading cause of blindness, often progressing asymptomatically until significant vision loss occurs. Early detection is crucial for preventing irreversible damage. The pupillary light reflex (PLR) has proven useful in glaucoma diagnosis, and mobile technologies like the AI-based smartphone pupillometer (AI Pupillometer) offer a promising solution for accessible screening. This study assesses the reliability of the AI Pupillometer in detecting glaucoma.Methods: In Experiment 1, 20 healthy participants were assessed using both the AI Pupillometer and the NPi-200 device to evaluate equivalence in measuring PLR. Each eye underwent three trials. Experiment 2 included 46 participants, 24 with primary open-angle glaucoma (POAG) and 22 healthy controls. PLR measurements from the AI Pupillometer were correlated with structural and functional ocular parameters. An additional study expanded the sample to 387 participants (103 glaucoma patients, 284 controls), focusing on differential pupillometry parameters to minimize ambient light interference.Results: In Experiment 1, the AI Pupillometer demonstrated strong correlations with the NPi-200 in key parameters like initial pupil size (r = 0.700), constricted pupil size (r = 0.755), and constriction velocity (r = 0.541), confirming its reliability. In Experiment 2, although no statistically significant differences in light-corrected PLR parameters were found between groups, glaucoma patients had a marginally higher constricted pupil size (p = 0.1632). Significant correlations were observed between pupillometry and advanced ocular imaging results, notably between constriction amplitude and visual field loss. The additional study revealed significant differences in constriction amplitude (p = 0.014) and relative pupil size change (p = 0.0072) between glaucoma patients and controls, reinforcing the AI Pupillometer’s diagnostic potential.Conclusion: This study confirms the AI Pupillometer as a reliable, accessible tool for glaucoma screening. Mobile diagnostics could enhance early detection, improving outcomes for glaucoma patients.

Resistance to systemic therapy is one of the hallmarks of renal cell carcinoma (RCC). Recently, TOLLIP has emerged as a possible driver of autophagy and chemoresistance. We explored the relationship between primary and metastatic RCC tumor characteristics, patient survival, and TOLLIP expression. The tissue microarrays cohort contained 95 cores of the primary tumor, matched metastases, and matched adjacent tissues derived from 32 RCC patients. TOLLIP expression in tumor samples was evaluated using the H-score. All examined samples showed cytoplasmic TOLLIP expression, with a median value of 100 in primary tumors, 107.5 in metastases, and 220 in the control group. The expression was significantly higher in the normal adjacent tissues compared to primary or metastatic RCC (p < 0.05). We found a positive correlation between expressions of TOLLIP in the primary tumor and its metastases (p < 0.05; k = 0.48). TOLLIP expression significantly correlates with a lower overall survival rate (p = 0.047). TOLLIP functions as a ubiquitin-LC3 adaptor in the intracellular pathway associated with autophagy. Relative TOLLIP overexpression may augment autophagy-related signaling, limiting susceptibility to therapy. The blockade of TOLLIP physiological function seems to be a promising approach to overcoming resistance to systemic therapy.

Prostate cancer remains a leading cause of cancer-related death in men worldwide. Recent research advances have emphasized the critical roles of mismatch repair (MMR) and double-strand break (DSB) in prostate cancer development and progression. Here, we provide a comprehensive review of the molecular mechanisms underlying DSB and MMR defects in prostate cancer, as well as their clinical implications. Furthermore, we discuss the promising therapeutic potential of immune checkpoint inhibitors and PARP inhibitors in targeting these defects, particularly in the context of personalized medicine and further perspectives. Recent clinical trials have demonstrated the efficacy of these novel treatments, including Food and Drugs Association (FDA) drug approvals, offering hope for improved patient outcomes. Overall, this review emphasizes the importance of understanding the interplay between MMR and DSB defects in prostate cancer to develop innovative and effective therapeutic strategies for patients.

Background/Aim: Renal cell carcinoma (RCC) continues to pose a challenge due to our limited understanding of its underlying pathophysiology. Aconitase 2 (ACO2) is a mitochondrial Fe–S cluster enzyme that catalyzes the stereospecific isomerization of citrate to isocitrate in the second step of the Krebs cycle. We investigated the relationship between ACO2 protein expression and the clinical course of RCC. Materials and Methods: Tumor samples were evaluated in a commercial tissue microarray for ACO2 expression using the H-score. The tissue microarrays contained a total of 96 cores from primary tumors, matched metastases, and matched adjacent tissues derived from 32 patients with RCC. The mean follow-up was 82.74 months. Correlation analysis of clinicopathological data and survival was performed. Expression levels of ACO2 mRNA were compared using publicly available data. Results: All the tissue samples showed cytoplasmic ACO2 expression, with median H-scores of 139.7, 130.3 and 166.7 in primary tumor, metastatic tissue, and matched control tissue, respectively. A significantly higher ACO2 expression was found in normal tissues compared to primary and metastatic RCC. The analysis demonstrated a significantly positive correlation between ACO2 expression in primary tumors and their metastases. The results also showed a significant correlation between the expression of ACO2 and worse overall survival among patients with RCC. Conclusion: ACO2 may be used as a prognostic factor in RCC. Significant alterations in ACO2 expression are thought to occur in the early stages of RCC carcinogenesis. Considering the physiological role of ACO2, its dysregulation may constitute an adaptive trait of RCC for escaping the equilibrium phase of immunoediting.