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Some studies have highlighted the role of Janus kinase 3 (JAK3) in the development of various cancers. To manage this condition, inhibitors such as decernotinib and facitinib are commonly used, although these drugs can cause elevations in liver enzymes and increased lipid levels. It is essential to recognize that new therapies are being developed to inhibit cancer cell growth, using both theoretical and experimental approaches. This study aimed to investigate whether carbazole derivatives (1-25) could interact with JAK3, using the 3pjc protein, decernotinib, and facitinib as reference compounds in the DockingServer tool. The results showed that the carbazole analogs engage with different regions of the 3pjc protein compared to facitinib and decernotinib. Additionally, the inhibition constant (Ki) for carbazole-protein interactions with compounds 2, 5, 9, 17, 18, and 22 was lower than that of the reference drugs, suggesting that these carbazole analogs could be effective JAK3 inhibitors and may help reduce cancer cell growth.

For many years, various drugs have been utilized to treat different cancer types, but some of these treatments come with adverse effects such as liver damage, hypertension, and erectile dysfunction. In the pursuit of alternative therapeutic options, several new compounds have been developed to address this clinical challenge. Yet, the interactions of these compounds with biomolecules involved in cancer development remain largely unclear. With this context in mind, the present study aimed to explore the potential theoretical interaction of a series of pyrimidinone derivatives (compounds 1-27) with the X-linked inhibitor of apoptosis protein (XIAP), a key player in cancer progression, using the Docking model. The findings indicated that certain pyrimidinone derivatives (compounds 1-6, 10, 11, 14, 15, 22-24, 26, and 27) exhibited the ability to bind with the surface of the XIAP protein. In conclusion, these results suggest that some pyrimidinone derivatives may modulate XIAP’s biological activity, making them promising candidates for cancer therapy.

This investigation examined the bacterial profile and patterns of antibiotic resistance among cancer patients receiving care at B.P. Koirala Memorial Cancer Hospital in Bharatpur, Chitwan. Employing a hospital-based cross-sectional design, the study processed 384 clinical specimens obtained from cancer patients. Once bacterial growth was observed on selective and differential culture media, Gram staining was used as a preliminary identification method. Organisms were subsequently characterized based on their biochemical features, and antibiotic susceptibility testing was performed using the Kirby-Bauer disk diffusion technique. The results, measured by determining the diameter of the inhibition zones, adhered to the Clinical and Laboratory Standards Institute (CLSI) guidelines established in 2020. Data analysis was conducted using SPSS version 20.0.Among the 384 individuals included, 55.4% were male and 44.6% female. Bacterial growth was detected in 43.5% of the total specimens analyzed. A comparison between cancer types showed that hematogenous malignancies accounted for 40.7% of the positive cultures, while 45.5% were associated with non-hematogenous cancers. The most frequently isolated organism was Escherichia coli, making up 38.9% of isolates, followed by Klebsiella species (20.4%), Pseudomonas species (19.2%), Citrobacter species (9.0%), and Acinetobacter species (4.8%). Additionally, Staphylococcus aureus and Enterobacter aerogenes were detected in 3.6% and 3.0% of cases, respectively, while Proteus species and coagulase-negative Staphylococci (CoNS) accounted for 0.6% each. Regarding antibiotic resistance, E. coli demonstrated substantial resistance to amoxicillin (98.5%), followed by ciprofloxacin (73.9%) and cotrimoxazole (67.7%), whereas resistance to amikacin remained low. In contrast, S. aureus, the predominant gram-positive isolate, exhibited complete resistance (100%) to amoxycillin, ciprofloxacin, cloxacillin, and cephalexin (each at 66.7%), but remained fully sensitive to both Amikacin and Tigecycline. Overall, gram-negative bacteria were more frequently identified than gram-positive bacteria. The findings highlight the vulnerability of cancer patients to infections by opportunistic organisms, including multidrug-resistant (MDR) strains, underscoring the urgent need for robust antimicrobial stewardship and ongoing surveillance of antibiotic resistance trends.

The present investigation retrospectively examined the therapeutic impact of crizotinib in a cohort of patients diagnosed with ALK-positive metastatic lung cancer. A total of 25 individuals participated, and survival outcomes were assessed using Kaplan-Meier estimation and Cox proportional hazards modeling. Among the participants, 52% (13 patients) were male, and the mean age was 55 years, spanning from 30 to 80 years. Notably, 92% (23 patients) presented with de novo metastatic disease. Central nervous system involvement was observed in 32%, while 20% exhibited hepatic metastases. Before the administration of crizotinib, 64% had received systemic chemotherapy, and 20% underwent palliative radiation. The median progression-free survival was calculated at 16.8 months (95% CI: 5.7–27.9). Adverse effects of grade 1–2 severity were recorded in 36% of cases, whereas 12% experienced grade 3–4 toxicities. Upon disease progression, 52% (13 patients) transitioned to alternative therapies, including second-generation ALK inhibitors such as alectinib, ceritinib, or lorlatinib, or received additional chemotherapy. Median overall survival reached 44.2 months (95% CI: 28.5–59.9), with a 37.4% survival rate at the four-year mark. Multivariate analysis identified the ALK positivity ratio as a statistically significant prognostic variable for overall survival (P = 0.02). These results highlight the clinical benefit and tolerability of crizotinib in the management of ALK-mutant metastatic non-small cell lung cancer and reinforce the prognostic relevance of ALK positivity in predicting long-term survival.