Colorectal cancer is the third most common cancer worldwide with a high mortality rate at the advanced stages. However, colorectal cancer is not a single type of tumor; its pathogenesis depends on the anatomical location of the tumor and differs between right side and left side of the colon. Tumors in the proximal colon (right side) and distal colon (left side) exhibit different molecular characteristics and histology. In the right-sided tumors, mutations in the DNA mismatch repair pathway are commonly observed; and these tumors generally have a flat histology. In the left-sided tumors, chromosomal instability pathway-related mutations, such as KRAS, APC, PIK3CA, p53 mutations are observed and these tumors demonstrate polypoid-like morphology. Therapy responses are totally different between these tumor entities. Left-sided colorectal cancer (LCRC) patients benefit more from adjuvant chemotherapies such as 5-fluorouracil (5-FU)-based regimes, and targeted therapies such as anti- epidermal growth factor receptor (EGFR) therapy, and have a better prognosis. Right-sided colorectal cancer (RCRC) patients do not respond well to conventional chemotherapies, but demonstrate more promising results with immunotherapies because these tumors have high antigenic load. For the development of effective therapy regimes and better treatment options, it is essential to evaluate right-sided and left-sided tumors as separate entities, and design the therapy regime considering the differences between these tumors.

Neuroblastoma (NB) is the most common extracranial solid tumor in children with incidence rate 10.2 per 1 million children under 15 years old. NB has great diversity in clinical behavior while some tumors are easily curable and spontaneously regressed, the others are resistant to chemotherapies and exhibiting high relapse rates. Despite intensive usage of chemotherapies, still 5-year survival rate is about 40% for advanced stage bad prognostic patient group. Hence, there is need for more effective therapeutics and novel biomarkers for early detection of high-risk patients. In the present study we aimed to study molecular mutation profile of both good and bad prognostic NB patients with whole exome sequencing (WES). The NB patients whose risk group previously was confirmed according to TPOG-2009 protocol. 5 patients with good prognosis (low risk & intermediate with good histology) and 5 patients with bad prognosis (intermediate poor histology & high risk) were chosen. As a result, 23 common mutations were found in both prognostic group. While 7 mutations were found to be specific to bad prognostic group, 2 mutations were only observed in good prognostic group patients. The commonly mutated genes were located commonly in cell membrane and extracellular space and mostly interfering with cell signaling and cell communication pathways.

Ewing sarcoma is a bone and soft tissue tumor either neuroectodermal or mesenchymal originated and affecting children and adolescents. In the present study, we aimed to find out prognostic and predictive biomarkers for Ewing sarcoma. Hence, we examined the copy number alterations (and related possible genes) among ten Ewing sarcoma patient samples and possible associations with the clinical outcome. DNA extraction from formalin fixed paraffin embedded archive tissues was performed. Whole genome Comparative Genomic Hybridization (CGH) was performed by NimbleGen and recorded as single Panel Rainbow through chromosomes 1–22, X and Y. Data was interpreted by SignalMap software and genetic regions matching the deletion or amplification loci were recorded. The mean age of the patients was 8.6 years. Three of the cases were male, while seven were female. According to CGH analysis, the most common DNA copy number alterations were found in SLIT-ROBO Rho GTPase activating protein (srGAP2), RANBP2 like GRIP domain (RGPD5), nephrocystin 1 (NPHP1), GTF2I repeat domain containing 2 (GTF2IRD2), pyridoxal dependent decarboxylase domain containing 1 (PXDC1), which were found down-regulated among 7 of 10 patients. In conclusion, in our dataset the copy number alterations are mostly found in genes related with cytoskeletal elements, migration and protein trafficking among our patient group. Gene functional studies are required for better understanding the role of these genes in Ewing Sarcoma pathogenesis

Necroptosis is a regulated inflammatory form of programmed cell death mediated by RIPK1, RIPK3, and MLKL, but its clinical relevance in surgically resected non-small cell lung cancer (NSCLC) remains uncertain. This study evaluated the transcript-level expression of these genes and their associations with survival in 41 patients who underwent complete NSCLC resection without preoperative therapy. RNA was isolated from frozen tumor tissues, and mRNA expression was quantified using RT-qPCR. Expression was analyzed primarily as continuous log₂(expression + 1)-transformed variables in Cox proportional hazards models; median-based groups were used only for exploratory Kaplan–Meier visualization. The cohort comprised 34 males and 7 females, with a mean age of 61.0 years; 41.5% had adenocarcinoma and 58.5% had squamous cell carcinoma. The maximum follow-up was 145 months, and the 5-year overall survival rate was 46.3%. None of the three genes was significantly associated with overall or disease-free survival in either univariable or restricted adjusted Cox models. Median-based analyses similarly showed no significant survival differences. These findings do not support RIPK1, RIPK3, or MLKL transcript levels as standalone prognostic biomarkers in surgically resected NSCLC. Larger studies integrating transcriptomic, protein-level, and functional assessments are warranted.