RNA-binding proteins (RBPs), a class of molecules that play a crucial role in regulating gene expression, have attracted considerable attention in cancer biology research. RBPs influence osteosarcoma progression by modulating RNA metabolism and participating in cellular proliferation, differentiation, apoptosis, and interactions within the tumor microenvironment. Understanding the current status and future trends of RBPs is crucial for the advancement of osteosarcoma research.

This study was conducted to assess the diagnostic accuracy of long non-coding RNAs (lncRNAs) in differentiating patients with oral squamous cell carcinoma (OSCC), and to explore their potential role in early detection.

This study aims to conduct a systematic review of the prognostic value of miR-21 expression levels in patients with colorectal cancer (CRC), pancreatic ductal adenocarcinoma (PDAC), and esophageal squamous cell carcinoma (ESCC).

Endometrial cancer represents one of the most common gynecological cancers in women. In recent years, there has been increasing interest in immunotherapy, including the use of pembrolizumab, particularly for the treatment of cancers with deficient mismatch repair (dMMR) and microsatellite instability-high (MSI-H). A systematic review of the literature from 2020 to 2025 was conducted according to the PICO model. Six studies were included in this review, comprising four randomized clinical trials (RCTs) and two pre-specified subgroup analyses derived from previous RCTs involving a total of 3684 patients with early-stage or advanced disease or metastatic or recurrent endometrial cancer. Interventions included the use of pembrolizumab in monotherapy and in combination with chemotherapy or lenvatinib. Pembrolizumab showed a significant improvement in progression-free survival (PFS) and overall survival (OS) in the dMMR patient groups. Therapeutic benefit was limited in the proficient mismatch repair (pMMR) groups. The incidence of side effects was high but comparable to the control group. Pembrolizumab, especially in combination therapy with lenvatinib, is a promising therapeutic option for patients with dMMR/MSI-H endometrial cancer. The results suggest a potential long-term treatment effect, although the limitations of the RCT and the variability in the therapeutic regimens require further research.

ALK receptor tyrosine kinase (ALK) rearrangements occur in 4-8% of non-small cell lung cancer (NSCLC) and are often associated with aggressive clinical behavior. Although ALK-targeted tyrosine kinase inhibitors significantly improve overall survival in advanced-stage NSCLC, their role in early-stage disease remains unclear. This meta-analysis (PROSPERO CRD420251012874) aimed to systematically evaluate recurrence rates and disease-free survival (DFS) outcomes in surgically resected patients with ALK-rearranged NSCLC compared to ALK-wild type (WT).

DNA damage-induced genomic instability represents a fundamental hallmark of cancer progression. Natural products with multi-target and low toxicity characteristics can effectively utilize this mechanism for cancer treatment.

To date, no meta-analysis has studied the general outcomes of personalized cancer drug therapy with a focus on current targeted, immunotherapy, and multi-agent phase II clinical trials.

Head and neck adenoid cystic carcinoma (ACC) is a common malignancy often associated with an aggressive clinical course and a wide array of gene mutations. This systematic review aimed to determine the prevalence of these mutations and their association with prognosis and recurrence in ACC. A search of the scientific literature was carried out from inception till 31 July 2024 in the electronic databases - PubMed, EMBASE, Scopus, Web of Science, Ovid/MEDLINE, and Science direct following specific eligibility criteria. The methodological quality of the included studies was assessed using the Newcastle-Ottawa tool. 31 studies were included, and numerous genes like MYB, NOTCH, TP53, PIK3CA, ARID1A, KDM6A, RAS, SPEN, and many more were identified and were related to poor prognosis. Identification of different genes using wide NGS panels and combination of molecular techniques becomes necessary as multiple genes might be involved in ACC pathogenesis and subsequent targeted therapies can be designed.

Immune checkpoint inhibitors (ICIs) are used in epidermal growth factor receptor (EGFR)-mutant nonsmall-cell lung cancer (NSCLC) after resistance to targeted therapy; however, responses remain limited. This study identified predictors of ICI efficacy to inform treatment strategies.

Neoadjuvant targeted therapy with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) is emerging as a strategy to improve outcomes in resectable stage IIIA/IIIB non-small cell lung cancer (NSCLC) with EGFR mutations. We conducted a systematic review of clinical trials and studies, following PRISMA guidelines, to evaluate the efficacy, safety, and surgical feasibility of neoadjuvant EGFR-TKI therapy in this setting. Literature was searched for studies reporting outcomes of neoadjuvant TKIs (e.g., gefitinib, erlotinib, afatinib, osimertinib) in resectable stage III NSCLC. Key endpoints included radiologic response rates, pathological response (pCR and major pathologic response, MPR), complete resection (R0) rates, surgical outcomes, and adverse events. A total of 15 studies (including one randomized trial and multiple phase II trials/cohorts) were analyzed, encompassing over 400 patients. Neoadjuvant EGFR-TKIs yielded high objective response rates (pooled ORR ~ 57%, up to 70-80% with third-generation TKIs). However, pathological complete response was rare (pooled pCR ~ 3%) and MPR rates remained modest (often < 15%), underscoring a difference compared to neoadjuvant chemoimmunotherapy. Complete resection (R0) rates were excellent (approximately 90% in patients undergoing resection), and neoadjuvant TKIs enabled surgical downstaging in ~ 40-74% of cases. Treatment was well tolerated, with primarily grade 1-2 rash and diarrhea; severe adverse events ≥ grade 3 were under 10%. Importantly, surgery after TKI therapy was feasible, with no increase in perioperative morbidity reported. In some cases, tumor shrinkage allowed conversion of an initially unresectable or complex case to a less extensive resection (e.g., sleeve lobectomy instead of pneumonectomy). In comparison to historical neoadjuvant chemotherapy, EGFR-targeted therapy significantly improved radiologic response and progression-free survival, while avoiding the added toxicity of chemotherapy. Compared to neoadjuvant chemo-immunotherapy (which achieves higher pCR rates), targeted therapy is specific to oncogene-driven tumors and has shown efficacy in EGFR-mutant tumors where immunotherapy alone is often ineffective. This review highlights that neoadjuvant EGFR-TKI therapy is a safe and feasible approach that can increase resectability and preserve lung tissue in stage III EGFR-mutant NSCLC. The combination of novel targeted agents with advanced surgical techniques (including sleeve resections and robotic-assisted approaches) offers promising results. Nevertheless, due to the lack of significant pathological complete responses, adjuvant therapy and long-term outcomes remain concerns. Ongoing trials (e.g., NeoADAURA) will further clarify the role of EGFR-TKIs ± chemotherapy in the neoadjuvant setting. In conclusion, for resectable stage III EGFR-mutant NSCLC, neoadjuvant EGFR-targeted therapy achieves high response rates and surgical success with manageable toxicity. Multimodal therapy incorporating targeted agents and lung-sparing surgical strategies may improve patient outcomes. Future research should focus on optimizing combination regimens, identifying predictive molecular markers of response, and confirming survival benefits in this subset of lung cancer.

Hereditary breast cancer, primarily linked to pathogenic BRCA1 and BRCA2 mutations, accounts for 5%-10% of all breast cancer cases in the United States. Despite national guidelines recommending genetic testing for individuals at elevated hereditary risk, uptake remains disproportionately low among African American and Hispanic/Latina women. Despite elevated risk in Black women data on genetic testing uptake in St. Louis is absent.

Artificial intelligence (AI) is transforming histologic assessment, evolving from a diagnostic adjunct to an integral component of clinical decision-making. Over the past decade, AI applications have significantly advanced histopathology, facilitating tasks from tissue classification to predicting cancer prognosis, gene alterations, and therapy responses. These developments are supported by the availability of high-quality whole-slide images (WSIs) and publicly accessible databases like The Cancer Genome Atlas (TCGA), which integrate histologic, genomic, and clinical data. Deep learning techniques replicate and enhance pathologists' decisions, addressing challenges such as inter-observer variability and diagnostic reproducibility. Moreover, AI enables robust predictions of patient prognosis, actionable gene statuses, and therapy responses, offering rapid, cost-effective alternatives to conventional methods. Innovations such as histomorphologic phenotype clusters and spatial transcriptomics have further refined cancer stratification and treatment personalization. In addition, multimodal approaches integrating histologic images with clinical and molecular data have achieved superior predictive accuracy and explainability. Nevertheless, challenges remain in verifying AI predictions, particularly for prognostic applications and ensuring accessibility in resource-limited settings. Addressing these challenges will require standardized datasets, ethical frameworks, and scalable infrastructure. While AI is revolutionizing histologic assessment for cancer diagnosis and treatment, optimizing digital infrastructure and long-term strategies is essential for its widespread adoption in clinical practice.

To assess the variations in Single Nucleotide Polymorphisms (SNPs) that affect susceptibility of CRC in Saudi patients.

ObjectiveTo synthesize recent molecular advances that inform diagnosis, risk-stratification, and perioperative treatment in early-stage and locally advanced non-small cell lung carcinoma (NSCLC), with emphasis on comprehensive genomic profiling, minimal residual disease (MRD) detection by circulating tumor DNA (ctDNA), and the translation of biomarkers into targeted and immunotherapy strategies.MethodsSystematic review registered in PROSPERO (CRD420251076423). Searches of PubMed, Scopus, Web of Science, and Embase (January 2015-April 2025) followed PRISMA 2020/PRISMA-S. From 4640 records, 890 duplicates were removed; 3750 titles/abstracts were screened; 150 full texts were assessed; 75 studies met inclusion criteria. Risk of bias used Newcastle-Ottawa Scale (NOS) for observational studies and Cochrane RoB 2 tool for randomized controlled trials; certainty was summarized with GRADE where applicable.ResultsActionable alterations (e.g. EGFR, ALK, KRAS, MET, RET, BRAF, NTRK) are prevalent in early-stage NSCLC and comparable to advanced disease, supporting routine comprehensive genomic profiling in curative-intent settings. Next-generation sequencing (NGS) and ctDNA enable the detection of MRD, earlier relapse prediction, and dynamic treatment monitoring. Perioperative strategies integrating targeted therapy and immunotherapy (e.g. adjuvant EGFR-TKI, neoadjuvant chemo-immunotherapy) improve pathological and disease-free outcomes in selected biomarker-defined populations. Evidence profiles generally show low-to-moderate risk of bias and moderate-to-high certainty for key outcomes related to profiling and MRD, with heterogeneity across platforms and endpoints.ConclusionsMolecular advances-particularly broad NGS and ctDNA-based MRD-are reshaping the perioperative management of early and locally advanced NSCLC, enabling precision selection for targeted and immunotherapy approaches. Standardization of testing workflows and reporting, and cost-effective implementation are priorities for equitable adoption and for future trials that combine NGS, MRD, and multi-omic/AI-driven risk stratification.

P53 mutation (TP53m) is a common intrinsic factor involved in relapsed or refractory (R/R) B cell malignancies that associates with treatment resistance. As a novel immunotherapy, CAR-T has been increasingly applied in TP53m B cell malignancies, yet whether it can overcome the poor outcome of the TP53m population is controversial. We searched MEDLINE and EMBASE to identify population-based cohort studies that evaluated the CAR-T treatment outcomes between wild type and TP53m patients in B cell malignancies. Meta-analysis on their complete response (CR), partial response (PR), overall response rate (ORR), progression-free survival (PFS) and overall survival (OS) was carried out and pooled risk ratios (RR) or hazard ratios (HR) were estimated. A total of 10 eligible studies reporting 848 patients with B cell malignancies from wild type and TP53m groups receiving CAR-T therapy were selected. The CR and ORR were comparable in both wild type and TP53m patients either with B cell lymphoma or leukaemia (all p > 0.05). However, the TP53m group was associated with shorter PFS and OS in both diseases (all p < 0.05). In traditional single targeting CAR-T therapy, the PFS and OS were shorter in the TP53m group than in the wild type group (all p < 0.05). In contrast, the former outcomes of the wild type and TP53m groups were comparable when receiving dual-targeting CAR-T treatment (all p > 0.05). Though the CR and ORR of wild type and TP53m groups were similar, the PFS and OS of B cell malignancy patients bearing TP53m were inferior to wild type patients receiving CAR-T cell treatment. Notably, the CR, PFS and OS of wild type and TP53m groups exhibit the same therapeutic effect via CD19/22 CAR-T cocktail therapy. In other words, the poor prognosis of TP53m patients may be overcome by double targeting CAR-T mode.

Fms-like tyrosine kinase 3 (FLT3) mutations are associated with poor prognosis in patients with acute myeloid leukaemia (AML).

BRAF V600E-mutated metastatic colorectal cancer (mCRC) represents a biologically aggressive subset with poor prognosis and limited response to conventional therapies. While dual inhibition of BRAF and EGFR with encorafenib and cetuximab has emerged as a promising therapeutic strategy, a comprehensive quantitative synthesis of its efficacy and safety has been lacking.

Current treatments for locally advanced rectal cancer (LARC) include preoperative radiotherapy, chemotherapy and chemoradiotherapy followed by total mesorectal excision (TME), which can severely impact quality of life. Recently, anti-PD1 immunotherapy in microsatellite instability high (MSI-H) LARC has shown 100% clinical complete responses, allowing patients to avoid surgery with minimal toxicity. This review assesses the safety, toxicity, pathological impact, and long-term benefits of incorporating immunotherapy into the neoadjuvant treatment of microsatellite stable (MSS) and MSI-H LARC. This systematic review, conducted following PRISMA guidelines, investigates neoadjuvant immunotherapy in LARC. Data on study characteristics, treatment protocols, and outcomes were extracted. Quality assessment was conducted by using the Methodological Index for nonrandomized studies (MINORS) and the RoB2 tool. Patients were categorized into MSI-H, MSS, and unknown microsatellite status cohorts. We found twelve published studies including 547 patients. In the MSS cohort, postneoadjuvant surgery rates ranged from 57.6% to 100%, with a watch-and-wait approach adopted in up to 27.1% of cases. For MSI-H patients, surgery and watch-and-wait rates varied widely (0%-100%), reflecting heterogeneity in management. R0 resection rates were high across cohorts (70%-100% MSS, 80%-100% MSI-H). Pathological complete response (pCR) rates were 25% to 50% in MSS and 50% to 60% in MSI-H cohorts. Grade 3-4 adverse events ranged from 3.9% to 45.2% (MSS), 0% to 60% (MSI-H), with immune-related events generally below 10%. The role of immunotherapy in MSS rectal cancer remains unclear; phase III trials and translational research are needed urgently for guidance.

The clinicopathological and molecular characteristics of early-onset colorectal cancer (EOCRC) are unclear. In this study, we compared the clinicopathological features, biomarkers, and prognoses between EOCRC and late-onset colorectal cancer (LOCRC).

Proteomics can play an important role in advancing the discovery of cancer biomarkers. We aimed to synthesize current evidence concerning proteome signatures and molecular pathways involved in human breast cancer (BC).