Colorectal Adenocarcinoma

Neoadjuvant immune checkpoint inhibition demonstrates high pathological and clinical response rates in dMMR/MSI-H colorectal cancer, with organ preservation achievable in selected rectal cancer patients. Neoadjuvant immunotherapy may become an alternative to surgery as the primary treatment for MSI-H/dMMR colorectal cancer if long-term quality of life is superior and toxicity and cost are competitive with standard surgical approaches. However, longer follow-up, predictive biomarkers, and randomized comparisons with upfront surgery are required before its routine clinical use.

According to in vivo experiments, UA inhibited CRC tumor growth by regulation of above genes. This study demonstrated that UA could effectively inhibit CRC proliferation by inducing ferroptosis via regulation of system xc- subunits and miR-214-3p/Stat3/GPX4 axis, suggesting UA could serve as a promising anti-colorectal cancer candidate requiring further validation and optimization.

Here, we show that sotorasib, adagrasib, and the RAS-ON inhibitor RMC-6291 are effective in a neuroblastoma cell line altered by KRAS(G12C). Importantly, sotorasib also decreased ERK phosphorylation in a NRAS(G12C)-altered cell line xenograft model; however, this treatment did not prolong survival as a single agent. These results suggest that combinations of targeted agents that include sotorasib may be required for clinical benefit in pediatric patients with H- or NRAS(G12C)-altered malignancies in addition to those with KRAS(G12C)-altered malignancies.

The results highlighted a small number of tumor entities that could be targeted by anti-L1CAM drugs, once these are proved to be sufficiently safe and efficient. L1CAM expression does not appear to confer an aggressive phenotype to affected cancer cells.

Considering the prognostic implications of DLAT in tumors and its correlations with immune indicators, it is plausible to regard DLAT as both a prognosis feature for certain malignancies and an evaluative metric for immunotherapy efficacy. The findings suggest that DLAT could be a potential therapeutic target and serve as a biomarker for predicting patient outcomes and guiding treatment strategies in various cancers, with its prognostic and immunological implications likely to be context-dependent across different tumor types.

Our findings identify glycolysis as a shared but oppositely regulated pathway linking cancer and neurodegeneration. ACAA2 may serve as a molecular mediator of this metabolic divergence, offering new insights into disease crosstalk and potential therapeutic targets.

Further exploration using the datasets from the Genotype-Tissue Expression (GTEx) Portal and The Cancer Genome Atlas (TCGA) showed that rs3825071 genotypes affected NEAT1 expression in the colon tissues, and elevated NEAT1 levels were associated with a worse survival rate in relatively younger patients (< 65 years old) with colon adenocarcinoma. These data suggest that altered expression levels of NEAT1 due to genetic polymorphisms may influence the progression of colon cancer.

Integrating microbiome and transcriptome analysis shows significant potential in COAD diagnosis and prognostic assessment. These findings provide important insights for further clinical applications and cancer treatment strategies.

We report promising downstaging and pCR/cCR rate of ICI for initially-unresectable MMRd CRC. ICI-first can permit curative resection, with risk of local complication from significant treatment response. Larger, multi-centre studies are needed to validate these findings.

For the first time, the expression of IL-23 and IL-28  has shown a highly significant interrelation in MA patients, suggesting a possible interplay between them. High IL-23 and IL-28 expressions may have adverse prognostic effects on survival in MA. Molecular studies are necessary to further investigate the interaction between IL-23 and IL-28 in CRC.

Immunophenotyping demonstrated TTF-1 nuclear positivity in the metastatic tumor alongside a classic colorectal profile: cytokeratin 7 (CK7) negativity, cytokeratin 20 (CK20) positivity, strong caudal-type homeobox transcription factor 2 (CDX2) and special AT-rich sequence-binding protein 2 (SATB2) nuclear expression, and absence of Napsin A. The patient underwent surgical resection of the primary sigmoid colon tumor and received 16 cycles of capecitabine plus bevacizumab chemotherapy. We discuss how the comprehensive immunohistochemical panel and genetic findings confirmed the colorectal origin of the lung lesions, emphasizing that combined marker profiles (TTF-1 +/CK7 -/CK20 +/CDX2 +/SATB2 +/Napsin A -) are more consistent with metastatic colorectal adenocarcinoma rather than an enteric-type adenocarcinoma of the lung, primary. The report reviews relevant literature and underscores the importance of correlating clinical history with pathology to avoid misdiagnosis.

In line with this, HnRNPU deletion induced ferroptosis and increased sensitivity to RSL3 treatment and cysteine deprivation...Findings demonstrate that HnRNPU promotes proliferation and inhibits ferroptosis by regulating the mRNA stability of SLC7A11 and SLC3A2. Targeting HnRNPU is a potential therapeutic approach for COAD treatment.