ReviewJournal of gastrointestinal cancer2026
Emerging Molecular Insights and Targeted Therapeutics in Colorectal Cancer: From Emerging Approaches to Personalized Medicine.
Review in Journal of gastrointestinal cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is the third most prevalent malignancy and the second leading cause of cancer-related deaths globally. Recent research emphasizes personalized medicine as it tailors treatment to the patient’s tumor genetics, improving therapeutic response and reducing toxicity. It improves illness management by enabling precise targeted immunotherapies, better treatment outcomes, and early identification and risk assessment. On a molecular level, CRC is driven by a spectrum of genetic alterations involving oncogenes, tumor suppressor genes, and genes responsible for maintaining genomic integrity. Based on the nature and origin of these mutations, CRC is typically classified into sporadic, familial, and hereditary subtypes. The disease is underpinned by three principal molecular mechanisms: chromosomal instability (CIN), microsatellite instability (MSI), and the CpG island methylator phenotype (CIMP). KRAS, BRAF, PIK3CA, PTEN, SMAD2, SMAD4, and c-MYC are oncogenic and tumor suppressor genes that are frequently altered in CRC. These genes affect tumor biology and clinical outcomes, making them useful biomarkers. Besides protein-coding gene changes, dysregulation of non-coding RNAs (ncRNAs) has been linked to colorectal carcinogenesis, presenting promising early detection and prognostication methods. Therapeutically, advances have included the integration of monoclonal antibodies targeting vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) pathways. More recently, the development of targeted agents, such as tyrosine kinase inhibitors and next-generation biologics, aims to optimize therapeutic efficacy while reducing systemic toxicity. This review focuses on the Targeted and personalized CRC treatment, highlighting low-toxicity regimens, significant clinical trial outcomes, ongoing challenges, and potential future directions in personalized medicine.
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Identifiers
41874786What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.