Cancer / Oncology/Gastric cancer
Gastrointestinal · type
Gastric cancer
Clinical / Scientific
Gastric adenocarcinoma includes chromosomal-instable, MSI, genomically stable/diffuse (RHOA/CDH1) and EBV-positive classes. HER2 amplification, , PD-L1 and metabolic programmes vary by class. H. pylori-related is a classic initiator.
Core Biological Drivers
HER2 / RTKs
Amplifications in CIN tumours.
CDH1 / RHOA
Diffuse/genomically stable biology.
Inflammation / NF-κB
H. pylori and tone.
MSI / EBV
Immune-visible subsets.
Key Pathways
Scientific explanation
HER2/ERBB2 amplification or overexpression produces ligand-independent ERBB signalling, classically in a subset of breast and gastroesophageal cancers and rarely in colorectal cancer.
Scientific explanation
phosphorylates PIP2 to PIP3, recruiting . supports growth, survival, glucose uptake and mTORC1 input. Pathway activation is common via PIK3CA mutation, PTEN loss or -tyrosine- signalling.
Scientific explanation
Canonical Wnt signalling stabilizes β-catenin, driving TCF/LEF . APC loss is a classic colorectal initiating event; the pathway also contributes to stemness in several tissues.
Scientific explanation
NF-κB factors link inflammatory cytokines and innate sensors to survival, production and sometimes therapy resistance.
Scientific explanation
family ligands drive endothelial sprouting and vascular permeability, a canonical tumour axis.
Scientific explanation
PD-1 on T cells engaging PD-L1/PD-L2 restrains cytotoxic function. Tumour or myeloid PD-L1 is a canonical adaptive immune-evasion axis.
Scientific explanation
Epithelial–mesenchymal plasticity, driven by TWIST/SNAIL/ZEB and TGF-β/Wnt/Notch inputs, reduces adhesion and increases motility and stem-like features.
Scientific explanation
Aerobic (Warburg metabolism) supports ATP, biomass and redox buffering even when oxygen is available. Hexokinase, PKM2 and lactate export are frequent nodes.
Scientific explanation
TP53 encodes a stress-responsive factor controlling cell-cycle arrest, and metabolic adaptation. Loss or mutation is among the most common cancer events.
Pathway Convergence
Target → pathway → downstream effect → biological consequence. Shared intersections are mechanistic maps, not protocols.
Growth-factor signalling
Ligand or mutation-driven RTK input feeds PI3K/AKT and mTORC1, supporting anabolic growth. This is a map of signalling, not a treatment protocol.
Hypoxia to vessels
Low oxygen stabilizes HIF-1α, inducing VEGF and endothelial sprouting. Anti-angiogenic pharmacology intersects this axis but does not erase the tumour ecosystem.
Inflammatory survival
Chronic cytokine tone activates NF-κB and STAT3 transcriptional programmes that favour survival, invasion and sometimes immune evasion.
Metabolic Vulnerabilities
Aerobic supports ATP, biomass and acidification even when oxygen is available. Extent varies by tumour and remains a vulnerability hypothesis rather than a uniform target.
Tumor Microenvironment
Disordered vasculature creates , HIF-1α stabilization, induction and immune-suppressive adenosine/lactate milieus.
Tumour-associated macrophages and myeloid-derived suppressor cells secrete cytokines that support invasion and blunt cytotoxic T cells.
Metastasis Module
, protease-mediated invasion, , circulating tumour-cell survival and organ-specific colonization form the metastatic cascade. Pre-metastatic niches and vascular permeability influence tropism.
Resistance Biology
Resistance can arise from drug efflux, secondary mutations, bypass RTK signalling, apoptotic threshold elevation, -mediated survival, metabolic adaptation and lineage plasticity.
Cancer Stemness
Wnt, Notch, Hedgehog, ALDH and CD44-associated programmes can mark stem-like fractions with quiescence and therapy tolerance. These markers are not interchangeable across tumour types.
Mechanism-Based Adjunctive Strategies
Compounds appear only where a mechanistic overlap exists for this cancer. Evidence tiers are not equivalent. Nothing here is a treatment recommendation.
Target / Mechanism
Modest complex I inhibition raises AMP:ATP, activating and restraining hepatic and -linked anabolism. Direct antineoplastic efficacy is not established from that pharmacology alone.
Cancer relevance
activation and restraint provide a metabolic rationale in - and -linked tumours. Human data are mixed and do not establish metformin as cancer therapy.
Metabolic adjunctive research context. Convergence: AMPK, mTOR, Glycolysis.
Curcumin
Target / Mechanism
Polyphenol with promiscuous in-vitro NF-κB, and ROS effects. Bioavailability is poor; dish activity does not establish clinical anticancer efficacy.
Cancer relevance
In-vitro NF-κB/ effects are frequent. Poor bioavailability and absence of robust clinical anticancer efficacy keep this pathway-level.
Inflammatory-signalling dish models. Convergence: NF-κB, JAK/STAT.
Celecoxib
Target / Mechanism
Selective -2 reducing PGE2. Relevant to -associated epithelial neoplasia; cardiovascular risk and lack of broad anticancer approval constrain interpretation.
Cancer relevance
-2/PGE2 biology is relevant in some epithelial neoplasias. Cardiovascular risk and lack of broad anticancer approval apply. Do not equate polyp or biomarker studies with tumour cure.
Inflammation-associated epithelial neoplasia research. Convergence: COX / inflammatory signalling, Angiogenesis.
Target / Mechanism
Benzimidazole that binds β-. Mammalian disruption, mitotic arrest and related signalling in cancer models are preclinical and are not an approved anticancer use.
Cancer relevance
disruption can trigger mitotic stress and in cell and animal models. This is not an established oncology use.
Experimental antimitotic / microtubule stress. Convergence: Apoptosis, p53.
Target / Mechanism
uncoupler in cestodes; mammalian models report , Wnt/β-catenin and modulation. Those host-signalling findings are investigational/preclinical.
Cancer relevance
Models report Wnt/β-catenin, and effects. Host signalling findings remain investigational.
Wnt / STAT3 signalling models. Convergence: Wnt/β-catenin, JAK/STAT, mTOR.
Target / Mechanism
Azole antifungal; off-target reports include Hedgehog-pathway antagonism and anti-angiogenic endothelial effects in experimental and early clinical settings. Not a licensed antineoplastic.
Cancer relevance
Hedgehog antagonism and anti-angiogenic endothelial reports exist, including early clinical probes. Not a licensed antineoplastic.
Hedgehog / angiogenesis research. Convergence: Hedgehog, Angiogenesis.
Research Context
- Hallmarks. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-674. https://doi.org/10.1016/j.cell.2011.02.013
- Checkpoints. Pardoll DM. The blockade of immune checkpoints in cancer immunotherapy. Nat Rev Cancer. 2012;12(4):252-264. https://doi.org/10.1038/nrc3239
- NF-κB. Karin M. NF-κB as a critical link between inflammation and cancer. Cold Spring Harb Perspect Biol. 2009;1(5):a000141. https://doi.org/10.1101/cshperspect.a000141
This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.