Stomach Neoplasms

The grounding supports a multifactorial aetiology involving both environmental and genetic influences. Carcinogenesis is described as a multistage process driven by progressive mutations and epigenetic alterations in gene expression. Chronic atrophic gastritis, intestinal metaplasia, and persistent Helicobacter pylori gastritis are also linked to gastric adenocarcinoma risk.

The literature describes gastric carcinogenesis as a stepwise process involving mutations, epigenetic changes, altered gene expression, and changes in cell proliferation. Tumor biology is also associated with the tumor microenvironment, DNA mismatch repair, and immune-related pathways including PD-1/PD-L1 signaling. Drug resistance and noncoding RNA regulation are highlighted as important mechanisms in advanced disease.

Risk increases with age, and the incidence rises progressively over time. Chronic atrophic gastritis, intestinal metaplasia, incomplete intestinal metaplasia, persistent Helicobacter pylori gastritis, and a family history of gastric cancer are identified as risk factors or factors used for risk stratification. The literature also notes that younger patients may represent a model for genetically driven early-onset disease.

For advanced or metastatic disease, systemic therapy is the main treatment modality, with chemotherapy remaining the backbone of care. The grounding supports fluorouracil-based combination chemotherapy and platinum-containing regimens, and it also notes targeted and immunotherapy approaches such as trastuzumab, nivolumab, and pembrolizumab in biomarker-selected disease. Surgery and endoscopic surveillance are also part of management in appropriate settings, particularly for diagnosis, staging, and earlier lesions or precancerous conditions.