Gastric Adenocarcinoma

Slide 1 · GASTRIC ADENOCARCINOMA

Morphologic patterns • etiopathogenesis • molecular subtypes • clinical behavior

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Distinguish intestinal-type from diffuse-type gastric adenocarcinoma.

Trace environmental, hereditary, and molecular mechanisms of tumor development.

Recognize gross and microscopic patterns and their mechanistic basis.

Integrate clinical presentation, metastatic patterns, stage, and prognosis.

Slide 3 · Adenocarcinoma dominates gastric malignancy

>90%

Of gastric cancers are adenocarcinomas account.

The core morphologic distinction is gland-forming intestinal type versus discohesive diffuse type.

Slide 4 · Two principal patterns of gastric adenocarcinoma

Intestinal-type

Usually forms a bulky or ulcerated tumor.

Shows cohesive, gland-forming malignant epithelium.

Often follows metaplasia and dysplasia.

Diffuse-type

Infiltrates gastric wall without a dominant mass.

Cells are poorly cohesive; Signet-ring forms are typical.

Closely linked to defects of cell adhesion.

Slide 5 · Why diagnosis may be delayed

Early dyspepsia, dysphagia, and nausea overlap with benign gastric disease.

Symptoms become more specific as tumor burden and wall involvement increase.

Weight loss, anorexia, anemia, or gastrointestinal bleeding often signal advanced disease.

Diffuse infiltration may produce early satiety without a conspicuous luminal mass.

Slide 6 · Geographic variation is pronounced

Up to 20-fold

Higher gastric cancer incidence in selected high-risk regions.

Textbook examples: Japan, Chile, Costa Rica, and Eastern Europe versus several lower-incidence regions.

Slide 7 · Population risk differs by geography

High-incidence settings

Marked regional burden, including parts of East Asia.

Endoscopic screening can identify early lesions.

Intestinal-type cancers historically predominated.

Low-incidence settings

Population screening is generally less cost-effective.

Advanced stage at presentation is more frequent.

Diffuse-type disease shows less geographic variation.

Slide 8 · Screening changes stage at diagnosis

35%

Early cancers among newly detected cases in Japan, as reported.

Early gastric cancer is confined to mucosa or submucosa, regardless of nodal involvement.

Slide 9 · Early detection remains uncommon in low-risk regions

<20%

Early gastric cancers detected in North America and northern Europe account.

This historical textbook comparison should not be treated as a current national surveillance estimate.

Slide 10 · The long-term incidence decline has etiologic clues

An 85% decline in U.S. Incidence since 1930.

Decline is linked mainly to reduced H. Pylori infection and intestinal-type cancers.

Changes in preserved foods and refrigeration are additional plausible contributors.

The decline does not apply equally to every site and histologic subtype.

Slide 11 · Environmental influences on intestinal-type disease

H. Pylori exposure

Chronic gastric inflammation

Multifocal atrophy

Loss of normal glands

Intestinal metaplasia

Altered epithelial lineage

Dysplasia / adenoma

Neoplastic precursor

Adenocarcinoma

Invasive gland-forming tumor

Conceptual progression: Not every infected or metaplastic stomach progresses to carcinoma.

Schematic

Slide 12 · Helicobacter pylori: The major infection association

H. Pylori–associated gastritis is frequent in gastric cancer development.

Host–bacterial interactions help determine whether atrophy develops.

The falling prevalence of infection is linked to a decline in intestinal-type cancer.

Carcinogenesis is multifactorial; Infection does not imply inevitable neoplasia.

Slide 13 · Atrophy and intestinal metaplasia alter cancer risk

Chronic gastritis

Persistent mucosal injury

Gland loss

Multifocal atrophy

Intestinal metaplasia

Risk-bearing altered mucosa

Dysplastic transformation

Preinvasive epithelial atypia

Precursor-associated pathway is characteristic of intestinal-type adenocarcinoma.

Schematic

Slide 14 · Environmental contributors extend beyond infection

Dietary carcinogens cited include N-nitroso compounds and benzo[a]pyrene.

Historic salt preservation and smoking of food increased relevant exposures.

Greater refrigeration access contributed to changed food preservation practices.

These associations support a substantial environmental contribution to risk.

Slide 15 · Migrant populations support environmental causation

First-generation migrants

May retain country-of-origin risk

Next generation

Adopts environment of new country

Intestinal-type risk

Approaches destination population

The generational change is difficult to explain by inherited variants alone.

Schematic

Slide 16 · Atrophic and metaplastic mucosa marks susceptibility

Multifocal gastric mucosal atrophy is associated with increased cancer risk.

Intestinal metaplasia is a background lesion linked to adenoma and carcinoma.

Risk is not equivalent to a diagnosis of dysplasia or invasive carcinoma.

Assessment must distinguish the background field from a focal neoplastic lesion.

Slide 17 · Gastric adenomas as epithelial precursors

Background

Most arise with atrophic gastritis and intestinal metaplasia.

Hereditary APC- or MUTYH-associated lesions are exceptions.

Usually located in the antrum.

Clinical importance

Adenomas are dysplastic epithelial neoplasms.

Carcinoma risk rises with increasing adenoma size.

Large lesions require careful assessment for coexisting carcinoma.

Slide 18 · Dysplasia is graded by cytology and architecture

Low-grade dysplasia

Nuclear enlargement, elongation and hyperchromasia.

Pseudostratified dysplastic epithelium.

Architectural changes less severe than high-grade.

High-grade dysplasia

Greater nuclear and architectural atypia.

Gland budding and complex gland-in-gland structures.

Cribriform arrangements may develop.

Slide 19 · Size increases carcinoma risk in gastric adenoma

>2 cm

Adenomas of this size have particularly elevated carcinoma risk.

Up to 30% cancer risk among large gastric adenomas; Not a universal risk for all adenomas.

Slide 20 · Peptic ulcer and post-gastrectomy risk are different

Peptic ulcer disease

Reported association with reduced gastric carcinoma risk.

Do not treat every benign gastric ulcer as premalignant.

Residual gastric stump

Prior partial gastrectomy for ulcer disease increases later cancer risk.

Potential mechanisms: Hypochlorhydria and bile reflux.

Slide 21 · Cardia cancers do not follow every distal trend

Rising gastric cardia adenocarcinoma despite declining overall incidence.

Increasing reflux, Barrett esophagus, and obesity may contribute.

Cardia and distal esophageal adenocarcinoma share clinicobiologic features.

Avoid combining proximal and distal tumors uncritically in etiologic discussions.

Slide 22 · Distal and cardia adenocarcinoma: Different contexts

Feature

Distal gastric site

Cardia / proximal site

Major association

H. Pylori / mucosal atrophy

GERD–Barrett-related context

Trend in textbook

Intestinal-type incidence declines

Incidence rising

Molecular overlap

Heterogeneous intestinal subtypes

Similarity to distal esophageal tumors

Interpretive caution

Background mucosal field matters

Precise anatomic classification matters

Contextual comparison; Not a formal clinicopathologic subclassification.

Slide 23 · Intestinal-type and diffuse-type epidemiology

Intestinal type

More frequent in high-incidence populations.

Mean presentation age approximately 55 years.

Male:female ratio approximately 2:1.

Diffuse type

Incidence varies less between countries.

Sporadic frequency similar between sexes.

Germline CDH1-associated tumors may present around age 40.

Slide 24 · Adenocarcinoma evolves through distinct mechanisms

Intestinal type

Inflammatory precursor field; Molecular heterogeneity.

Diffuse type

Disrupted epithelial adhesion and discohesive infiltration.

Chromosomal instability

Aneuploidy and signaling-pathway alterations.

Microsatellite instability

Mismatch-repair dysfunction, often via MLH1 silencing.

EBV-associated cancer

Epigenetic alterations and immune-associated phenotype.

Slide 25 · E-cadherin loss creates the diffuse growth phenotype

Intact E-cadherin junctions

CDH1 loss → reduced cell cohesion

Adhesion failure explains single-cell infiltration and the absence of cohesive glands.

Schematic — native editable shapes

Slide 26 · CDH1 encodes the adhesion protein E-cadherin

E-cadherin is an adherens-junction component maintaining epithelial cohesion.

Loss of function permits individual cells and small clusters to infiltrate.

A noncohesive growth pattern explains the diffuse histologic phenotype.

CDH1 alteration is central in hereditary and many sporadic diffuse cancers.

Slide 27 · Hereditary diffuse gastric cancer: CDH1

CDH1

A major inherited susceptibility gene for hereditary diffuse gastric cancer.

Other heritable mechanisms exist, including CTNNA1; Genetic heterogeneity matters.

Slide 28 · Two routes to E-cadherin loss in diffuse carcinoma

Germline CDH1 loss-of-function variants predispose to hereditary disease.

Somatic CDH1 mutations occur in approximately half of sporadic diffuse tumors.

Promoter hypermethylation may silence CDH1 when sequence variants are absent.

Epigenetic silencing may also affect the remaining normal allele in hereditary cases.

Slide 29 · Hereditary CDH1 tumor development

Inherited CDH1 defect

First allele predisposed

Wild-type allele silenced

Frequently by promoter methylation

Reduced E-cadherin

Defective epithelial cohesion

Diffuse carcinoma

Individual-cell infiltration

This is a mechanism schematic; Individual patients may have differing second-hit mechanisms.

Schematic

Slide 30 · CTNNA1 adds another hereditary adhesion pathway

CTNNA1 encodes α-catenin, an adherens-junction component.

α-Catenin links the E-cadherin/β-catenin complex with actin organization.

Germline CTNNA1 alterations also occur in hereditary diffuse gastric cancer.

Different inherited defects converge on loss of organized epithelial adhesion.

Slide 31 · Additional sporadic diffuse cancer alterations

RHOA

RHOA mutation is associated with sporadic diffuse gastric cancer.

Contributes to altered cell behavior in this adhesion-related subtype.

CLDN18::ARHGAP26

Fusion is associated with sporadic diffuse gastric cancer.

RHOA mutations and this fusion are reported as mutually exclusive.

Slide 32 · Diffuse cancers may be relatively genomically stable

Many diffuse gastric cancers carry fewer mutations than intestinal cancers.

Genomic stability does not mean biologically indolent behavior.

Discohesive infiltration and wall stiffening can be extensive.

Morphologic aggressiveness and total mutation burden are different concepts.

Slide 33 · Three intestinal-type molecular patterns

CIN

Chromosomal instability, aneuploidy, signaling activation.

MSI

MLH1 promoter silencing and mismatch-repair dysfunction.

EBV-associated

Extensive promoter methylation, PIK3CA changes, PD-L1/2 upregulation.

Slide 34 · Chromosomal instability defines a major molecular subset

CIN tumors exhibit aneuploidy and chromosomal copy-number abnormalities.

Receptor tyrosine kinase–RAS signaling is frequently altered.

ERBB2 (HER2), EGFR, MET, KRAS, and VEGFA are implicated in the source account.

CIN tumors are particularly associated with the antrum and pyloric channel.

Slide 35 · CIN: Interacting signaling pathways

Receptor/RAS network

ERBB2 (HER2), EGFR, MET, KRAS and VEGFA-related signaling.

Wnt pathway

APC and CTNNB1 alterations are prevalent.

TGF-β pathway

SMAD2 and SMAD4 may be altered.

Genome integrity

TP53 alterations also occur frequently.

Slide 36 · HER2 in the molecular context of gastric cancer

ERBB2 encodes the HER2 receptor, part of oncogenic growth signaling.

ERBB2 among frequently altered CIN-associated genes.

Molecular subtype, morphologic subtype, and actionable biomarkers are distinct axes.

Do not infer HER2 positivity from intestinal-type morphology alone.

Slide 37 · MSI tumors often silence MLH1

Microsatellite instability reflects defective DNA mismatch repair.

The source describes MLH1 silencing within CpG-island hypermethylation (CIMP).

MSI cancers more commonly involve the gastric body.

This mechanism differs from the copy-number–driven CIN pathway.

Slide 38 · MSI and CIN differ in their typical mutation pattern

MSI-associated findings

MLH1 promoter silencing / mismatch-repair deficiency.

BRAF and mitosis-regulating gene changes are described.

TP53 and KRAS changes are comparatively uncommon.

CIN-associated findings

Aneuploidy and receptor/RAS pathway changes.

Alterations involving Wnt, TGF-β and TP53.

Often located toward the antrum and pylorus.

Slide 39 · EBV-associated cancers form a smaller subset

<10%

Gastric carcinomas associated with Epstein–Barr virus.

They often arise in the fundus or proximal gastric body.

Slide 40 · EBV-associated gastric cancer has a distinct epigenome

More extensive promoter hypermethylation is described than in MSI tumors.

CDKN2A may be epigenetically silenced, without corresponding MLH1 silencing.

PIK3CA mutations are frequent account.

Increased PD-L1/2 expression helps explain the immune-associated phenotype.

Slide 41 · EBV tumor biology links genetics to host response

EBV-associated tumor

Distinct epigenetic state

Promoter methylation

CDKN2A silencing

PD-L1 / PD-L2 expression

Immune checkpoint engagement

Lymphocytic-rich phenotype

Immune context influences treatment response

PD-L1/2 expression to lymphocytic infiltrates and checkpoint-inhibitor sensitivity.

Schematic

Slide 42 · Molecular subtype comparison

Axis

Typical abnormalities

Pattern emphasized

CIN

Aneuploidy; RTK/RAS; TP53

Antrum / pyloric channel

MSI

MLH1 silencing, CIMP

Gastric body

EBV-associated

CDKN2A methylation, PIK3CA, PD-L1/2

Fundus / proximal body

Diffuse-associated stable

CDH1; RHOA or CLDN18::ARHGAP26

Discohesive growth

Molecular and histologic classification systems overlap; They are not exact synonyms.

Slide 43 · Anatomic setting of distal gastric adenocarcinoma

Most distal adenocarcinomas arise in the antrum.

The lesser curvature is affected more often than the greater curvature.

Location and architecture both contribute to morphologic classification.

Location alone cannot establish intestinal or diffuse histologic type.

Slide 44 · Gross growth pattern: Mass versus infiltrative wall

Intestinal: Localized mass or ulcer

Diffuse: Circumferential wall infiltration

Conceptual wall cross-section — not gross pathology photographs

Slide 45 · Intestinal-type tumors form cohesive masses

An elevated mass with heaped-up borders may have central ulceration.

Some tumors form ulcerated infiltrative lesions rather than exophytic masses.

The invasive front is often broad and relatively cohesive.

Gross ulceration is not by itself proof of invasive adenocarcinoma.

Slide 46 · Diffuse-type tumors may conceal their extent

Discohesive neoplastic cells permeate the gastric wall.

The stomach may become thickened without a circumscribed tumor mass.

Desmoplastic stromal reaction contributes to rigidity.

Flattening of rugal folds reflects broad mural involvement.

Slide 47 · How diffuse infiltration produces linitis plastica

Loss of cohesion

Single cells infiltrate wall

Diffuse mural permeation

No single dominant mass

Desmoplastic reaction

Stroma becomes firm

Linitis plastica

Rigid thickened “leather bottle” wall

Linitis plastica is a gross morphologic pattern, not a separate genetic subtype.

Schematic

Slide 48 · Histologic architecture: Glands versus separate cells

Gland-forming intestinal pattern

Discohesive diffuse pattern

Schematic representation — not histology images

Slide 49 · Intestinal-type histology is gland-forming

Neoplastic epithelial cells form irregular infiltrative glands.

Glands traverse a reactive, often desmoplastic stroma.

Apical mucin vacuoles may be visible in the malignant cells.

Mucin may accumulate within neoplastic gland lumina.

Slide 50 · Why mucin can be abundant in gland-forming tumors

Malignant glandular cells retain variable secretory differentiation.

Intracellular apical mucin produces epithelial vacuolation.

Luminal mucin supports the gland-forming morphologic phenotype.

Mucin location must be distinguished from stromal extracellular pools.

Slide 51 · Diffuse carcinoma infiltrates as single cells

Cells appear singly or in small poorly cohesive clusters.

Well-formed glands are absent in the classic diffuse pattern.

Infiltrative cells may spread widely beyond grossly obvious lesions.

Discohesion follows loss of the adhesion apparatus, especially E-cadherin.

Slide 52 · Signet-ring morphology is produced by mucin

Large intracellular mucin vacuoles expand the cytoplasm.

The nucleus is displaced to one side of the cell.

The compressed peripheral nucleus gives a signet-ring appearance.

The signet-ring cell is a morphologic finding, not a standalone site-of-origin diagnosis.

Slide 53 · Low-power diffuse carcinoma can be missed

Scattered poorly cohesive tumor cells may resemble inflammatory cells.

Attention to atypical nuclei and intracellular mucin is important.

A gland-free infiltrate does not exclude epithelial malignancy.

The distinction between inflammation and carcinoma requires full morphologic assessment.

Slide 54 · Extracellular mucin pools occur in either type

Extracellular mucin may escape into the surrounding tissue.

Large mucin lakes can dissect stromal planes.

The finding is not exclusive to intestinal-type or diffuse-type tumors.

Record extracellular pools separately from intracellular signet-ring mucin.

Slide 55 · Desmoplasia explains a crucial gross feature

Invasive tumor stimulates a fibrous stromal response.

Desmoplasia contributes to wall firmness and diffuse thickening.

Extensive involvement may flatten the gastric mucosal rugae.

A stiff wall can have advanced infiltration despite no bulky exophytic lesion.

Slide 56 · Intestinal and diffuse type: Morphologic contrasts

Feature

Intestinal type

Diffuse type

Growth pattern

Mass-forming or ulceroinfiltrative

Widespread mural permeation

Cell cohesion

Relatively cohesive

Poorly cohesive

Histology

Neoplastic glands

Single cells / small clusters

Mucin

Apical / luminal; Sometimes extracellular

Intracellular signet-ring; Sometimes extracellular

Stromal change

Desmoplasia can surround glands

Desmoplasia stiffens the wall

Slide 57 · Precursors distinguish the principal morphologic types

Intestinal-type pathway

Background atrophy and intestinal metaplasia.

Flat dysplasia and gastric adenomas as recognized precursors.

More strongly influenced by population-level exposures.

Diffuse-type pathway

No identified precursor lesions.

Cell-adhesion abnormalities often precede the phenotype.

Familial risk can exist without an endoscopically obvious precursor.

Slide 58 · Do not conflate dysplasia and invasive cancer

Gastric dysplasia

Neoplastic epithelial atypia and altered architecture.

Adenoma shows dysplasia but is not automatically invasive carcinoma.

Grade describes the degree of intraepithelial atypia.

Invasive adenocarcinoma

Malignant gland-forming or discohesive cells invade tissue.

Tumor depth and spread directly affect prognosis.

The question is invasion, not simply cytologic severity.

Slide 59 · Histologic interpretation integrates site and invasion

Document whether tumor forms glands or diffusely infiltrates as separate cells.

Describe intracellular and extracellular mucin appropriately.

Assess depth of tissue invasion in available material.

Do not infer the entire wall extent from a limited mucosal biopsy.

Slide 60 · Early complaints are often nonspecific

Dyspepsia is a common initial symptom account.

Dysphagia and nausea may also occur.

Overlap with gastritis and peptic ulcer disease lowers symptom specificity.

Persistent symptoms alone cannot determine morphology or stage.

Slide 61 · Advanced disease changes the symptom pattern

Weight loss and anorexia may reflect established tumor burden.

Anemia and gastrointestinal hemorrhage can follow mucosal ulceration.

Early satiety is particularly associated with diffuse wall infiltration.

Clinical manifestations depend on local extent and metastatic spread.

Slide 62 · Why diffuse disease produces early satiety

Diffuse mural tumor

Cells infiltrate much of gastric wall

Desmoplastic stiffening

Reduced gastric compliance

Impaired distension

Small meal volumes feel excessive

Early satiety

Symptom may appear without bulky mass

Mechanistic explanation of the association reported.

Schematic

Slide 63 · Bleeding and anemia are clinicopathologic consequences

Ulcerated tumors can expose vessels and produce hemorrhage.

Chronic blood loss can contribute to anemia.

The severity of anemia does not independently define depth of invasion.

The bleeding presentation may resemble benign peptic ulcer disease.

Slide 64 · Characteristic metastatic sites to recognize

Left supraclavicular node

Virchow node.

Periumbilical region

Sister Mary Joseph nodule.

Ovaries

Krukenberg tumor.

Additional locations

Left axillary nodes and pouch of Douglas are listed.

Slide 65 · Krukenberg tumor identifies ovarian spread

The ovaries are a characteristic metastatic destination of gastric carcinoma.

Krukenberg tumor designates a characteristic metastatic ovarian tumor pattern.

Its recognition should prompt consideration of an extraovarian primary.

This metastatic association does not establish a particular gastric molecular subtype.

Slide 66 · Local extension adds to clinical burden

Adjacent duodenum, pancreas, and retroperitoneum can be invaded.

Extensive local invasion may preclude curative surgical treatment.

Nodal and distant metastatic deposits frequently coexist at diagnosis.

Anatomic disease distribution determines management feasibility.

Slide 67 · Depth of invasion is prognostically central

Mucosa

Submucosa

Muscularis propria

Serosa / outer surface

Depth through gastric wall layers is a key determinant of outcome; Schematic progression only.

Slide 68 · Early gastric cancer is anatomically defined

Early gastric adenocarcinoma is confined to mucosa or submucosa.

The definition does not require absence of regional nodal metastases.

Stage and prognosis depend on both local tumor extent and spread.

Endoscopic early detection is important in high-incidence screening programs.

Slide 69 · Early resected cancers have favorable survival

>90%

Five-year survival after surgical resection of early cancer.

The source states this can hold even when lymph-node metastases are present.

Slide 70 · Advanced gastric cancer has poor outcomes

<20%

Five-year survival reported for advanced gastric cancer.

Historical textbook figure; Prognosis varies with stage, tumor biology, and treatment context.

Slide 71 · Depth and metastatic extent dominate prognosis

Depth of invasion is a major prognostic factor.

Regional nodal burden and distant metastases are also critical.

Morphologic subtype helps explain behavior but does not replace staging.

The stage distribution at diagnosis strongly influences population survival.

Slide 72 · Treatment context follows anatomic extent

Potentially resectable disease

Surgery is a preferred option when feasible in the source account.

Earlier detection improves the possibility of curative management.

Extensively invasive disease

Local extension and metastasis can limit surgery.

Systemic treatment, radiation, and palliation may become major components.

Slide 73 · Case: An ulcerated antral mass

A 58-year-old man presents with dyspepsia and anemia. Endoscopy identifies an elevated antral lesion with central ulceration. The biopsy shows infiltrative, irregular malignant glands in desmoplastic stroma.

Which major morphologic type best fits this description?

A. Intestinal-type adenocarcinoma

B. Diffuse-type adenocarcinoma

Slide 74 · Case analysis: Ulcerated antral mass

Antral location, a bulky ulcerated lesion, and gland formation favor intestinal type.

Desmoplastic stroma supports the invasive character of the biopsy.

Clinical anemia is compatible with tumor-associated gastrointestinal bleeding.

Further assessment is needed to establish local depth and nodal extent.

Slide 75 · Case: A rigid stomach without a mass

A younger patient has early satiety and weight loss. Imaging/endoscopy identifies diffuse wall thickening with flattened folds. Histology demonstrates isolated mucin-filled cells with peripheral nuclei.

What mechanism best explains the infiltrative pattern?

A. Disruption of epithelial cell adhesion

B. Increased benign foveolar cell proliferation

Slide 76 · Case analysis: Diffuse rigid stomach

Signet-ring cells and mural infiltration support diffuse-type carcinoma.

Loss of epithelial cohesion, commonly involving E-cadherin, is central.

The stiff, thickened wall corresponds to linitis plastica.

In a younger patient, family history may suggest inherited susceptibility.

Slide 77 · Integrated classification: Four separate questions

Classification axis

Question it answers

Representative categories

Morphology

How does it grow?

Intestinal; Diffuse

Site

Where does it arise?

Distal/antral; Cardia/proximal

Molecular

Which tumor biology?

CIN; MSI; EBV; Adhesion-related stable

Extent

How far has it spread?

Mucosal/submucosal vs deeper; Nodes/metastases

Slide 78 · Five pathology principles to retain

Intestinal tumors are gland-forming; Diffuse tumors infiltrate as discohesive cells.

Atrophy, intestinal metaplasia, and dysplasia mark the principal intestinal pathway.

CDH1/E-cadherin dysfunction explains diffuse morphology and hereditary predisposition.

CIN, MSI, and EBV are overlapping molecular rather than purely histologic groups.

Invasion depth and metastatic spread are the strongest prognostic determinants.

Slide 79 · Principal reference and evidentiary limits

Robbins, Cotran & Kumar: Pathologic Basis of Disease, 11th edition (2026), Chapter 17, Gastric Adenocarcinoma, pp. 705–707.

Adjacent Robbins sections on chronic gastritis and gastric adenoma provide the precursor context.

All morphology visuals in this lecture are original editable schematics, not authentic micrographs.

Textbook epidemiologic and survival figures are reproduced as historical source statements, not current estimates.