Gastric Polyps and Tumors

Slide 1 · Gastric Polyps and Tumors

An integrated clinicopathologic approach

Reactive polyps · epithelial tumors · lymphoma · NET · GIST

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Classify common gastric mucosal polyps by pathogenesis and histology.

Differentiate reactive polyps and adenomas from malignant neoplasms.

Relate adenocarcinoma morphology to molecular mechanisms.

Recognize key features of gastric MALT lymphoma, NET, and GIST.

Slide 3 · What is a gastric polyp?

A mucosal projection that rises above the surrounding gastric surface.

Detected in up to 5% of upper gastrointestinal endoscopies.

The term describes a shape—not a single biologic diagnosis.

Slide 4 · Four mechanisms generate polypoid lesions

Epithelial / stromal hyperplasia

Chronic inflammation

Ectopic tissue

Neoplasia

Polypoid protrusion seen at endoscopy

Slide 5 · Lineage—not shape—organizes gastric masses

Gastric polyp or tumor

Epithelial

Hyperplastic polyp · fundic gland polyp · adenoma · adenocarcinoma

Lymphoid

Gastric MALT lymphoma

Neuroendocrine

Well-differentiated gastric neuroendocrine tumor

Mesenchymal

Gastrointestinal stromal tumor (GIST)

Slide 6 · A mucosal polyp and a mural mass are different

Surface / mucosa

Muscularis mucosae

Submucosa

Muscularis propria

Serosa

Original conceptual cross-section (schematic)

Hyperplastic polyps and adenomas arise in the mucosa.

Neuroendocrine tumors often form intramural/submucosal nodules.

GIST typically forms a mass in the gastric wall and may ulcerate mucosa.

Slide 7 · Endoscopy provides shape; Histology provides identity

Endoscopic description

Polypoid / nodular / ulcerated / infiltrative

Solitary or multiple

Antrum versus oxyntic mucosa

Tissue assessment

Gland architecture and cytology

Lymphoid versus neuroendocrine cells

Spindle / epithelioid mesenchymal cells

Slide 8 · Inflammatory and hyperplastic polyps dominate

Together account for up to 75% of gastric polyps.

Share inflammatory associations but differ by the histologic emphasis.

Other common polyp diagnoses include fundic gland polyps and adenomas.

Slide 9 · Helicobacter-associated mucosal injury matters

H. Pylori–associated chronic inflammation

Foveolar epithelial regeneration

Architectural elongation and distortion

Reactive polyp formation

Association, not a universal obligatory pathway

Slide 10 · Inflammatory and hyperplastic are related—not identical

Feature

Hyperplastic polyp

Inflammatory polyp

Surface

Usually smooth

Superficial erosion common

Predominant emphasis

Foveolar gland change

Inflammatory / erosive change

Shared background

Often chronic gastritis

Often chronic gastritis

Slide 11 · Age and multiplicity provide context

Most common in the fifth to sixth decades of life.

Most lesions measure less than 1 cm.

They may be multiple, particularly with atrophic gastritis.

Regional prevalence tracks the prevalence of H. Pylori infection.

Slide 12 · Gross morphology: Smooth versus eroded

Hyperplastic

Commonly ovoid

Smooth mucosal surface

Frequently less than 1 cm

Inflammatory

Often superficial erosions

Similar reactive gland changes

Inflammation more conspicuous

Slide 13 · The foveolar apparatus is the site of hyperplasia

SCHEMATIC — not a histologic specimen

Tortuous / dilated foveolae

Surface and pit epithelium expands into irregular elongated glands.

Marked tortuosity produces a “corkscrew” architectural pattern.

Variable cystic dilation adds luminal size variation.

Slide 14 · Histology: Distorted and dilated foveolar glands

Irregular gland profiles replace uniform foveolar architecture.

Some glands are long and corkscrew-shaped; Others are cystically dilated.

This is a predominantly regenerative epithelial response.

Architectural distortion alone is not evidence of adenomatous dysplasia.

Slide 15 · The lamina propria is edematous and inflamed

SCHEMATIC — not a histologic specimen

Foveolar change + stromal inflammation

Edema expands the interglandular stroma.

The inflammatory infiltrate varies in acuity and intensity.

Foveolar growth and stromal inflammation coexist.

Slide 16 · Why erosions occur in an inflammatory polyp

Raised mucosal projection

Surface exposure and injury

Superficial epithelial erosion

Visible inflammation

Mechanistic interpretation of described morphology

Slide 17 · Multiplicity suggests a mucosal field process

Single protrusion

Characterize its surface

Assess gland architecture

Check background mucosa

Multiple protrusions

Consider accompanying atrophy

Look for diffuse chronic gastritis

Do not equate multiplicity with malignancy

Slide 18 · Hyperplastic polyp versus adenoma

Axis

Hyperplastic polyp

Gastric adenoma

Core biology

Reactive hyperplasia

Dysplastic epithelial neoplasm

Histology

Tortuous dilated foveolae

Nuclear atypia / stratification

Background

Chronic gastritis

Atrophy / intestinal metaplasia frequent

Slide 19 · Applied morphology: A small eroded polyp

Teaching vignette — constructed from textbook descriptions

Presentation A patient in the sixth decade has multiple small gastric protrusions in a stomach with chronic gastritis.

Finding The biopsied nodule shows elongated foveolar glands, edematous lamina propria, and a superficial erosion.

Interpretation Most consistent with an inflammatory/hyperplastic polyp; Assess histology rather than shape alone.

Slide 20 · Fundic gland polyps arise in oxyntic mucosa

Typical distribution: Gastric body and fundus.

Well-circumscribed lesions with a smooth surface.

May occur singly or in multiples.

Can be sporadic or associated with inherited polyposis syndromes.

Slide 21 · Proton-pump inhibition alters the oxyntic trophic axis

Suppression of gastric acid output

Compensatory rise in gastrin

Oxyntic gland growth

Increased sporadic fundic gland polyps

Association

Slide 22 · Sporadic and syndromic polyps have different contexts

Feature

Sporadic / PPI-associated

Hereditary context

Setting

Often prolonged PPI exposure

Germline APC or MUTYH

Dysplasia

Not a significant neoplasia risk

Dysplasia may occur in FAP

Risk signal

Clinical medication context

Polyposis syndrome context

Slide 23 · Microscopy: Cystic dilation of oxyntic glands

SCHEMATIC — not a histologic specimen

Cystic oxyntic glands

Cystically dilated, irregular glandular spaces.

Lining includes parietal, chief, and foveolar mucous cells.

The background inflammatory infiltrate is absent or minimal.

Slide 24 · Histologic pitfall: Cysts do not imply adenoma

Fundic gland polyp

Cystically dilated glands

Recognizable oxyntic cell types

Little inflammation

Gastric adenoma

True epithelial dysplasia

Nuclear elongation / hyperchromasia

Architectural atypia at higher grade

Slide 25 · Dysplasia risk depends on clinical setting

FAP-associated fundic gland polyps can harbor dysplasia.

Rare cancers have been described in that inherited setting.

Sporadic lesions, including PPI-associated polyps, do not carry a significant neoplastic risk.

Slide 26 · Applied morphology: Body/fundus cystic polyps

Teaching vignette — constructed from textbook descriptions

Presentation A patient taking a proton-pump inhibitor has several smooth gastric body polyps.

Finding Histology shows dilated oxyntic glands with parietal and chief cells and scant inflammation.

Interpretation Interpretation: Fundic gland polyp; Distinguish sporadic from inherited-polyposis context.

Slide 27 · Adenoma is epithelial neoplasia with dysplasia

Unlike a reactive polyp, a gastric adenoma is defined by dysplastic epithelium.

Usually develops in chronic atrophic gastritis with intestinal metaplasia.

APC- or MUTYH-associated syndromic adenomas are exceptions to that common background.

Slide 28 · Adenomas are antral lesions in older adults

Usually solitary, commonly located in the antrum.

Frequency rises with age; Typical patient age is 50–60 years.

Male predominance is described.

Population prevalence parallels gastric carcinoma risk.

Slide 29 · Chronic injury creates a permissive precursor mucosa

Chronic gastritis

Mucosal atrophy

Intestinal metaplasia

Dysplastic gastric adenoma

Typical background; Not a mandatory sequence for every lesion

Slide 30 · Low-grade dysplasia has recognizable nuclear changes

SCHEMATIC — not a histologic specimen

Dysplastic nuclei

Nuclear enlargement, elongation, and hyperchromasia.

Nuclear pseudostratification within glandular epithelium.

Architectural disorder less severe than in high-grade dysplasia.

Slide 31 · High-grade dysplasia adds complex architecture

Cytology

More pronounced nuclear atypia

Greater epithelial disorder

Altered epithelial maturation

Gland architecture

Budding of dysplastic glands

Gland-within-gland profiles

Cribriform configurations

Slide 32 · Size is a meaningful neoplastic risk variable

Carcinoma risk within an adenoma increases with polyp size.

Lesions exceeding 2 cm deserve particular concern.

Cancer in up to 30% of large gastric adenomas.

This risk justifies a more aggressive approach than for typical colonic adenomas.

Slide 33 · Distinguish a dysplastic gland from a reactive gland

Observation

Reactive foveolar proliferation

Dysplastic adenoma

Architecture

Elongated, tortuous or dilated

Crowded, atypical glands

Nuclei

No defining neoplastic atypia

Hyperchromasia + pseudostratification

Grade

Not assigned as adenoma grade

Low-grade or high-grade dysplasia

Slide 34 · Applied morphology: Antral polyp with pseudostratification

Teaching vignette — constructed from textbook descriptions

Presentation A solitary antral polyp is found in a patient with atrophic gastritis.

Finding The epithelial cells show enlarged hyperchromatic, elongated and pseudostratified nuclei.

Interpretation A diagnosis of gastric adenoma requires histologic grading and assessment for carcinoma.

Slide 35 · Adenocarcinoma dominates gastric malignancy

Accounts for more than 90% of gastric cancers.

The major morphologic patterns are intestinal-type and diffuse-type.

This division predicts differences in gland formation, growth pattern, and pathogenesis.

Slide 36 · Symptoms are subtle until disease is advanced

Early / nonspecific

Dyspepsia

Nausea

Dysphagia

Later / advanced

Weight loss and anorexia

Anemia and hemorrhage

Early satiety (especially diffuse type)

Slide 37 · Gastric cancer burden varies by geography

Marked regional differences are documented.

High-incidence areas have used population endoscopic screening.

Reduced H. Pylori burden is associated with declining intestinal-type cancer.

Risk also correlates with multifocal atrophy and intestinal metaplasia.

Slide 38 · A mucosal field can progress toward intestinal-type cancer

Chronic H. Pylori gastritis

Atrophy and intestinal metaplasia

Dysplasia / adenoma

Intestinal-type adenocarcinoma

Conceptual precursor pathway from textbook associations

Slide 39 · Intestinal and diffuse cancers build different lesions

Feature

Intestinal type

Diffuse type

Gross form

Bulky exophytic / ulcerated mass

Diffuse infiltration / wall rigidity

Cell organization

Cohesive malignant glands

Discohesive cells; no glands

Typical pattern

Mucin within glands

Mucin-filled signet-ring cells

Slide 40 · Intestinal-type cancer forms cohesive glandular fronts

SCHEMATIC — not a histologic specimen

Irregular malignant glands

Invasive irregular gland structures within desmoplastic stroma.

Cohesive fronts may produce an exophytic or ulcerated mass.

Tumor cells can have apical mucin vacuoles and luminal mucin.

Slide 41 · Diffuse-type cancer is a cell-adhesion disorder

Loss of E-cadherin function

Reduced epithelial cohesion

Single cells and small clusters infiltrate wall

Diffuse mural thickening

Central biology of diffuse gastric carcinoma

Slide 42 · CDH1 connects hereditary and sporadic diffuse cancer

CDH1 encodes the adhesion protein E-cadherin.

Germline loss-of-function mutations predispose to hereditary diffuse gastric cancer.

Sporadic tumors frequently lose E-cadherin through mutation or promoter methylation.

CTNNA1 is another hereditary diffuse gastric cancer-associated gene.

Slide 43 · Signet-ring morphology reflects intracellular mucin

SCHEMATIC — not a histologic specimen

Discohesive mucin-filled cells

An expanded mucin vacuole displaces the nucleus to the cell periphery.

Diffuse tumors infiltrate individually or in small cell clusters.

At low power malignant cells can resemble inflammatory cells.

Slide 44 · Linitis plastica results from infiltrative desmoplasia

Surface / mucosa

Muscularis mucosae

Submucosa

Muscularis propria

Serosa

Diffuse infiltrating cells

+ stromal fibrosis

Original conceptual cross-section (schematic)

Diffuse infiltration occurs without a conspicuous dominant mass.

A desmoplastic response stiffens and thickens the wall.

Loss of rugal folds produces the characteristic “leather bottle” stomach.

Slide 45 · Molecular diversity in intestinal-type tumors

CIN

Chromosomal instability

RTK–RAS, TP53, Wnt / TGF-β alterations

MSI

Mismatch-repair defect pattern

Often MLH1 promoter silencing

EBV-related

Extensive methylation

PIK3CA / PD-L1/2 associated features

Slide 46 · CIN tumors often harbor receptor-signaling alterations

Chromosomal instability is associated with aneuploidy.

Commonly altered signaling genes include ERBB2, EGFR, MET, and KRAS.

APC, CTNNB1, SMAD2, SMAD4, and TP53 can also be involved.

An antral / pyloric predilection.

Slide 47 · MSI gastric tumors have a distinct methylation axis

CpG island hypermethylation

MLH1 silencing

Mismatch-repair dysfunction

Microsatellite instability

Book-described molecular subtype

Slide 48 · EBV-associated tumors form another molecular group

A minority of gastric adenocarcinomas with EBV.

Extensive promoter methylation may suppress CDKN2A, without MLH1 silencing.

PIK3CA mutations and increased PD-L1/2 expression are frequent.

Lymphocytic infiltrates commonly accompany these tumors.

Slide 49 · Diffuse-type pathogenesis differs from CIN tumors

Axis

Diffuse pathway

CIN-rich intestinal pathway

Biologic defect

Cell–cell adhesion

Receptor signaling + genomic instability

Examples

CDH1; RHOA; CLDN18::ARHGAP26

ERBB2; EGFR; KRAS; TP53

Growth

Discohesive single cells

Cohesive malignant glands

Slide 50 · Local growth and dissemination determine clinical stage

Surface / mucosa

Muscularis mucosae

Submucosa

Muscularis propria

Serosa

Increasing

Invasion

Original conceptual cross-section (schematic)

Invasion advances through gastric wall layers and adjacent structures.

Regional nodal spread and distant metastases markedly influence prognosis.

Depth, nodal disease, and metastases outweigh gross appearance as prognostic factors.

Slide 51 · Recognizable metastatic presentations

Lymphatic / cutaneous

Left supraclavicular (Virchow) node

Periumbilical Sister Mary Joseph nodule

Left axillary nodes

Other sites

Ovaries: Krukenberg tumor

Pouch of Douglas

Direct extension to neighboring organs

Slide 52 · Early detection sharply changes prognosis

“Early gastric cancer” is confined to mucosa or submucosa.

Extent of invasion and metastasis are the strongest prognostic determinants.

Markedly better survival following resection of early disease than of advanced disease.

Slide 53 · Applied morphology: Infiltrative thick-walled stomach

Teaching vignette — constructed from textbook descriptions

Presentation Endoscopy shows rigid thickened wall and flattened rugae without a prominent mass.

Finding Biopsy contains isolated mucin-filled cells with eccentric crescent-shaped nuclei.

Interpretation Diagnosis: Diffuse-type gastric adenocarcinoma; Consider altered E-cadherin pathway.

Slide 54 · The stomach is a favored extranodal lymphoma site

The GI tract—particularly the stomach—is the most common extranodal lymphoma site.

Approximately 5% of gastric malignancies are primary gastric lymphomas.

Extranodal marginal zone B-cell lymphoma of MALT type is a major subtype.

Slide 55 · MALT is acquired in a stomach with chronic gastritis

H. Pylori chronic gastritis

Acquired mucosa-associated lymphoid tissue

Persistent antigen-dependent B-cell stimulation

Gastric MALT lymphoma

Normal gastric mucosa lacks organized MALT

Slide 56 · NF-κB links antigen dependence to cell survival

Lymphocyte antigen-receptor signaling

BCL10 and MALT1 activation

NF-κB-dependent transcription

B-cell growth and survival

Translocations can bypass the antigen stimulus

Slide 57 · Translocations create alternative routes to activation

Rearrangement

Target / consequence

t(11;18)

API2::MALT1 fusion

t(1;14)

BCL10 upregulation

t(14;18)

MALT1 upregulation

t(3;14)

FOXP1 upregulation

Slide 58 · MALT lymphoma infiltrates and damages gastric glands

SCHEMATIC — not a histologic specimen

Lymphocytes breach gastric glands

Dense neoplastic lymphoid cells expand the lamina propria.

Infiltration of gland epithelium creates lymphoepithelial lesions.

Reactive-appearing follicles and plasmacytic differentiation may occur.

Slide 59 · Immunophenotype supports marginal-zone B-cell lineage

Typical positive

CD19

CD20

Sometimes CD43

Usually negative / clonality

CD5 and CD10 negative

Light-chain restriction may demonstrate clonality

Clonal IGH rearrangements may be informative

Slide 60 · Dependence on H. Pylori predicts eradication response

Feature

More likely H. pylori-responsive

More likely resistant

Activation

Antigen-dependent signals

MALT1/BCL10-related translocations

Depth

More superficial

Muscularis propria invasion

Spread

Limited disease

Nodal involvement

Slide 61 · Applied morphology: Lymphocytes invade gastric glands

Teaching vignette — constructed from textbook descriptions

Presentation A patient with chronic H. Pylori gastritis presents with dyspepsia and epigastric pain.

Finding A gastric biopsy shows a dense B-cell infiltrate forming lymphoepithelial lesions.

Interpretation Favor MALT lymphoma; Integrate morphology, immunophenotype, and clonality if required.

Slide 62 · Gastric NETs arise from endocrine-lineage cells

Well-differentiated NETs were historically termed carcinoids.

Gastric lesions often arise in oxyntic mucosa and form submucosal nodules.

Associations include autoimmune atrophic gastritis, MEN1, and Zollinger–Ellison syndrome.

PPI-associated endocrine-cell hyperplasia rarely progresses to neoplasia.

Slide 63 · Hypergastrinemic settings can produce endocrine hyperplasia

Autoimmune oxyntic atrophy / gastrinoma

Sustained gastrin trophic signals

Enterochromaffin-like cell hyperplasia

Some gastric NET contexts

Schematic association; Not every NET has this pathway

Slide 64 · NET morphology: Uniform cells and stippled chromatin

SCHEMATIC — not a histologic specimen

Organoid cell nests / trabeculae

Nests, trabeculae, strands, glands, or sheets of uniform cells.

Scant pink granular cytoplasm with round-to-oval nuclei.

Coarse and fine chromatin creates a “salt-and-pepper” pattern.

Slide 65 · Differentiate well-differentiated NET from NEC

Axis

Well-differentiated NET

Poorly differentiated NEC

Morphology

Uniform cells; organoid pattern

Small-cell or large-cell carcinoma

Proliferation

Mitotic / Ki-67 assessment

High proliferative activity

Molecular note

Not specified here

TP53 and RB alterations common

Slide 66 · Neuroendocrine markers and prognostic variables

Lineage evidence

Synaptophysin

Chromogranin A

Compatible neuroendocrine morphology

Risk stratification

Degree of differentiation

Mitotic rate and Ki-67 index

Tumor size and location

Slide 67 · Applied morphology: A small oxyntic NET

Teaching vignette — constructed from textbook descriptions

Presentation An intramural gastric nodule arises in the setting of autoimmune atrophic gastritis.

Finding Biopsy shows monotonous cells with salt-and-pepper chromatin and synaptophysin expression.

Interpretation Diagnosis: Gastric NET; Assess differentiation, proliferation, size and clinical background.

Slide 68 · GIST is a mesenchymal tumor of Cajal-cell lineage

Most common mesenchymal tumor of the abdomen.

More than half of GISTs arise in the stomach.

Interpreted as arising from interstitial cells of Cajal or related precursors.

Distinguish from rare leiomyoma, schwannoma, and glomus tumors.

Slide 69 · Constitutively active kinases drive most GISTs

KIT activating mutation OR PDGFRA activating mutation

Constitutive receptor tyrosine kinase signal

Downstream growth / survival pathways

GIST development

KIT and PDGFRA mutations are generally mutually exclusive

Slide 70 · A subset is linked to succinate dehydrogenase loss

SDHA / SDHB / SDHC / SDHD defect

Mitochondrial SDH loss

Metabolic dysregulation

A molecularly distinct GIST subset

An incompletely understood oncogenic mechanism

Slide 71 · Inherited contexts can signal GIST predisposition

Familial / syndromic

KIT or PDGFRA germline variants

SDH-related Carney–Stratakis syndrome

Neurofibromatosis type 1

Carney triad

GIST

Paraganglioma

Pulmonary chondroma

Slide 72 · Gross GIST: A fleshy wall-based mass

Surface / mucosa

Muscularis mucosae

Submucosa

Muscularis propria

Serosa

GIST mass

Original conceptual cross-section (schematic)

Often a solitary, well-circumscribed mural mass.

May show a whorled cut surface and overlying mucosal ulceration.

Bleeding and anemia may result from mucosal breakdown.

Slide 73 · Spindle and epithelioid patterns are morphologic variants

Pattern

Spindle-cell GIST

Epithelioid GIST

Cytology

Thin elongated cells

Plump epithelial-like cells

Architecture

Fascicles / bundles

Sheets or less-defined fascicles

Pitfall

Other spindle-cell tumors

May mimic carcinoma

Slide 74 · KIT and DOG1 provide a useful diagnostic pair

KIT (CD117)

Expressed by normal Cajal cells

Detected in most gastric GISTs

Can be absent in epithelioid tumors

DOG1

Strongly useful GIST marker

Also detects many KIT-negative tumors

Interpret with morphology and site

Slide 75 · Risk assessment combines size, mitoses, and location

Tumor maximum size

Mitotic activity

Anatomic site

Estimated recurrence / metastasis potential

Gastric tumors generally behave less aggressively than small-bowel GISTs

Slide 76 · Kinase genotype informs systemic drug sensitivity

Mutation-driven tumors

KIT / PDGFRA alterations

May respond to kinase inhibition

Secondary variants can confer resistance

Mutation-negative tumors

Many lack the target alteration

Often less sensitive to imatinib

Interpret genotype in clinical context

Slide 77 · Applied morphology: An ulcerated spindle-cell mass

Teaching vignette — constructed from textbook descriptions

Presentation A gastric wall mass causes gastrointestinal blood loss and anemia.

Finding Histology demonstrates bundles of spindle cells; KIT and DOG1 are positive.

Interpretation Diagnosis: GIST. Record size, mitotic activity, location, and relevant mutation testing.

Slide 78 · Gastric lesions are separable by cellular lineage

Lesion

Dominant cells

Useful clue

Hyperplastic polyp

Foveolar epithelium

Dilated corkscrew glands

Adenoma

Dysplastic glandular epithelium

Nuclear pseudostratification

MALT lymphoma

B lymphocytes

Lymphoepithelial lesions

NET

Neuroendocrine cells

Salt-and-pepper chromatin

GIST

Cajal-lineage mesenchyme

Spindle / epithelioid; DOG1

Slide 79 · A site-based orientation narrows the possibilities

Antrum

Gastric adenoma common

Intestinal-type carcinoma often distal

Body and fundus

Fundic gland polyp

Gastric NET within oxyntic mucosa

Deep gastric wall

GIST, submucosal NET

Diffuse cancer may rigidly thicken wall

Slide 80 · Four actionable clues in a pathology report

State the histologic lineage and whether dysplasia or invasion is present.

Link the lesion to its background mucosa, especially atrophy and H. Pylori-associated injury.

For malignant neoplasms, report extent of involvement and salient classification/risk features.

Apply markers and molecular tests only when they answer a diagnostic or treatment question.

Slide 81 · Integrated case: Three lesions, three questions

Teaching vignette — constructed from textbook descriptions

Presentation Smooth body polyps with cystic parietal/chief-cell glands → fundic gland polyps; Identify syndromic setting.

Finding Solitary antral polyp with pseudostratified hyperchromatic epithelium → dysplastic adenoma; Assess grade.

Interpretation Wall mass with spindle cells and DOG1 expression → GIST; Estimate risk using size and mitoses.

Slide 82 · Take-home distinctions

Polypoid gross appearance is not a diagnosis: The cellular lineage determines behavior.

Reactive hyperplastic polyps, fundic gland polyps, and adenomas have different mechanisms and risks.

Intestinal-type gastric cancer forms glands; Diffuse type loses cohesion and infiltrates as individual cells.

MALT lymphoma, NET, and GIST have distinct morphology, immunophenotype, and therapeutic implications.

Slide 83 · Primary reference

Robbins, Cotran & Kumar: Pathologic Basis of Disease. 11th edition. 2026.

Chapter 17 — The Gastrointestinal Tract.

Gastric Polyps and Tumors and related source sections, printed pages 704–709.

Histologic diagrams in this lecture are original editable schematics, not actual specimens.