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FRCPath Histopathology Part 1 > Stomach > Flashcards

Stomach Flashcards

1
Q

What is the normal stomach anatomy?

A

MUCOSA:
* epithelium
* lamina propria
* muscularis mucosa
* gastric pits/surface invaginations - foveolar cells containing neutral mucin
* deep glands - vary with anatomic regions

Cardia, antrum, pylorus: mucus secreting glands
* Antrum - G Cells - Gastrin

Fundus, body: oxyntic mucosa
* Pink paretial cells - Acid, Intrinsic factor (for B12 absorption)
* Purple chief cells - Pepsinogen

SUBMUCOSA:
* Loose connective tissue
* blood vessels, lymphatics, nerve fibres, ganglion cells

MUSCULARIS PROPRIA:
* Smooth muscle:
Inner oblique
Middle circular
Outer longitudinal
* Myenteric plexus

SUBSEROSA and SEROSA:
* Thin layer of collagen
* Mesothelium

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2
Q

What types of gastritis are there?

A
  • Acute haemorrhagic
  • H Pylori
  • Autoimmune
  • Reactive/Chemical
  • Eosinophilic
  • Lymphocytic
  • Collagenous
  • Granulomatous
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3
Q

Describe Haemorrhagic gastritis

A
  • Hyperemic edematous mucosa
  • Bleeding, erosions, ulcers

Microscopy:
* dilation and congestion of mucosal capillaries
* oedema
* lamina propria haemorrhage
* fibrinoid necrosis of superficial capillaries (seen in doxycycline gastritis)
* adjacent epithelium - reactive changes with mucin depletion

Causes:
* severe stress, trauma, shock
* binge drinking
* caustic agents
* large doses of NSAIDS
* steroids
* doxycycline

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4
Q

Describe H. pylori gastritis

A
  • gram negative curved rods
  • commonly colonize antrum first, but –> pangastritis –> mucosal atrophy –> intestinal metaplasia –> dysplasia –> carcinoma

major risk factor for extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma).

Endoscopy:
* erythema, erosions, hypertrophy or atropic changes
* superficial mononuclear inflammatory infiltrate, prominent lymphoid follicles
* Neutrophils

  • Slender curved bacilli - typically seen in mucin coat of lining epithelial cells
  • intracellular invasion and cocci forms can be seen with PPI treatment
  • After successful eradication therapy - acute inflammation disappears rapidly, chronic persists longer.
  • helicobacter heilmannii gastritis - similar to h. pylori gastritis but less severe
  • Acquired from farm animals and household pets -> more common in children
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5
Q

How do you diagnosis H Pylori?

A
  • Biopsy Urease test
  • Urea breath test
  • 13C urea assay
  • PCR

**Special stains: **
Giemsa
Warthin Starry

H. Pylori IHC

Grading system: Updated Sydney System:
* Inflammation
* Neutrophil activation
* Glandular atrophy
* Intestinal metaplasia
* H Pylori intensity

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6
Q

What is the prognosis of H.Pylori

A

Generally cured by treatment

Can progress to **MALToma **
Increased risk of **Adenocarcinoma ** - CagA-positive H Pylori strain

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7
Q

Describe Autoimmune/Atrophic gastritis

A
  • Occurs in oxyntic muscosa - body/fundus
  • Cause: anti-parietal cell and anti-intrinsic factor antibodies

Seen in patients with:
* T1DM
* Hashimoto’s
* Addison’s

  • lack of intrinsic factor –> B12 deficiency –> Pernicious anaemia

Gastrin acts on parietal cells –> triggers intinsic factor and H+ release

H+ causes negative feedback on G cells, suppressing Gastrin

Antibodies remove this negative feeback loop –>** increased gastrin ** (but still low acidity)

  • Antrum: normal, features of reactive gastropathy, G-cell hyperplasia

**Macro: **
* atrophic body mucosa
* absence of rugal folds
* hyperplastic polyp (advanced disease)

Micro:
* Patchy lymphoplasmacytic infiltrate in lamina propria
* Gastric gland atrophy
* Focal intestinal metaplasia
Increased risk of** gastric NETs**

Tests:
* gastrin stain —> should be negative –> confirm from body, not antrim
* synaptophysin and **chromogranin **–> highlight enterochromafffin-like cell hyperplasia.
* Pseudopyloric metaplasia can be highlighted by mucin 6

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8
Q

What are the phases of Autoimmune Gastritis?

A

EARLY Phase
* Dense lamina propria lymphoplasmacytic infiltrate +/- eosinophil and mast cells
* Patchy lymphocytic infiltration and destruction of individual oxyntic glands
* Hypertrophic changes of residual parietal cells.
* Pseudopyloric metaplasia (mucinous)

FLORID phase
* Marked atrophy of oxytinic glands
* Diffuse lamina propria lymphoplasmacytic infiltration
* Extensive pseudopyloric metaplasia
* Prominent intestinal metaplasia

END stage
* Marked reduction in oxyntic glands, foveolar hyperplasia and hyperplastic polyp formation.
* Increasing pseudopyloric, pancreatic and intestinal metaplasia
* Parietal cells are hard to detect
* Linear/Nodular enterochromaffin-like cell hyperplasia due to achlorhydria –> physiologic hypergastrinemia

Can progress to intramucosal and invasive neuroendocrine tumours

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9
Q

Describe Reactive (Chemical) Gastritis

A

**Endoscopy: **
* Mucosa erythema and oedema

Micro:
* Foveolar hyperplasia - tortuous/corkscrew gastric pits
* Mucin depletion, oedema, ectatic capillaties
* Extension of smooth muscle bands in lamina propria
* Minimal inflammation

Causes:
* Bile reflux
* Chronic use of medications - NSAIDs/Iron
* Alcohol
* Chemoradiation

**Gastric Antral Vascular Ectasia (GAVE): **
* Endoscopic appearance of watermelon stomach - hyperemic mucosal streaks converging on antrum
* Resembles reactive gastropathy
* Antral vasucular ectasia
* Intravascular fibrin thrombia

Portal Hypertensive Gastropathy:
* Cirrhotic and Non-Cirrhotic portal hypertension
* Endoscopically: mosaic or snakeskin pattern
* Resembls reactive gastropathy
* Dilated capillaries and veins in mucosa and submucosa

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10
Q

Describe Eosinophillic Gastritis

A

Unknown aetiology for primary

Secondary:
* Food Allergies
* Medications
* H.Pylori
* Parasites - Strongloides, Anisakis
* IBD
* Connective tissue diseases

  • Increased eosinophilic infiltration of GI tract
  • > 30 eosinophls/HPF
  • Intraepithelial, muscularis mucosae and subucosal eosinophils
  • Eosinophillic crypt abscesses
  • May see mast cells
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11
Q

Describe Lymphocytic Gastritis

A
  • Increased mature intraepithelial lymphocytes
  • > 25 per 100 epithelial cells
  • Mixed lymphoplasmacytic infiltration of lamina propria

Endoscopy:
* Normal to mucosal nodularity
* Erosions (varioliform gastritis)

Causes:
* Coeliac
* Crohns
* Menetrier disease
* H. Pylori
* HIV
* Meds - Ticlopidine, immune check point inhibitors, NSAIDs

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12
Q

Describe Collagenous Gastritis

A
  • Diffuse/patchy thickened subepithelial collagen band
  • > 10 microns
  • Highlight with Trichrome
  • Entrapped inflammatory cells and capillaries
  • Increased intraepithelial lymphocytosis
  • Increased lamina propria lymphplasmacytic infiltration with eosinophils
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13
Q

Describe Granulomatous Gastritis

A
  • Multiple gastric mucosal granulomas

Causes:
* Infection - TB, fungi, parastitic
* Systemic conditions - sarcoid, crohns, common variable immunodeficiency, langerhans cell histicytosis
* Foreign bodies
* Lymphoma

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14
Q

Describe PPI Therapy Effect

A
  • Dilated oxyntic glands
  • Hypertrophic parietal cells - snouts, cytoplasmic blebs

PPI use causes increased gastrin levels through feedback –> parietal cell hypertrophy

Long term use may lead to** fundic gland polyps**

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15
Q

Describe Menetrier Disease

A
  • Hyperplastic gastropathy
  • Worse in adults, often self-limiting in children
  • Low acid production
  • Protein losing enteropathy

Macro
* Thickened body/fundus folds… Spares antrum
* May mimic carcinoma or lymphoma

Micro
* Marked foveolar hyperplasia - tortuous gastric pits, cystically dilated atrophic glands
* Lamina propria with oedema and variable inflammation

Cause:
* increased signalling of EGFR
* Viral infections

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16
Q

Describe Zollinger-Ellison Syndrome

A
  • Pancreatic or duodenal neuroenodrine tumour (Gastrinoma)
  • Serum hypergastrinaemia
  • Increased acid secretion
  • Gastric mucosal hypertrophy

Can be seen in MEN 1 syndrome

Endoscopy:
* Enlarged gastric body/fundus mucosal folds
* Duodenal ulcers

Micro:
* Foveolar hyperplasia
* Dilated oxyntic glands
* Parietal cell hypertrophy

Can progress to:
* Secondary ECL-cell hyperplasia
* Dysplasia
* Gastric Neuroendocrine tumours

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17
Q

What types of Gastric Polyps are there?

A
  • Fundic gland polyps
  • Gastric Hyperplastic polyps
  • Pyloric gland adenoma
  • Intestinal-type adenoma (dysplastic)
  • Foveolar-type adenoma (dysplastic)
  • Oxyntic gland adenoma
  • Inflammatory fibroid polyp
  • Gastric xanthoma
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18
Q

Describe fundic gland polyps

A
  • Benign
  • Most common type of gastric polyp

Micro:
* Hyperplastic expansion of deep oxyntic mucosa with cystically dilated oxyntic glands
* Parietal cell hyperplasia
* Foveolar hyperplasia can be seen

  • Often **sporadic **- linked to PPI usage
  • Dysplasia is rare <1%

Associated with APC beta catenin alteration in both sporadic and syndromic cases

If numerous - consider polyposis syndromes:
* Familial adenomatous polyposis (FAP)
* Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS)
* Zollinger-Ellison syndrome

FAP and GAPPS:
* APC mutations
* increased incidence of dysplasia
* HG dysplasia and adenocarcinoma rare, though

ICH: B-catenin nuclear +ve

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19
Q

Describe gastric hyperplastic polyps

A
  • Benign
  • Usually <1cm
  • Second most common gastric polyp

Micro:
* Elongated, tortuous, hyperplastic foveolar epithelium
* Cystically dilated glands
* Stroma oedema, inflammation, surface erosion
* Hapazardly distributed smooth muscle bundles extending to the surface

Hyperproliferative response to tissue injury:
* Chronic gastritis
* Reactive gastropathy
* Reflux
* Barrett oesophagus
* Autoimmune gastritis

Precursor is polypoid foveolar hyperplasia

If multiple, rule out:
* Juvenile polyposis
* Peutz-Jeghers
* FAP

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20
Q

Describe Pyloric gland adenoma

A
  • Polypoid proliferation of closely packed pyloric-type glands
  • Lined with cuboidal to low-vcolumnar epithelial cells
  • Clear/lightly eosinophilic ground-glass cytoplasm
  • Basally located nuclei
  • Can develop high-grade dysplasia and adenocarcinoma

IHC:
Diffuse
* MUC6
* MUC5AC

SPORADIC:
* associated with autoimmune atrophic gastritis

POLYPOSIS Syndromes:
* FAP
* GAPPS
* McCune-Albright syndrome
* Juvenile polyposis
* Lynch syndrome

Mutations:
Sporadic and FAP-associated:

Activating GNAS and/pr KRAS mutations.
**Inactivating **APC mutations

21
Q

Describe intestinal type gastric adenoma

A
  • Localised polypoid lesion with dysplastic intestinal-type epithelium
  • Dysplastic tubules, columnar epithelium
  • Varying degrees of Paneth and goblet cells
  • Third most common type of gastric polyp

More prone to progress to cancer than foveolar-type - risk based on size

Risk factors:
* H Pylori
* Autoimmune gastritis

22
Q

Describe foveolar-type adenoma

A
  • Polypoid dysplastic foveolar epithelium
  • Mostly occurs in the oxyntic compartment - body/fundus
  • Distinctive **PAS-positive **apical neutral mucin cap

Rate of cancer is low.
BUT
Hybrid phenotype (intestinal and gastric differentiation) - high risk

Associated with FAP and GAPPS
Coexist with fundic gland polyps and pyloric gland adenoma

23
Q

Describe oxyntic gland adenoma

A
  • Benign
  • Columnar cells with pale basopghillic cytoplasm
  • Mild nuclear atypia
  • Predominant chief cell component, mimicking oxyntic glands
  • Occurring in areas with oxyntic mucosa, mainly in** upper third** of stomach
  • High risk of progression to adenocarcinoma (gastric adenocarcinoma of fundic-gland type)

IHC:
Chief cell:
* Pepsinogen I
* MUC6

Parietal cell:
* H+/K+ ATPase

  • MUC5AC negative

Mutations:
Missense/Nonsense mutations in **WNT/Beta-catenin **signalling pathway

24
Q

Describe Inflammatory fibroid polyp

A
  • Benign
  • Occurs throughout GI tract
  • Most common in stomach
  • Submucosal proliferation of vascular fibrous tissue
  • Bland spindle cells with **onion skin arrangement **around small vessels
  • Eosinophil rich inflammatory infiltrate
  • Oedematous background

Associated with Devon Polyposis Syndrome

CD34 positive
CD117 negative

Mutation:
**PDGFRA **mutation (platelet-derived growth factor receptor alpha).

dfxcgvycydfcfxyxyy vbiibvhg vbd

25
Q

Describe Gastric Xanthoma

A
  • Collection of bland, foamy histiocytes in the lamina propria
  • No mitotic activity
  • No background inflammation

Endoscopy:
Single/multiple white/yellow nodules

IHC:
CD68 positive
Cytokeratin negative

Associations:
* H pylori
* bile reflux
* hypercholesterolemia

26
Q

What are the risk factors for gastric adenoca?

A

H Pylori
* Correa’s cascade
* Chronic infection –> chronic inflammation –> intestinal metaplasia –> dysplasia –> Carcinoma

EBV infection

Tobacco smoking

Dietary factors

Rubber manufacturing industry

X and gamma radiation

27
Q

What is the IHC for gastric Ca?

A
  • CK7+ (50-70%)
  • CK20+ (30-50%)
  • CDX2 (60%)
  • MUC2+ (30%)
  • MUC5AC+ (70%)
  • GATA3-

All diffuse type gastic carcinomas should be differentiated from metastatic lobular carcinoma of the breast

28
Q

Describe Gastric carcinoma macroscopic subtypes

A

EARLY gastric Adeno:
Three types

  • 0-I -protruding (polypoid)
  • 0-IIa (superficialk elevated)
  • 0-IIb (superficial flat)
  • 0-IIIc (superficial depressed)
  • 0-III (excavated)

ADVANCED gastric Adeno:
Borrmann Classification

  • Type I
    Polypoid tumors that protrude into the gastric cavity and have sharp demarcation from the surrounding tissue
  • Type II
    Ulcerative tumors with a clear margin and raised surface
  • Type III
    Ulcerative tumors with an unclear margin that infiltrate deeply into the surrounding tissue
  • Type IV
    Diffusely infiltrating tumors, also known as linitis plastica
29
Q

Describe the LAUREN histological classifications of Gastric AdenoCa

A

Lauren Classification

**Intestinal: **
Characterized by cohesive cells that form gland-like structures.
It’s more common in males and older patients.

** Diffuse: **
Characterized by tumor cells that lack cell-to-cell interactions and infiltrate the stroma.
It’s more common in women and younger patients.

Mixed: **
Tumors that exhibit features of both the intestinal and diffuse types
**
Most important prognostic factor is clinical stage

30
Q

Describe the WHO classification of Gastric AdenoCa

A

WHO classification

Tubular:
Most common.
Dilated and slit-like branching tubules
Solid structures and barely rdcognisable tubles are classed as poorly diff tubular carcinoma.

Papillary:
Relatively rare
Exophytic growth pattern
Cuboidal/columnar cells, fibrovascular core
Frequent invasion by inflammatory cells
Associated with higher frequency of liver mets
Poor prognosis

Mucinous:
Malignant epithelium in extracellular pools of mucin
Mucin >50% of tumour area

**Poorly cohesive, which includes signet ring cell carcinoma: **
Second most common
Cells in small aggregates without well-formed glands
CDH1 mutations (e-cadherin)

1) Signet ring type

2) Non signet ring type
Neoplastic cells resembling histiocytes or lymphocytes
Deeply eosinophilic cytoplasm and pleomoprhic nuclei

**Mixed **
Contains two or more histiological subtypes

31
Q

What are other subtypes of Gastric Ca?

A

(Adeno)carcinoma with lymphoid stroma
* AKA lymphoepithelioma or medullary
* Polygonal cells embedded in prominent lymphocytic infiltrate
* Favours proximal stomach or gastric stump
* Associated with** EBV **
* Subest of gastric Ca with** microsatellite instability**

Hepatoid adenocarcinoma
* Large polygonal eosinophilic hepatocyte-like cells
* Bile and **PAS-D **positive - intracytoplasmic globules
* **AFP, HepPar-1 **positive

**Micropapillary adenocarcinoma **
* Without fibrovascular cores
* Small clusters protruding into clear spaces
* Worse prognosis

Gastric adenocarcinoma of fundic-gland type
* Very rare
* Assumed to develop from oxyntic gland adenoma
* Three subcategories
Chief-cell predominant (99%)
Parietal-cell predominant
Mixed phenotype

32
Q

What are the predictive biomarkers/treatments

A

NB… <2cm into the stomach from GOJ -> treat as oesophagheal ca

HER2 therapy
* unresectable
* metastatic/recurrent ERBB2-positive Ca

Immune checkpoint inhibitor therapy
* PD-L1 expression

33
Q

What are the molecular subtypes?

A

Proposed by The Cancer Genome Atlas (TCGA)

EBV (9%)

  • Gastric carcinoma with lymphoid stroma
  • Better prognosis
  • CpG island (CIMP) promoter hypermethylation
  • CDKN2A promoter hypermethylation
  • PIK3CA mutations
  • ARID1A mutations
  • PD-L1 amplified
  • PD-L2 amplified

Mictosatellite Unstable (22%)

  • Better prognosis
  • CpG island (CIMP) promoter hypermethylation
  • CDKN2A promoter hypermethylation
  • MLH1 promoter hypermethylation

Genomically Stable (20%)

  • Poorly cohesive (diffuse) moprhology
  • Poorer prognosis
  • CDH1 alterations/mutations
  • RHOA alterations/mutations

Chromosomally Unstable (50%)

  • Predominantly intestinal type morphology
  • TP53 mutations
  • Receptor Tyrosine kinase (RTK)/ RAF pathway amplifications
    (EGFR, FGFR2, VEGFA, KRAS, MET, HER2/ERBB)
  • Extensive DNA copyt number variations
34
Q

Describe GISTs

A
  • Gastrointestinal stromal tumor
  • Most common mesenchymal tumour
  • Arises from intersitial cells of Cajal
    within myenteric plexus of muscularis propria

Can occur anywhere in the GI tract
* Stomach (60%)
* Jejunum and ileum (30%)
* Duodenum (5%)
* Rectum (4%)
* Colon and appendix (2%)
* Oesophagus (1%)

Can occur outside of the GI tract
* Omentum
* Mesentery
* Retroperitoneum
* Pleura

Four histologic types:
* Spindle
* Epithelioid (typically SDH-deficient)
* Mixed
* (last two more common in stomach)
* Dedifferentiated

Five Molecular types:
* KIT mutated (c-KIT/DOG1 +ve)
* PDGFR mutated (DOG1 +ve)
* SDH deficient (SDHB -ve)
* RAS-P mutated (SDHB +ve)
* Quadruple wild type (SDHB +ve)

35
Q

What is the IHC for GISTs?

A

CD117 (c-KIT) +ve - membranous, diffusely cytoplasmic, dot-like perinuclear

**CD34+

DOG1+**

SDHB-, S100-

CD117 and DOG1 are sensitive markers, not specific

Ki67 to assess proliferation rate not superior to mitotic count

36
Q

What are the molecular abnormalites of GIST?

A
  • Activating KIT (95%)
  • Platelet derived growth factor alpha (PDGFRA)
  • Receptor tyrosine kinase (5%)
  • SDH deficient (<5%)

Do mutational analysis:
* All resected moderate or high risk GISTs of any site
* All biopsies diagnostic of GIST prior to TKI treatment
* All biopsies from unresectable/widely metastatic GIST

37
Q

What is the prognosis/treatment for GIST?

A

PROGNOSIS

Depends on:
* Site
* Size
* Mitosis

Gastric GISTs better than intestinal
Oesophageal worst - diagnosed late
Small intestine and Rectal - high risk

TREATMENT

Surgical Resection

Neoadjuvant small molecule tyrosine kinase inhibitors

KIT juxta mebrane domain (exon 11) mutations -> confers better response to tyrosine kinase inhibitor therapy (imatinib)

KIT (exon 9) mutant –> benefit from higher dose imatinib’

Resistant to imatinib –> benefit from sunitinib

38
Q

What are they syndromes associated with GIST?

A

Associated with:

1) SDH deficient GIST:

CARNEY TRIAD
SDH deficient GIST
Pulmonary chondroma
Paraganglioma

  • Non hereditary
  • SDHC promoter hypermethylation
  • Small percentage have germline SDH mutations
**CARNEY-STRATAKIS SYNDROME**
GIST
Paraganglioma
  • Hereditary, autosomal dominant
  • Germline mutations –> SDHB, SDHC or SDHD
Lymph nodes --> not core item, but raises suspicion of Carney's triad or Carney-Stratakis syndrome
	
	2) Neurofibromatosis (NF):

7% patients with NF1 develop one or more GIST (usually small bowel)

39
Q

Describe the types of Gastric NETS

A

Neuroendocrine tumour
* Well-differentiated neuroendocrine tumour (NET)
* Poorly differentiated neuroendocrine carcinoma (NEC) - small and large cell
* Mixed neuroendocrine-non-neuroendocrine neoplasm (MiNEN)

Micro:
Well-differentiated cells
Nests, acini, trabeculae, ribbons
Abundant eosinophilic cytoplasm
monoimorphic round nuclei (salt and pepper chromatin)

Type I:
Derived from enterochromaffin-like (ECL) cells
Occurs in a setting of chronic atrophic gastritis (type A) and hypergastrinemia
More frequent in women

Type II:
Derived from ECL cells
Occurs in a setting of **hypergastrinemia **due to Zollinger-Ellison syndrome
Can be seen in patients with multiple endocrine neoplasia type 1 (MEN1) syndrome
Affects men and women equally

Type III:
Sporadic
More frequent in men

Type IV:
Discussed in the literature but not currently recognized by the WHO

Serotonin producing EC cell NET:
Rare and usually nonfunctional

Gastrin producing G cell NET:
Usually nonfunctional but can cause Zollinger-Ellison syndrome and is then referred to as a gastric gastrinoma

All types tend to occur in the age range of 50 - 60 years

PROGNOSIS

Type I: excellent prognosis with a 5 year survival of 90 - 95%

Type II: good prognosis with a 5 year survival of 60 - 90%

Type III: worse prognosis with a 5 year survival rate of < 35%

40
Q

What is the grading of Gastric NETS

A

**G1 **
Mitotic count <2 per 20 HPF
Ki-67 <2%

G2
Mitotic count 2-20 per HPF
Ki-67 3-20%

G3
Mitotic count >20 per HPF
>30%
TP53 and RB1 mutations can distinguish from from NEC

41
Q

What is the IHC markers of Gastric NETs?

A

Positive:
Chromogranin
synaptophysin
CD56

**Negative: **
CD7
CD20

42
Q

Describe MALToma

A
  • Extranodal marginal zone lymphoma of mucosa associated lymphoid tissue (MALT lymphoma).

Strong association of H. Pylori

Treatment of H pylori induces regression

indolent behaviour and generallly excellent prognosis

Lugano staging system: most widely accepted staging system

Endoscopy:
Most arise in antrum
Early lesions form a plaque or small erosions
Advanced lesions cause ulcers, diffuse thickening, masses

Micro:

Heterogenous inflitrate - neoplastic lymphocytes

Centrocyte-like cells: Small lymphocytes with irregular nuclear contours and pale cytoplasm.
Monocytoid B-cells
Centroblasts/Immunoblasts: Large cells
Lymphoepithelial lesion: classic finding
Neoplastic Plasma cells

Lymphoid follicles:
Germinal centres
MALToma can infiltrate germinal centers –> Follicular colonisation

Can get Amyloid deposition

43
Q

What is the IHC profile of MALTOMA?

A

POSITIVE:
CD20
CD43 (variable)
BCL-2
CD79a

NEGATIVE:
CD3
CD5
CD10
CD23
Cyclin D1

CD43 and CD5 support the diagnosis

Kappa / lambda: can be useful to demonstrate light chain restriction (especially if there are abundant neoplastic plasma cells)

Congo red: can highlight amyloid deposition present in a subset of cases

44
Q

What are the Cytogenetics of MALToma?

A

**t(11;18): BIRC3 (API2)-MALT1 (6 - 26%) **
Associated with resistance to H. pylori eradication therapy

t(14;18)(q32;q21): IGH-MALT1 (1 - 5%)

Trisomy 3 (11%)
Trisomy 18 (6%)

TNFAIP3 deletion / hypermethylation

45
Q

Describe Squamous Cell Carcinoma

A

Very rare
Presents late, poor outcome

46
Q

Describe Gastric Undifferentiated Carcinoma

A

Micro:
Anaplasic cells, diffuse sheets
Variable cytology - Polygonal, rhabdoid, spindled, osteoclast-like giant celkls

Driven by SWI/SNF chromatin-remodeling complex

Aggressive

IHC:
Variable pan-cytokeratin
Vimentin +ve
EMA may be helpful in keratin-poor tumour

46
Q

Describe Gastric Adenosquamous Carcinoma

A

Very rare
Males more affected

Glandular and Squamous - squamous must be >25%

Aggressive - mets to LN, liver and peritoneum are common

Mucin stain
p63/p40

47
Q

Describe Gastroblastoma

A

Micro:
Biphasic tumour
* Uniform spindle cells
* Epithelial cells arranged in nests

Molecular:
MALAT1-GL1

IHC:

EPITHELIAL COMPONENT
* Pan cytokeratins
* Focal CD56+
* Focal CD10+

SPINDLE CELL COMPONENT
* negative for keratins
* CD56+
* CD10+

Negative for C-KIT, DOG1, CD34, SMA, Desmin, Synaptophysin, Chromogranin, S100

FRCPath Histopathology Part 1 (28 decks)

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