Stomach Flashcards
What is the normal stomach anatomy?
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
What types of gastritis are there?
- Acute haemorrhagic
- H Pylori
- Autoimmune
- Reactive/Chemical
- Eosinophilic
- Lymphocytic
- Collagenous
- Granulomatous
Describe Haemorrhagic gastritis
- 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
Describe H. pylori gastritis
- 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
How do you diagnosis H Pylori?
- 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
What is the prognosis of H.Pylori
Generally cured by treatment
Can progress to **MALToma **
Increased risk of **Adenocarcinoma ** - CagA-positive H Pylori strain
Describe Autoimmune/Atrophic gastritis
- 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
What are the phases of Autoimmune Gastritis?
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
Describe Reactive (Chemical) Gastritis
**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
Describe Eosinophillic Gastritis
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
Describe Lymphocytic Gastritis
- 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
Describe Collagenous Gastritis
- 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
Describe Granulomatous Gastritis
- Multiple gastric mucosal granulomas
Causes:
* Infection - TB, fungi, parastitic
* Systemic conditions - sarcoid, crohns, common variable immunodeficiency, langerhans cell histicytosis
* Foreign bodies
* Lymphoma
Describe PPI Therapy Effect
- 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**
Describe Menetrier Disease
- 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
Describe Zollinger-Ellison Syndrome
- 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
What types of Gastric Polyps are there?
- 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
Describe fundic gland polyps
- 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
Describe gastric hyperplastic polyps
- 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
Describe Pyloric gland adenoma
- 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
Describe intestinal type gastric adenoma
- 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
Describe foveolar-type adenoma
- 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
Describe oxyntic gland adenoma
- 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
Describe Inflammatory fibroid polyp
- 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).
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Describe Gastric Xanthoma
- 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
What are the risk factors for gastric adenoca?
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
What is the IHC for gastric Ca?
- 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
Describe Gastric carcinoma macroscopic subtypes
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
Describe the LAUREN histological classifications of Gastric AdenoCa
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
Describe the WHO classification of Gastric AdenoCa
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
What are other subtypes of Gastric Ca?
(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
What are the predictive biomarkers/treatments
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
What are the molecular subtypes?
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
Describe GISTs
- 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)
What is the IHC for GISTs?
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
What are the molecular abnormalites of GIST?
- 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
What is the prognosis/treatment for GIST?
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
What are they syndromes associated with GIST?
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)
Describe the types of Gastric NETS
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%
What is the grading of Gastric NETS
**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
What is the IHC markers of Gastric NETs?
Positive:
Chromogranin
synaptophysin
CD56
**Negative: **
CD7
CD20
Describe MALToma
- 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
What is the IHC profile of MALTOMA?
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
What are the Cytogenetics of MALToma?
**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
Describe Squamous Cell Carcinoma
Very rare
Presents late, poor outcome
Describe Gastric Undifferentiated Carcinoma
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
Describe Gastric Adenosquamous Carcinoma
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
Describe Gastroblastoma
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
