GI ONCOLOGY

GASTRIC, PANCREATIC, & COLONIC

TUMOURS
BENIGN GASTRIC NEOPLASMS
 
Leiomyoma
 Lesions <2 cm are usually asymptomatic and benign.
 Larger lesions have greater malignant potential and risk of Cx as
bleeding, obstruction, or acute pain.

Lipoma

 Polyps
 GASTRIC POLYPS
There are essentially five types of benign epithelial polyps
• 1- Adenomatous second common

• 2- Hyperplastic (regenerative) most common (75%)

• 3- Hamartomatous

• 4- Inflammatory

• 5- Heterotopic (e.g., ectopic pancreas).

  
Indications of resection (endoscopic)

1- Adenomatous/ hyperplastic

2- Size > 2 cm

3- Symptomatic

If histopathology revealed malignant transformation, either

endoscopic mucosal resection (EMR) or gastrectomy.
MALIGNANT NEOPLASMS OF THE STOMACH

•1- Adenocarcinoma (95%)

•2- Lymphoma (4%)

•3- Malignant GIST (1%).

•4- Other rare primary malignancies include carcinoid.

• 5- Secondaries
 AETIOLOGY
1. Atrophic gastritis or pernicious anaema is by far the most common
precursor for gastric cancer,

2. Family Hx and hereditary diseases

• FAP-10%
• HNPCC-10% (Lynch II syndrome)
• Ménétrier's disease-10%.
• CDH1 gene encoding for E-cadherin is responsible for diffuse type.
• P53 and COX-2 genes (Aspirin a COX inhibitor is protective)
 AETIOLOGY
3. Diet as canned food with preservatives (nitrates), salt, pickles,
scorched animal fat, and smoked foods.
 AETIOLOGY

3. Gastric adenomatous polyps

4. Previous gastrectomy or
gastrojejunostomy (>10 y ago)

5. Tobacco use

6. Blood group A

7. Helicobacter pylori infection.

Early Gastric Cancer
Adenocarcinoma limited to the mucosa and submucosa of the stomach, regardless of lymph node status.

•Type I Exophytic lesion

•Type II Superficial variant

•IIA Elevated lesions
•IIB Flat lesions
•IIC Depressed lesions

•Type III Excavated lesions

• 
 Gross Morphology

Bormann’s classification:
1. polypoidal

2. fungating

3. ulcerative

4. scirrhous.
 Gross Morphology

Lauren classification
1. intestinal type

2. diffuse type

3. unclassified
 TNM STAGING

T: Primary tumor
Tis Carcinoma in situ
T1 Tumor mucosa & submucosa
T2 Tumor invades muscularis propria
T3 Tumor penetrates serosa
T4 Tumor invades adjacent structures

N: Regional lymph node

N0 No regional LN metastasis
N1 Metastasis in 1 to 6 LNs
N2 Metastasis in 7 to 15 LNs
N3 Metastasis in more than 15 LNs

M: Distant metastasis
M0 No distant metastasis
M1 Distant metastasis
• 
 CLINICAL MANIFESTATIONS
1. Three As (Anaemia, Anorexia, and Asthenia).

2. Dyspepsia

3. Acute GI bleeding

4. Obstuctive symptoms as dysphagia and recurrent vomiting

5. Paraneoplastic syndromes such as Trousseau's syndrome

(thrombophlebitis), acanthosis nigricans (hyperpigmentation of the axilla
and groin), or peripheral neuropathy are rarely present.
1. supraclavicular (Virchow's node)

2. metastatic pleural effusion, or aspiration pneumonitis

3. Abdominal mass could indicate a large (usually T4 incurable)

4. A palpable umbilical nodule (Sister Joseph's nodule)

5. Malignant ascites.

6.Rectal exam may reveal heme-positive stool and hard nodularity

extraluminally and anteriorly, indicating so-called drop metastases, or
rectal shelf of Blumer in the pouch of Douglas.
 DIAGNOSIS

•Upper endoscopy and biopsy is the gold standard test to evaluate

patient with dyspepsia or those with Alarm Features:

Dysphagia
Recurrent vomiting
Bleeding
Weight loss
 STAGING

1- Abdominal/pelvic CT scanning
with IV and oral contrasts.

2- MRI

3- EUS (Depth of tumor penetration

& LAP >5 mm).

4- PET scan

5-Staging Laparoscopy
CT SCAN
EUS & PET
 TREATMENT

•Surgical resection (radical subtotal or total gastrectomy with adequate

lymphadenectomy) is the only curative treatment for gastric cancer.

Reconstruction is usually by Billroth II gastrojejunostomy, but if a small

gastric remnant is left (<20%), a Roux-en-Y reconstruction is
considered.

•Extent of lymphadenectomy include D1, D2, and D3

lymphadenectomy where D1 nodes are perigastric, D2 nodes are along
the hepatic and splenic arteries, and D3 nodes are the most distant.
• 
RADICAL TOTAL & SUBTOTAL GASTRECTOMY
 Chemotherapy and Radiation

1. Postoperative adjuvant therapy for stage II and III.

2. Preoperative neoadjuvant therapy to downstage advanced tumours

3. Palliative chemotherapy for stage IV.

 Endoscopic Resection

1. Small tumors (<2 cm)

2. Confined to the mucosa by EUS

3. No detectable LN metastasis

4. No ulceration
 Gastric Lymphoma

The stomach is the most common site of primary GI lymphoma

Over 95% are non-Hodgkin's type

Most are B-cell type

Thought to arise in MALT (Mucosa- associated lymphoid tissue)

It is divided into two distinctive types: low and high grade Maltomos
 Low-grade gastric lymphoma
•When the H. pylori is eradicated and the gastritis improves, the low-
grade MALT lymphoma often disappears.

•If low-grade lymphoma persists after H. pylori eradication, Radiation

should be considered for disease clinically confined to the stomach
(stage I),

Chemotherapy with/without radiation is used for more advanced lesions

 High-grade gastric lymphoma
TREATMENT
currently treated with chemotherapy and radiation, without surgical resection.

For disease limited to the stomach and regional nodes, radical subtotal D2
gastrectomy may be performed, especially for bulky tumors with bleeding and/or
obstruction.
 Gastrointestinal Stromal Tumor (GIST)
•GISTs arise from interstitial cells of
Cajal (ICC)

•Almost all GISTs express CD117

and CD34

•GISTs smaller lesions are usually

asymptomatic.

•Larger lesions: weight loss,

abdominal pain, fullness, early
satiety, and bleeding or an abdominal
mass.
 Treatment options

•1-Surgical resection is the best treatment option in form of wedge

resection, partial or total gastrectomy with no lymphadenectomy as LN
metastasis are rare.

•2- Anti- CD117 as imatinib (Gleevec R), sunitinib, Sorafenib, dasatinib,

erlotinib, and everolimus.
IMATINIB & SUNITINIB
SORAFENIB & DASATINIB
 Gastric Carcinoid Tumors

•Carcinoids commonly involve

•the appendix followed by ileum and rectum.

•Gastric carcinoids comprise about 1% of all carcinoid tumors and less

than 2% of gastric neoplasms.

• They arise from gastric enterochromaffin-like (ECL) cells

•Clearly have malignant potential.

 TYPES
•Type I (75% ) occurring in those with chronic hypergastrinemia secondary to pernicious
anemia or chronic atrophic gastritis

•Type II gastric carcinoids are associated with MEN1 and ZES.

•Type III gastric carcinoids are sporadic tumors. They are usually solitary (usually >2 cm) .
They are not associated with hypergastrinemia.
 Gastric Carcinoid Tumors

•Gastric carcinoids should be resected. Small lesions confined to the

mucosa (typically type I or type II lesions) may be treated
endoscopically with EMR.

• Larger lesions should be removed by D1 or D2 gastrectomy.

• Because somatostatin has an antiproliferative effect on gastric ECL

cells, there may be a possible primary treatment role for octreotide, and
lanreotide.
OCTREOTIDE & LANREOTIDE
PANCREATIC NEOPLASM
 NEUROENDOCRINE TUMOURS
Insulinomas are the most common

Arising from B-cells

Secrete insulin.

Evenly distributed throughout the

head, body, and tail of the pancreas.

(90%) of insulinomas are benign and

solitary,

10% are malignant or multiple

 Whipple's triad
The triad consists of
1. Symptomatic fasting
hypoglycemia

2. A documented serum
glucose level <50 mg/dL

3. Relief of symptoms with

the administration of
glucose.
 
DIAGNOSIS
Whipple triad + elevated C-peptide ( to rule out factitious
hypoglycaemia)

LOCALIZATION
Combination of CT scanning and endoscopic ultrasound (EUS).
 
 Treatment
1- Simple enucleation for those < 2 cm

2- However, tumors located close to the main pancreatic

duct or large (>2 cm) tumors may require a distal
pancreatectomy or pancreaticoduodenectomy.
 
NONFUNCTIONING ISLET CELL TUMORS

 
• Second common

• Malignant

• Stain positive for pancreatic polypeptide (PP),

 GASTRINOMA

Zollinger-Ellison syndrome (ZES) is caused by a gastrinoma, a G-cell endocrine tumor that

secretes gastrin

Although most of the ulcers are solitary, any patient presenting with
• Recurrent

• Persistent

• Multiple

• Giant

• Unusually sited ulcers

• Having associated hypercalcaemia or diarrhoea

 
 HYPERGASTRINAEMIA

•1- Pernicious anemia and atrophic gastritis

•2-Treatment with proton pump inhibitors

•3- Renal failure

•4- G-cell hyperplasia

•5- Retained or excluded antrum

•6- Gastric outlet obstruction.

 
 LOCATIONS
Duodenal wall submucosally
Panceatic head.

Passaro's triangle:

1. Junction of the cystic duct and common

bile duct

2. Junction of second and third portion of

the duodenum

3. the neck and body of the pancreas

 Localization
Combination of Somatostatin receptor (SSTR) scintigraphy
& EUS can localize 90 % of cases 

50% are solitary tumors

50% are malignant.

 Treatment
1- Pancreatic resection is justified for solitary gastrinomas

2- A highly selective vagotomy can be performed if unresectable

3-If patients have MEN1 syndrome, the parathyroid hyperplasia is

addressed with total parathyroidectomy

4-Chemotherapy with streptozocin, and 5-fluorouracil (5-FU)

5- Other approaches can be useful as such as somatostatin analogues,

interferon, and chemoembolization.
 SOMATOSTATINOMA
Triad of Gallstones + DM + Steatorrhea

Usually are malignant

Most somatostatinomas, PPPomas and gastrinomas originate in the

pancreatoduodenal groove (over 60%)

Localization: Combination of EUS and SSTR scintigraphy

Treatment: Complete excision of the tumor and cholecystectomy

 VIPOMA (Verner-Morrison syndrome)

WDHA syndrome due to the presence of watery diarrhea, hypokalemia,

and achlorhydria (low gastric acid).

Distal pancreas

Malignant.

Diagnosis: Serum VIP (episodic secretion).

Localization: EUS
 
Treatment: Palliative debulking+ Lanreotide
 GLUCAGONOMA
DM+Malnutrition+AV thrombosis+
Necrolytic migratory erythema (caused
by low levels of zinc, amino acids, and
fatty acids)

Distal pancreas

Usually are malignant.

LOCALIZATION: EUS + CT scan 

Rx: Complete resection or debulking with

DVT prophylaxis
 PANCREATIC CANCER
The Worst Prognosis of all malignancies with a 5% 5-YSR

Pancreatic intraepithelial neoplasia (PIN)

•PIN IA & PIN IB

•PIN II

•PIN III
 RISK FACTORS

1. DM (few fold),
2. Chronic pancreatitis (20-fold),
3. Hereditary pancreatitis (50 fold)
4. Diets high in fat and low in fiber, fruits, and vegetables
5. Oncogens as K-ras (approximately 90% of pancreatic tumors), and
HER-2/neu oncogene
6. Tumor-suppressor genes are involved in pancreatic cancer as p53
(breast, bone and leukaemia), Smad4 (colon), and BRCA2 (breast-
ovary).
7. Familial syndromes as FAP, HNPCC, Peutz-Jeghers syndrome are
associated with increased risk.
 STAGING
Tis: Carcinoma in situ
T1: Intra-pancreatic and is 2 cm in greatest dimension
T2: Intra-pancreatic and is >2 cm in greatest dimension
T3: Tumor extends beyond the pancreas but without
involvement of major arteries
T4: Tumor involves the celiac axis or the superior mesenteric
artery
 CLINICAL FEATURES
• pain
• jaundice.
• weight loss
• a distended gallbladder is palpable
(Courvoisier’s law).
• Malignant ascites, pleural effusion, liver
metastasis, Troisser’s sign are features of
advanced disease.
 DIAGNOSIS
1. CA19-9
2. Contrast-enhanced CT scan, is the single most versatile and cost-
effective tool
3. Abdominal MRI/ MRCP
4. ERCP is very useful in jaundiced patients as tissue biopsy is
applicable and it can be therapeutic (stenting the obstruction).
5. Positron emission tomography (PET) scan may help distinguish
chronic pancreatitis from pancreatic cancer.
6. EUS can be used to detect small pancreatic masses that could be
missed by CT scanning, and it can allow for transluminal biopsy
.
7.Diagnostic laparoscopy with the use of US is reported to improve the
accuracy of predicting resectability to about 98%.
CT SCAN
PANCREATICODUODENECTOMY
 PANCREATICODUODENECTOMY
Three phases:
• Phase I : Assessment of resectability

• Phase II : Resction

• Phase III: Reconstruction

Findings contraindicating resection
1. Liver metastases

2. Celiac lymph node involvement

3. Peritoneal implants

4. Fixed hepatic hilar lymph node involvement

5. SMA involvement
 Phase II: Resction
• The gallbladder

• Pancreatic head

• Pylorus

• All of duodenum with first loop of jejunum are resected.

•
• In modified Whipple or PPPD, the pylorus is preserved
along with first inch of duodenum.
Phase III: Reconstruction
1. Pancreaticojejunostomy

2. Choledochojejunostomy

3. Gastojejunostomy either antrum (Whipple) or proximal

duodenum (PPPD)

4. Feeding tube jejunostomy

RADICAL DISTAL
PANCREATECTOMY
 PALLIATIVE TREATMENT

• The mainstay of pain control is oral narcotics and celiac plexus nerve block
with alcohol

• Biliary obstruction …….endoscopic approach Sugical bypass

(choledochojejunostomy and cholecystojejunostomy)

• Duodenal obstruction …..gastrojejunostomy.

•  Palliative chemoradiation
• 
• Newer drugs such as EGFr inhibitors (erlotinib and cetuximab), and
VEGFinhibitor (bevacizumab).
• Periampullary cancer includes tumors arising from
the distal bile duct, duodenal mucosa, or pancreas just
adjacent to the ampulla,

• Ampullary cancer is more specific and is reserved for

tumors that arise at the ampulla,
 TREATMENT
Endoscopic resection for small benign tumors ( 2 cm or less)
 
Larger benign lesion are resected surgically transduodenally.  

Whipple procedure ( pancreaticoduodenectomy) for cancer.

FAP patients standard (not pylorus-sparing) Whipple procedure

CYSTIC NEOPLASMS OF THE PANCREAS
1. Pseudocyst

2. Serous cystadenoma

3. Mucinous cystic neoplasm (MCN)

4. Intraductal papillary mucinous neoplasm (IPMN)

5. Pancreatic adenocarcinoma with cystic necrosis or degeneration

6. Simple lymphatic cysts

7. Simple cysts in those with polycystic renal and liver diseases

8. Hydatid cyst (usually associated with liver cysts)

 TREATMENT
Cystic neoplasm > 3 cm or symptomatic → Resection

Cystic neoplasm 1-3 cm → EUS + MRCP/ERCP

Resection only if:
Mucin aspirate, CEA > 200, Low amylase, Atypical cells, Solid component,
Dilated main pancreatic duct

Neoplasm < 1 cm and those 1-3 cm with negative previous

criteria → strict follow up with CT/MRI every 6-12 months.
C OLON IC TUMOU R S
 COLONIC POLYPS
There are essentially five types of benign epithelial polyps
1- Hyperplastic (regenerative) most common (Hyperplastic polyposis)

2-Adenomatous second common (FAP)

3- Hamartomatous (PJS, Juvenile polposis)

4- Inflammatory (UC, CD, Amoebiasis, ischaemic colitis)

5- Heterotopic (e.g. pancreatic, gastric or endometrial).

  
 Familial Adenomatous Polyposis (FAP)
MALIGNANT TRANSFORMATION
POLYP TYPE
Tubular adenomas (5%)
Tubulovillous adenomas (20%).
villous adenomas may (40%)

POLYP SIZE
< 1 cm (5%)
1-2 cm (20 %)
Larger than 2 cm is 40%.
 FAP
• Autosomal dominant condition

• Accounts for only about 1% of all CRC due to a mutation in the APC gene

• Clinically, patients develop hundreds to thousands of adenomatous polyps.

• The lifetime risk approaches 100% by age 50 years.

• Sigmoidoscopy plus EGD

• FAP may be associated with extraintestinal manifestations such as desmoid

tumors, and osteomas (Gardner's syndrome), and CNS tumors (Turcot's
syndrome).
 Treatment
1. Total proctocolectomy with an end-ileostomy

2. Total abdominal colectomy with ileorectal

anastomosis

3. Restorative proctocolectomy with ileal pouch–anal

anastomosis with/without a temporary ileostomy.
 PJS
• Lip and buccal melanosis
• Small bowel and colonic hundreds
of hammartamatous polyps
• 17% risk of CA colon
• Increased risk of other
malignancies (ovary, testis, breast,
pancreas, and others)
COLORECTAL CARCINOMA (CRC)
Adenoma-carcinoma sequence
 Risk Factors
 Dietary factors
Consumption of diets high in animal fat. Diet high in vegetable fiber as well
as calcium, selenium, vitamins A, C, A and E, decrease the risk.
 Risk Factors
 Ageing
 Sedentary lifestyle and obesity.
 Risk Factors
 IBD
In UC and CD pancolitis, the risk of carcinoma is approximately 2% after 10
years, 8% after 20 years, and 18% after 30 years.
 Cigarette smoking

 Ureterosigmoidostomy

 Acromegaly

 Pelvic irradiation
Adenoma-carcinoma sequence
 GENETICS
Approximately 20% arise in patients with a known family history of CRC.
Oncogenes as K-ras and MYH gene
Tumor-suppressor genes as APC, DCC, p53, and PTEN.

Two major pathways:

LOH pathway (Left sided tumours with poor prognosis- 80%)

Replication Error (RER) pathway (right-sided tumours with better prognosis-20%)

 CLINICAL PRESENTATION
1. Change in bowel habits

2. Rectal bleeding.

3. Abdominal pain,

4. IO typically occur in left-sided tumors, because of the caliber of the bowel and
the consistency of the stool.

5. Rectal tumors may cause mucoid discharge, tenesmus, and perianal pain.

6. Unexplained anemia, weight loss, or poor appetite.

6, An intraabdominal mass (RIF or epigastric) seen usually in right-sided tumours

EXAMINATION
 DRE: lower rectal mass or ulcer

Liver : hepatomegaly in metastasis

Percussion: Ascites

Rarely: Sister Joseph or Verchow’s

LN
IMPORTANCE OF DRE
 TNM STAGING of CRC

Tumor stage (T) Definition

•Tis Carcinoma in situ
•T1 Tumor invades submucosa
•T2 Tumor invades muscularis propria
•T3 Tumor invades into nonperitonealized or perirectal tissues
•T4 Tumor directly invades other organs or perforates

Nodal stage (N)

•N0 No lymph node metastasis
•N1 Metastasis to 1-3LNs
•N2 Metastasis to >3 LNs
•N3 Metastasis to any LN along a major named vascular trunk
 
Distant metastasis (M)
•M0 No distant metastasis
•M1 Distant metastasis present
• 
 The modified Dukes' Classification
•Stage I: Tumour limited to bowel wall (5 years SR is 90-100%).

•Stage II: Tumour extends beyond bowel wall (5 years SR is 70%)

•Stage III: any T stage with LN metastasis (5 years SR is 30%)

•Stage IV: Distant metastases. (5 years SR is 10%)

 INVESTIGATIONS
1. Full colonoscopy to detect synchronous tumours (5%) and
metachronous tumours (10-40%)

2. EUS

3. A chest/abdominal/pelvic CT scan

4. MRI

5. Water-soluble contrast study (obstructing tumours).

6. PET scan

7. Preoperative CEA
CT SCAN
PET SCAN
 CRC TREATMENT
SURGICAL TREATMENT is the curative treatment option
TYPES:

A. Open
B. Laparoscopic
 Hand-assisted
 Laparoscopic assisted
 Totally laparoscopic
LAPAROSCOPIC COLECTOMY
 SURGICAL TREATMENT OF CRC

1. Caecal and ascending colon carcinoma → right hemicolectomy (RHC)

2. Hepatic flexure and transverse colon cancer → extended RHC

3. Splenic flexure and descending colon cancer → LHC

4. Sigmoid colon cancer → sigmoid colectomy (SC)

RHC & Extended RHC
LHC & SIGMOID COLECTOMY
SUBTOTAL & TOTAL COLECTOMY
 TREATMENT OF CRC
Rectal cancer are treated:

A.Upper third cancer: high anterior resection (AR) with (TME)

B.Middle third cancer: low anterior resection (AR) with (TME)

C.Lower third cancer that is more than 2 cm above anal spincter: extended low
anterior resection (AR) with (TME).

D.Lower third cancer that is less than 2 cm above anal spincter:

abdominoperineal resection (APR) with (TME)

E. Locally advanced cancer or recurrent cancer, pelvic exenteration.

ANTERIOR RESECTION & AP RESECTION
1.Those with isolated systemic metastasis as pulmonary or
hepatic can be treated with excision of primary cancer
along with segmental or lobar hepatic or pulmonary
resection.

2.If the tumour is inoperable: diversion colostomy or

ileostomy or a bypass procedure is indicated.

3.Early cancer (CIS and malignant polyp with no deeper

invasion) can be treated with local excision or
polypectomy
 Adjuvant Therapy

1. Systemic chemotherapy

2. Chemoradiation

3. Intraoperative radiation therapy (usually brachytherapy)

4. Target therapy
• Bevacizumab (anti-VEGF)
• Erlotinib (anti-EGF molecule)
• Cetuximab (anti-EGF monoclonal Ab)
BEVACIZUMAB, ERLOTINIB, & CETUXIMAB
 Prevention and Screening
 
1. Fecal occult blood testing (FOBT) annually.

2. Flexible sigmoidoscopy (every 5 years)

3. Combination of FOBT annually with flexible sigmoidoscopy every 5 years

4. Colonoscopy (every 10 years) best method and allows biopsy as well as it

may be therapeutic to remove a polyp, stop a bleeder, or stent an obstruction
 
5. Double-contrast barium enema

6. Computed tomographic colonography (virtual colonoscopy)

 Premalignant anal conditions

Anal intraepithelial neoplasia (AIN or Bowen’s disease)

squamous cell carcinoma in situ of the anus
HPV types 16 and 18,
HIV infection.

Treatment include topical immunomodulators as imiquimod and topical

cytotoxic agents as 5-FU and surgical ablation.
 
 Malignant anal conditions
1. Adenocarcinoma
2. Epidermoid Carcinoma
3. Buschke-Lowenstein tumour (variant of condylomata accuminata)
4. Basal cell carcinoma
5. Melanoma

Treatment
6. Chemoradiation
7. Sphincter-preserving wide local excision (WLE)
8. Radical excision (APR)