ca stomach premanagement

4. The stomach
Sphincters
 The cardiac sphincter
(lower esophagus
sphincter) closes off
the top end of the
stomach.
 The pyloric sphincter
closes off the bottom.

5. FUNCTIONS
 Temporary storage of ingested nutrients
 Mechanical breakdown of solid food
 Chemical digestion of proteins
 Regulation of the passage of chyme into the
duodenum
 Secretion of intrinsic factor for vitamin B12 absorption
 Secretion of gut hormones
 Secretion of acid to aid digestion

8. Japanese TNM staging

10.  I – 2/3 lesser curvature & large
part of the body Lt gastric
nodes  Celiac nodes
 II – distal part of lesser curvature
& pylorus  Rt. gastric nodes 
Supra-pyloric nodes  Hepatic
nodes Celiac & Aortic LN
 III- Part of greater curvature
Pancreatico –splenic nodes 
Celiac
 IV- Part of the greater curvature
and pylorus  RGE nodes 
Pyloric  Sub-pyloric Hepatic
nodes

11. EPIDEMIOLOGY
 4th most common cancer worldwide
 2nd leading cause of cancer related death worldwide
 Men > women
 Median age at diagnosis 65 years

12. GC Worldwide incidence
Male 16.4
Female 8.2
Male 36.3
Female 16.9
Male 77.9
Female 33.3
Male 10.8
Female 4.9
Male 43.6
Female 19.0
Male 5.9
Female 2.6
Male 11.5
Female 4.3
Male 18.6
Female 13.3
Male 8.4
Female 4.0
Eastern
Europe
Japan
Australia/
New Zealand
China
Northern
Africa
Southern
Africa
Central
America
Western
Europe
North
America

13. PATHOLOGY
Adenocarcinomas
Lymphomas
Leiomyosarcomas
Carcinoid tumors
Adenoacanthomas
Squamous Cell Carcinomas

14. RISK FACTORS
 Nutritional
■ High salt consumption
■ High nitrate consumption
■ Low dietary vitamin A and C
■ Poor food preparation (smoked, salt cured)
■ Lack of refrigeration
 Occupational
■ Rubber workers
■ Coal workers
 Cigarette smoking
 Helicobacter pylori infection
 Epstein-Barr virus
 Prior gastric surgery for benign gastric ulcer disease

15. Genetic Factors
■ Type A blood group
■ Pernicious anemia
■ Family history
■ Hereditary diffuse gastric cancer
■ Hereditary nonpolyposis colon cancer
■ Familial adenomatous polyposis
■ Li-Fraumeni syndrome
Precursor lesions
• Adenomatous gastric polyps
• Chronic atrophic gastritis
• Dysplasia
• Intestinal metaplasia
• Menetrier disease

16. Normal
Diet low in vitamin C, E
High salt diet
Helicobacterpylori
Chronic superficial
gastritis
Atrophic gastritis
Intestinalmetaplasia
Dysplasia
Cancer

17. H.Pylori
 3 to 6 times greater risk
 Intestinal type malignancy

18. Genetic factors
 CDH1 mutation loss of E-cadherin
function
E-cadherin is a molecule involved in cell-to-cell
adhesion; loss of its expression leads to noncohesive
growth, hence the diffuse type
 BRCA1/ BRCA 2 mutation

19. Molecular Biology
 Four major alterations
 Inactivation of p53 gene
 Alterations in mismatch repair genes: hMSH3, hMLH1
 C-met and k-sam proto-oncogenes
 ER, EGFR

20. CLINICAL PRESENTATION
Patients may have a combination of signs and symptoms such as
• weight loss
• anorexia
• fatigue,
• epigastric discomfort, or pain
• postprandial fullness heart burn,
• indigestion,
• nausea and vomiting
In addition, patients may be asymptomatic

21.  Signs and symptoms at presentation that are often related to spread of
disease are
• Ascites,
• jaundice, or
• a palpable mass.
 The transverse colon is a potential site of malignant fistulization and
obstruction from a gastric primary tumor.
 Diffuse peritoneal spread of disease frequently produces other sites of
intestinal obstruction.
 A large ovarian mass (Krukenberg’s tumor) or a large peritoneal implant in
the pelvis (Blumer’s shelf), which can produce symptoms of rectal
obstruction.

22. Pathologic Classifications
Borrmann’s Gross Morphology
Lauren’s Histopathology
WHO Histopathology
Ming Histopathology
Broder’s Histological Grade

24. Lauren’s classification
 Intestinal Type
 Diffuse Type

25. Intestinal
 Prevalent in high
incidence areas
 Gland formation
 Hematogenous Spread
 Better prognosis

26. Diffuse
 Blood type A
 Poorly
differentiated,
signet ring cells
 Decreased E-
cadhedrin
 Poor Prognosis

27. WHO Gastric Cancer classification
 Adenocarcinoma – divided according to the growth
pattern in:
- papillary
- tubular
- mucinous
- signet ring
 Adenosquamous cell carcinoma
 Squamous cell carcinoma
 Undifferentiated
 Unclassified

28. Early gastric cancer
 Defined as a tumor confined to the mucosal or submucosal
layer, with or without lymph node metastasis

29. Advanced gastric cancer
 Invasion depth beyond submucosal layer

30. Spread:-
 Local Extension
 Lymphatic metastasis
 Peritoneal metastasis
 Distant metastasis

31. LOCAL SPREAD
The initial growth of the tumour occurs by penetration into the
gastric wall, extension through the wall, within the wall
longitudinally, and subsequent involvement of an increasing
percentage of the stomach.
Local extension occurs by deep invasion through the wall to
adjacent structures (omentum, spleen, adrenal gland,
diaphragm, liver, pancreas, or colon).

32. LYMPHHATIC SPREAD
 Regional lymph nodes:
-lesser and greater curvature
-celiac
-splenic hilum
-hepatic hilum
-pancreatico-duodenal
 Lymph nodes where spread is considered metastasis:
-paraaortic
-mediastinal
-left supraclavicular (Virchow's)
-left axillary (Irish)
-umbilical (Sister Mary Joseph's)

34. Virchow’s Node

35. Peritoneal Spread
 Beyond the gastric wall to free peritoneal surface
 Krukenberg tumor
 Blumer’s shelf

36. Distant Metastasis
 Liver
 Lung
 Bone
 Brain

37. WORK UP
 BLOOD INVESTIGATIONS
 ENDOSCOPY
 CT SCAN
 MRI
 PET SCAN
 STAGING LAPROSCOPY AND PERITONEAL CYTOLOGY
 TUMOR MARKERS

38. I. Laboratory Studies
1) Complete Hemogram
2) Serum electrolytes.
3) Liver and Kidney function tests.

39. ENDOSCOPY
 Endoscopy is the best method to diagnose gastric cancer as it visualizes the
gastric mucosa and allows biopsy for a histologic diagnosis.
 Chromoendoscopy helps identification of mucosal abnormalities through
topical stains ( Lugol’s Iodine, methylene blue, crystal violet)
 Magnification endoscopy is used to magnify standard endoscopic fields by
1.5- to 150-fold.
 Confocal laser endomicroscopy permits in vivo, three-dimensional
microscopy including subsurface structures with diagnostic accuracy,
sensitivity, and specificity of 97%, 90%, and 99.5%, respectively.

40. Endoscopy
Room set-up and patient positioning for endoscopy

41. Adenocarcinoma of the cardia. Large, lobulated, ulcerated mass
at the gastroesophageal junction

42. Adenocarcinoma in the antrum manifested by ulcerated,
circumferential mass and gastric outlet obstruction

43. III. Endoscopic ultrasonography
(EUS)
EUS helps to determine the depth of tumor invasion.
Can be used to guide for biopsy.
Has the ability to detect sarcomas and other tumors arising
from the submucosa and the musculosa (GIST).

44. The gastric wall is visualized as 5 concentric bands

45.  EUS cannot permit assessment of tissue beyond a depth
of about 5 cm.
Can not be used to assess distant nodal or liver metastases.
Can not differentiate between malignant and benign
ulcers.

46. IV. Radiology
Barium study
 Barium meal showing infiltrating gastric carcinoma in the region of the
incisura. There is irregular narrowing affecting both the lesser and
greater curvatures (arrow) ‘Apple core sign”

47. Linitis plastica "leather-flask" appearing stomach

48. Computed Tomography (CT)
It is widely used for tumor staging.
Demonstrates accurately the size and location of the
tumor.
Helps to assess the presence of nodal or visceral spread
and involvement of other peritoneal structures (e.g.,
ovaries, liver).
Can not detect metastases smaller than 5 mm.

52. MAGNETIC RESONANCE
IMAGING
 MRI is not used routinely in preoperative staging of gastric
cancer.
 Several studies have demonstrated that CT and MRI are
comparable in terms of accuracy and staging.
 Useful modality to further characterize liver lesions identified
on preoperative CT staging workup

53. Overall accuracy
EUS MDCT MRI
T Stage 65-92% 77-89% 71-83%
N Stage 55-66% 32-77%

54. POSITRON EMISSION
TOMOGRAPHY

55. STAGING LAPROSCOPY AND
PERITONEAL CYTOLOGY

56. TUMOR MARKERS
 CEA, CA-125, CA 19-9, CA 72-4, CA 50 may be elevated
but have low sensitivity/specificity
 None are diagnostic
 Preoperative elevation in markers usually pretends high
risk of adverse outcome
 More helpful in follow up

57. STAGING
 AMERICAN JOINT COMMITTEE ON CANCER/
INTERNATIONAL UNION AGAINST CANCER
TUMOUR,NODE, METASTASIS STAGING
 JAPANESE STAGING SYSTEM

58. AJCC

61. AJCC Staging System

62. JAPANESE STAGING

64. Prognostic Factors
Tm extension within/beyond gastric wall
No of lymph nodes involved, location
Poor PS
Cardia lesions
Borrmann type IV
CD44 expression, telomerase reactivation, p53
suppression
Dysfunction of repair genes hMSH3, hMLH1
Overexpression of erb-B2, c-met and k-sam
ER expression

65. Thank
you!