This document discusses strategies for preventing gastrointestinal (GI) cancers. It outlines several key risk factors for GI cancers, including H. pylori infection for gastric cancer, obesity for pancreatic cancer, and family history for colon and gastric cancers. Prevention strategies discussed include H. pylori eradication, vaccination for hepatitis B, lifestyle modifications like diet and exercise, and cancer screening programs. The document emphasizes that while knowledge of risk factors is sound, interventions need improved implementation and awareness and education are critical to reducing the burden of GI cancers.

1. Prevention of GI malignancy
G N Ramesh
PVS Memorial Hospital
Cochin

3. Schema
• Principles of prevention
• H pylori and gastric cancer – should we eradicate
in all?
• Barrett’s and malignancy – do we need to
bother?
• Hepatitis virus and liver cancers – how could we
do more?
• Colonic cancers – applying guidelines to our
population
• Pancreatic cancer – we know the preneoplastic
situations .. But can we prevent?

4. Principles of prevention
• Primary – preventing the intitiation of the
carcinogenic process – elimination , avoiding
or neutralising the carcinogen
• Secondary – interfering with the metabolism
of carcinogen or preventing it from reaching
the target ( tissue DNA)
• Tertiary – preventing precancerous lesions
from progressing to cancer ( surveillance)

5. My aim
• Summary of factors that can be changed in
our population to decrease and prevent GI
cancers

6. My aim
• Summary of factors that can be changed in
our population to decrease and prevent GI
cancers
30% of cancer deaths are due to 5 behavioral risk factors
High BMI
Reduced intake of fruits/vegetables
Sedentary life style
Smoking
Alcohol use

7. Gastric cancer

9. The premalignant conditions
• Chronic atrophic gastritis
• Intestinal metaplasia
• H pylori
• Gastric adenoma

10. Gastric carcinogenesis: Histologic changes from normal gastric mucosa to neoplasia

11. Two ends of a spectrum
• Proximal cancers
• GERD
• Obesity
• Distal cancers
• Dietary factors
• H pylori

12. Primary prevention
• Decreased salt intake
• Increased vitamin C consumption
• Quit smoking
• H pylori eradication – class I carcinogen –
decreased Ca by 35%

14. The metanalysis

17. The final word?
• 1.8% vs 2.4% in controls
• NNT – 15 for Chinese , 245 for USA ,
• India?

18. Adenocarcinoma of the Esophagus

19. Gastroesophageal reflux/Barrett
esophagus
• Association exists between gastroesophageal
reflux disease (GERD) and adenocarcinoma –
duration and severity.
• Does elimination of gastroesophageal reflux
by surgical or medical means reduce the risk
of adenocarcinoma of the esophagus ???
• RFA of Barrett esophagus with severe
dysplasia may lead to eradication of both
dysplasia and intestinal metaplasia and a
reduced risk of disease progression

20. • When should you ablate? HGD or early
adenoca…..not metaplasia
• Does ablation reduce adenoca ? Perhaps yes
• Does surgery reduce adenoca? .. Series of
Swedish reports – no!
• Do we need surveillance in India? – no
evidence.

21. Hepatitis and liver cancer

22. Causes
• HBV and HCV – 80% of cases
• Cirrhosis
• Alcohol
• Steatosis and diabetes
• Medications/toxins
• Genetic / metabolic diseases

24. The impact of vaccination on liver
cancer

25. The Taiwan experience

26. Success of Hepatitis B vaccine

27. Other issues
• Antivirals and the impact on carcinogenesis –
not recurrence
• Improving the efficacy of screening programs
• Effective modification of the modifiable
factors

28. HCV and liver cancer
• Safe practices to prevent HCV
• New age antivirals and their potential impact
on carcinogenesis

29. NAFLD , cirrhosis and cancer

30. Non
modifiable modifiable

31. The final word…
• We can do lots more
• We aren’t doing enough.
• Education and awareness are the key

32. Colon cancer

33. Who is at risk?
• Age -> 50 yrs ( 90% of all CRCs)
• History
first degree relative ( < 55 yrs at diagnosis)
doubles the risk
personal h/o CRC / high risk
adenomas/ovarian ca
• Others – IBD , genetic ( hereditary GI cancer) ,
HNPCC , FAP

34. Factors and interventions to decrease
CRC
Increased risk
Alcohol – RR 1.41 > 45g/d
Smoking – RR 1.18
Obesity – RR 1.45 BMI>29
Decreased risk
Physical activity 24% reduction

35. Factors and interventions to decrease
CRC
Increased risk
Alcohol – RR 1.41 > 45g/d
Smoking – RR 1.18
Obesity – RR 1.45 BMI>29
Decreased risk
Physical activity 24% reduction
Interventions
NSAIDs
Aspirin
Physical Activity
Hormones – estrogen-progestin combination
High fiber, fruits , vegetables – inadequate evidence
Low fat/meat – inadequate evidence
Calcium supplementation – no evidence
Statins – insufficient evidence

38. When to start?
• Average risk – 50 yrs
• Moderate risk – ( Blacks , MS , abdominal
obesity ) 45 yrs
• High risk – familial - earlier

40. How often after polyp detection?
• Small rectal polyps – 10 yrs
• 1 or 2 small (<1 cm) with LGD – 5-10 YRS
• 3 or more adenomas , > 1 cm , villous/HGD – 3 yrs
• 10 or more - 3 yrs
• Sessile polyps / piecemeal removal / HGD – 2-6 mos
• HNPCC/FAP – more intensive

41. How often after polyp detection?
• Small rectal polyps – 10 yrs
• 1 or 2 small (<1 cm) with LGD – 5-10 YRS
• 3 or more adenomas , > 1 cm , villous/HGD – 3 yrs
• 10 or more - 3 yrs
• Sessile polyps / piecemeal removal / HGD – 2-6 mos
• HNPCC/FAP – more intensive
HOW EFFECTIVE IS IT?
Prevents 85% of cases of distal CRC ; less effective for proximal CRC
26% reduction of mortality with flexible sigmoidoscopy
Risk reduces with removal of polyps > 1 cm ; not proven with polyps <
1 cm

42. Prevention of colorectal ca
• Diet, exercise, smoking, and supplements
• daily aspirin may decrease the risk of
colorectal and extracolonic cancer in LS,
currently the evidence is not sufficiently
robust (CAPP1 , CAPP2 , CAPP3 trials)

43. The final word….
• Guidelines well established
• Putting guidelines into practice…not well
established
• Awareness , education , enforcement
• Whom? When ? What frequency ? For India

44. Pancreatic cancer

45. • Lethal
• Stage at diagnosis
• Lack of effective medical therapy
• No effective screening methods
• Primary prevention – most effective way to
reduce burden

47. 19 prospective studies ; 3 meta analyses
10-45% increase for every 5 BMI
Stronger association with obesity in the young
( 30-40 yrs)
? Related to pancreatic steatosis
Obesity and diabetes – risk cumulative

48. Who is at risk for adenoca?
• Genetic syndromes - hereditary breast–
ovarian cancer syndrome, familial
atypical multiple melanoma and mole
syndrome (FAMMM), PJS, LS, or other
gene mutations
• Three or more relatives with pancreatic
cancer
• Hereditary pancreatitis.

49. HOW?
• Surveillance for PC should be with
endoscopic ultrasound and/or MRI of the
pancreas annually starting at age 50
years, or 10 years younger than the
earliest age of PC in the family.
• Patients with PJS should start surveillance
at age 35 years

50. Screening tools ..and I whom?
• No guidelines
• Chronic pancreatitis; hereditary
pancreatic cancer; hereditary
pancreatitis
• How? MRI/EUS

51. Jack Andraka, the Teen Prodigy of
Pancreatic Cancer
A high school sophomore won the youth achievement Smithsonian
American Ingenuity Award for inventing a new method to detect a
lethal cancer
he won the $75,000 grand prize at this past spring’s Intel International
Science and Engineering Fair,
“Edison of our times,”
Follow us: @SmithsonianMag on Twitter

52. Conclusions
• Sound knowledge of factors associated with GI
cancer
• Interventions need to be executed
• Awareness and education is the key
• Common risk factors – smoking , obesity ,
diets , physical inactivity , alcohol – reduced
burden by 25-40%
• HBV,HCV – another 10-15%

58. FAP

59. Esophageal cancers
• The following risk factors may increase the
risk of esophageal cancer:
– Tobacco and alcohol use
– Gastric reflux and Barrett esophagus
• The following protective factors may
decrease the risk of esophageal cancer:
– Avoiding tobacco and alcohol use
– Diet
– Nonsteroidal anti-inflammatory drugs
– Radiofrequency ablation.

60. • Screening for gastric and proximal small bowel
tumors should be done using upper GI
endoscopy including duodenoscopy starting at
age 25–30 years.
• Annual thyroid screening by ultrasound should
be recommended to individuals affected with
FAP, MAP, and attenuated polyposis

61. Hereditary gastric cancer
• (i) ≥2 cases of diff use gastric cancer, with at least
one diagnosed at <50 years,
• (ii) ≥3 cases of documented diffuse cancer in first-
or second-degree relatives independent of age of
onset;
• (iii) diffuse gastric cancer diagnosed at <40 years;
and
• (iv) a personal or family history of diffuse gastric
cancer and lobular breast cancer with one
diagnosed at <50 years should be evaluated for
hereditary diffuse gastric cancer.

62. Management
• (i) prophylactic gastrectomy after age 20 years
(>80% risk by age 80 years);
• (ii) breast cancer surveillance in women
beginning at age 35 years with annual
mammography and breast MRI and clinical
breast examination every 6 months,
• (iii) colonoscopy beginning at age 40 years for
families that include colon cancer