Prevention of GI malignancy
G N RameshPVS Memorial Hospital
Cochin
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?
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)
My aim
• Summary of factors that can be changed in our population to decrease and prevent GI cancers
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 BMIReduced intake of fruits/vegetables
Sedentary life styleSmoking
Alcohol use
Gastric cancer
The premalignant conditions
• Chronic atrophic gastritis• Intestinal metaplasia• H pylori• Gastric adenoma
Gastric carcinogenesis: Histologic changes from normal gastric mucosa to neoplasia
Two ends of a spectrum
• Proximal cancers
• GERD• Obesity
• Distal cancers
• Dietary factors• H pylori
Primary prevention
• Decreased salt intake• Increased vitamin C consumption• Quit smoking• H pylori eradication – class I carcinogen –
decreased Ca by 35%
The metanalysis
The final word?
• 1.8% vs 2.4% in controls• NNT – 15 for Chinese , 245 for USA ,• India?
Adenocarcinoma of the Esophagus
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
• 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.
Hepatitis and liver cancer
Causes
• HBV and HCV – 80% of cases• Cirrhosis• Alcohol• Steatosis and diabetes• Medications/toxins• Genetic / metabolic diseases
The impact of vaccination on liver cancer
The Taiwan experience
Success of Hepatitis B vaccine
Other issues
• Antivirals and the impact on carcinogenesis – not recurrence
• Improving the efficacy of screening programs• Effective modification of the modifiable
factors
HCV and liver cancer
• Safe practices to prevent HCV• New age antivirals and their potential impact
on carcinogenesis
NAFLD , cirrhosis and cancer
Non modifiable modifiable
The final word…
• We can do lots more • We aren’t doing enough.• Education and awareness are the key
Colon cancer
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
Factors and interventions to decrease CRC
Increased riskAlcohol – RR 1.41 > 45g/d
Smoking – RR 1.18Obesity – RR 1.45 BMI>29
Decreased riskPhysical activity 24% reduction
Factors and interventions to decrease CRC
Increased riskAlcohol – RR 1.41 > 45g/d
Smoking – RR 1.18Obesity – RR 1.45 BMI>29
Decreased riskPhysical activity 24% reduction
InterventionsNSAIDsAspirin
Physical ActivityHormones – estrogen-progestin combination
High fiber, fruits , vegetables – inadequate evidenceLow fat/meat – inadequate evidence
Calcium supplementation – no evidenceStatins – insufficient evidence
When to start?
• Average risk – 50 yrs• Moderate risk – ( Blacks , MS , abdominal
obesity ) 45 yrs• High risk – familial - earlier
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 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 sigmoidoscopyRisk reduces with removal of polyps > 1 cm ; not proven with polyps <
1 cm
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)
The final word….
• Guidelines well established• Putting guidelines into practice…not well
established• Awareness , education , enforcement• Whom? When ? What frequency ? For India
Pancreatic cancer
• Lethal• Stage at diagnosis• Lack of effective medical therapy• No effective screening methods• Primary prevention – most effective way to
reduce burden
19 prospective studies ; 3 meta analyses10-45% increase for every 5 BMI
Stronger association with obesity in the young ( 30-40 yrs)
? Related to pancreatic steatosisObesity and diabetes – risk cumulative
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.
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
Screening tools ..and I whom?
• No guidelines• Chronic pancreatitis; hereditary
pancreatic cancer; hereditary pancreatitis
• How? MRI/EUS
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 cancerhe 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
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%
FAP
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.
• 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
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.
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
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