IBD and colon cancer

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Inflammatory Bowel disease and Colon Cancer

• Dr Ngemera Johannes A
• MD(HKMU), Mmed. Internal Medicine (MUHAS)
• July 17th, 2023

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DEFINITION

• Inflammatory Bowel Disease is defined as
• Conditions characterized by presence of
  idiopathic Intestinal Inflammation.
• - Bailey Love
• Chronic Condition resulting from Inappropriate
  Mucosal Immune Activation
• - Robbins Cotran

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Introduction

• Inflammatory bowel disease (IBD)
• a chronic, relapsing inflammation of bowel
  possibly due to abnormal immune response to
  enteric flora.
• The major forms of IBD are recognized as
• Crohns disease (CD)
• Ulcerative colitis (UC)
• Indeterminate Colitis

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Introduction

• Crohns disease (CD)
• Chronic inflammation potentially involving any
  part of the GIT from mouth to anus.
• It is a lifelong disease arising from an
  interaction between genetic and environmental
  factors
• Ulcerative colitis (UC)
• inflammatory disorder that affects the rectum and
  extends proximally to affect variable extent of
  the colon.

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Introduction

• these two conditions overlap in
• clinical features
• histological and
• radiological abnormalities
• In 10 of cases of IBD causing colitis, a
  definitive diagnosis is either UC or CD is not
  possible and the diagnosis is term as colitis of
  undetermined type and etiology (CUTE).
• Clinically useful to distinguished between these
  two conditions because of differences in their
  management, although in reality they may
  represent two aspect of the same disease.

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Epidemiology

• The incidence and prevalence of IBD are highest
  in westernized nations
• the incidence of CD varies from country to
  country but is approximately 4-10 per 100,000
  annually with the prevalence 25-100 per 100,000.
• The incidence of UC is stable at 6-15/10,000
  annually with a prevalence of 80-150/100,000.
• The disease is more prevalent in the west,
  particularly Caucasian and eastern European Jews.

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Etiology

• Exact etiology of ulcerative colitis and Crohns
  disease is unknown
• similar factors are believed responsible for both
  conditions.
• IBD represents the outcome of three essential
  interactive co-factors
• Genetic predisposition
• Environmental factors
• Host immune response

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INFLAMMATORY BOWEL DISEASE
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Etiology

• Genetic factors
• 1st degree relatives of an affected patient have
  a risk of IBD that is 4-20 times higher than that
  of general population
• Environmental
• Smoking - ???protects against UC but ?risk of CD
• NSAIDs - (?altered intestinal barrier)
• Hygiene
• Nutritional factors

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Etiology

• Host
• Appendectomy - Early appendectomy ?UC incidence
• The intestinal microbiota
• The intestinal immune system

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Crohns disease
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Crohns disease

• Chronic inflammatory condition affecting any part
  of the GI tract from mouth to anus
• has the tendency to affect the ileum and
  ascending colon (ileocolonic disease).
• Bimodal peak age of presentation
• 15-30 years and
• 60-80 years.

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Crohns disease

• The disease typically follows a remitting and
  relapsing course.
• Severe exacerbations may be
• life- threatening
• causing severe systemic upset,
• bowel perforation or obstruction.

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Pathophysiology of Crohns disease

• Mouth to anus
• commonly targets the distal ileum or proximal
  colon,
• characterized by
• transmural inflammation (affecting all layers of
  the bowel) in the affected region of bowel,
• producing deep ulcers and fissures (a
  cobblestone appearance)
• inflammation is not continuous, forming skip
  lesions throughout the bowel.

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Cobblestone
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Pathophysiology of Crohns disease

• The microscopic appearance of Crohns disease is
• non-caseating granulomatous inflammation.
• Due to the transmural nature of the inflammation,
  fistula can form from affected bowel to adjacent
  structures, resulting in
• perianal fistula (54), 
• entero-enteric fistula (24),
• recto-vaginal (9),
• entero-cutaneous fistula, or
• entero-vesicular fistula.

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Classification of CD

• Based on the area of the gastrointestinal tract
  which it affects
• Ileocolic Crohn's disease 50
• Affects both the ileum and the large intestine
• Crohn's ileitis 30
• Affects the ileum only
• Crohn's colitis 20
• Affects the large intestine

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Risk Factors

• Unknown etiology
• Environmental and Genetic factors are thought to
  play a role.
• The main risk factors for CD include
• Family history
• 20 have first degree relative affected.
• Smoking
• ??risk of developing Crohns disease and risk of
  relapse.
• White European descent
• particularly Ashkenazi Jews
• Appendicectomy
• ?? risk of developing CD directly after the
  surgery

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Clinical Features

• Abdominal pain
• may be colicky in nature and will vary in site
  depending on the region of bowel involved.
• Diarrhea
• often chronic and may contain blood or mucus.
• Systemic symptoms
• malaise, anorexia and low-grade fever
• may also result in malabsorption and malnutrition
  if severe,
• (in children, this may initially present as a
  failure to grow or thrive).

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Clinical Features

• As the disease affects the entire GI tract, both
  oral and perianal involvement are common
• Oral aphthous ulcers (can be painful and
  recurring)
• Perianal disease (as skin tags, perianal
  abscesses, fistulae, or bowel stenosis)

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Oral aphthous ulcers
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Clinical Features

• Examination features include
• Abdominal tenderness
• mouth or perianal lesions and
• signs of malabsorption or dehydration.
• Patients should also be examined for
  extra-intestinal features

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Extra-Intestinal Features of CD

• Musculoskeletal
• Enteropathic arthritis (sacroiliac and other
  large joints)
• Finger  clubbing
• Metabolic bone disease (secondary to
  malabsorption)
• Skin
• Erythema nodosum - tender red/purple subcutaneous
  nodules, typically found on the patients
  shins(Front of lower limbs)
• Pyoderma gangrenosum - erythematous
  papules/pustules that develop into deep ulcers
  and can occur anywhere (yet typically affect
  the shins)

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Erythema nodosum
Pyoderma gangrenosum
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Extra-Intestinal Features of CD

• Eyes
• Episcleritis,
• anterior uvetitis, or
• iritis
• Hepatobiliary
• Primary sclerosing cholangitis (more associated
  with UC)
• Cholangiocarcinoma (due to association
  with primary sclerosing cholangitis)
• Gallstones
• Renal
• Renal stones

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Investigations

• Routine blood test
• FBP Anaemia, ?WBC evidence of inflammation
• ?CRP - evidence of inflammation
• ?Serum Albumin Secondary to malabsorption
• Abdominal radiograph  or CT imaging
• in acute situation may be useful to exclude any
  potential toxic megacolon or bowel obstruction

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Investigations

• Colonoscopy with biopsy
• gold standard diagnostic investigation
• characteristic macroscopic finding is
• cobblestoning of the bowel (fissures and ulcers
  separate islands of healthy mucosa)
• non-caseating granulomatous inflammation on
  histology
• Proctosigmoidoscopy under anaesthesia 
• may also be considered to examine and treat
  fistulating peri-anal disease.

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Investigations

• CT scan - Abdomen
• usually warranted in severe Crohns disease,
  which may demonstrate
• bowel obstruction,
• perforation,
• collection formation, or
• fistulae
• MRI scan - Abdomen
• Same indications as CT scanning but in the
  non-acute (elective) setting
• particularly useful for looking for enteric
  fistulae and for peri-anal disease (as well as
  reducing radiation dosing)

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Management

• Note Avoid anti-motility drugs, e.g. Loperamide,
  in acute attacks as may precipitate toxic
  megacolon
• Any acute attacks
• aggressive fluid resuscitation
• nutritional support
• Smoking cessation 
• Enteral nutritional support
• Antibiotics
• only in concurrent infection or perianal disease
  (typically ciprofloxacin or metronidazole).

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Management

• INDUCING REMISSION
• Corticosteroid therapy 
• Prednisone is started a doses of 4060 mg/d
• I.V Hydrocortisone 300 mg/d, or
• I.V. Methylprednisolone, 4060 mg/d.
• Immunosuppresive agents, 
• mesalazine or azathioprine.
• Biological agents
• e.g infliximab

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Management

• MAINTAINING REMISSION
• Azathioprine or mercaptopurine
• recommended as a monotherapy to
  maintain remission. 
• Methotrexate
• Biological agents
• infliximab, adalumimab, or rituximab

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Surgical Management

• About 70-80 of Crohns patients require surgery
  at some point in their lifetime.
• Indications
• failed medical management,
• severe complications (such as strictures or
  fistulas), or
• growth impairment in younger patients.

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Surgical Management in CD

• Ileocaecal resection
• removal of terminal ileum and caecum with primary
  anastomosis
• Surgery for peri-anal disease
• e.g. abscess drainage, seton insertion, or laying
  open of fistulae
• Stricturoplasty
• division of a stricture that is causing bowel
  obstruction)
• Small bowel or large bowel resections

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Complications of Crohns Disease

• Gastrointestinal
• Fistula
• including enterovesical, enterocutaneous, or
  rectovaginal fistula
• Stricture formation
• Inflammation of the bowel can result in stricture
  formation, resulting in bowel obstruction(in
  about 40)
• Recurrent perianal abscesses / fistulae
• common and often difficult to treat,
• require multiple operations/examinations under
  anaesthesia
• GI malignancy
• about a 3 risk of developing colorectal cancer
  over 10 years
• small bowel cancer is about 30x more common in
  CD

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Complications of Crohns Disease

• Extraintestinal
• Malabsorption
• Growth delay in children
• Osteoporosis
• common if there is obstruction or fistula
  formation
• Secondary to malabsorption or long-term steroid
  use
• Increased risk of gallstones
• Due to ?? bile salts at reabsorption inflamed
  terminal ileum
• Increased risk of renal stones
• Due to malabsorption of fats in the small bowel
  which causes calcium to remain in the lumen
  oxalate is then absorbed freely (as normally
  bound to calcium and excreted in stool),
  resulting in hyperoxaluria and formation
  of oxalate stones in the renal tract

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Ulcerative Colitis
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Ulcerative Colitis

• The most common form of IBD
• ?Prevalence among the Caucasian population
• bimodal distribution
• 15-25yrs (most cases)
• 55-65yrs
• males and females affected equally.

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Ulcerative Colitis

• Typically follows a remitting and relapsing
  course.
• A severe fulminant exacerbation may be life
  threatening, resulting in
• severe systemic upset
• toxic megacolon and
• colonic perforation

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Pathophysiology of Ulcerative Colitis

• Characterised by
• diffuse continual mucosal inflammation of the
  large bowel
• beginning in the rectum and
• spreading proximally, potentially affecting the
  entire large bowel. 
• Backwash ileitis
• May occur if the ileocaecal valve is not
  competent
• A portion of the distal ileum can become affected
  in a small proportion of cases

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Pathophysiology of Ulcerative Colitis

• Histological changes include
• inflammation of the mucosa and submucosa,
• crypt abscesses, and
• goblet cell hypoplasia 
• Pseudopolyps
• Raised areas of inflamed tissue due to repeated
  cycles of ulceration and healing

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Types of Ulcerative colitis
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Clinical Features of Ulcerative Colitis

• Insidious/gradual in onset.
• Cardinal feature is bloody diarrhoea, with
  visible blood in stool reported in more than 90
  of cases.
• Proctitis
• most common manifestation,
• inflammation is confined to the rectum.
• Per Rectal bleeding and mucus discharge,
• increased frequency, urgency of defecation, and
• tenesmus.
• With more widespread colonic involvement
• bloody diarrhoea
• dehydration and electrolyte imbalance. 

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Clinical Features of Ulcerative Colitis

• Systemic symptoms
• malaise, anorexia, and low-grade pyrexia.
• Clinical examination
• generally unremarkable.
• Severe abdominal pain signs of peritonism in case
  of
• Fulminant colitis
• toxic megacolon or
• colonic perforation

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Disease Grading - Truelove and Witt Criteria

• Severity of an exacerbation
• Based on the presence of any one of the criteria
• Bowel movements per day
• Blood in stool
• Pyrexia
• Pulse gt90 bpm
• Anaemia
• ESR

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Disease Grading - Truelove and Witt Criteria
Criteria Mild Moderate Severe
Bowel movements per day lt4 4-6 gt6
Blood in stool Minimal Mild to severe Visible blood
Pyrexia No No Yes
Pulse gt90 bpm No No Yes
Anaemia No No Yes
ESR (mm/hour) 30 30 gt30
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Extra-Intestinal Manifestations

• Ulcerative colitis, much like Crohns disease, is
  associated with extra intestinal manifestations
  of disease
• Musculoskeletal
• enteropathic arthritis (typically affecting
  sacroiliac and other large joints)
• Finger clubbing
• Skin
• Erythema nodosum (tender red/purple subcutaneous
  nodules, typically found on the patients shins)
• Eyes
• Episcleritis, anterior uveitis, or iritis
• Hepatobiliary 
• Primary sclerosing cholangitis (chronic
  inflammation and fibrosis of the bile ducts)

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Differential Diagnosis

• Crohns disease
• as this can present in a similar fashion,
  however patients with UC patients typically
  experience a more bloody diarrhoea.
• Alternative forms of colitis include
• Chronic infections (schistosomiasis, giardiasis
  and TB)
• Mesenteric ischaemia, or
• Radiation colitis
• Malignancies
• Irritable Bowel Syndrome
• Coeliac disease.

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Investigations

• Blood tests
• FBP - for anaemia and evidence of inflammation
• CRP - evidence of inflammation
• Serum Urea and Cretinine
• Serum electrolytes
• LFTs and Clotting factors
• Serum Albumin - malabsorption
• Stool sample - for microscopy and culture
• Liver function tests may become deranged in
  patients on medical treatment and clotting can
  become deranged in severe attacks due to the
  large inflammatory response affecting the
  coagulation cascade.

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Investigations

• Colonoscopy with biopsy
• The definitive diagnosis for ulcerative colitis
• Characteristic macroscopic findings are
• Continuous inflammation with possible ulcers and
  pseudopolyps visible.
• full colonoscopy is only required if the
  diagnosis is unclear
• should be avoided in acute severe exacerbations  
• Flexible sigmoidoscopy
• may be sufficient and in clinical practice

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Investigations

• Abdominal radiograph  or CT imaging
• In acute exacerbation to assess for toxic
  megacolon and/or bowel perforation
• Abdominal radiograph of acute ulcerative colitis
  flares include
• mural thickening and thumbprinting, indicating a
  severe inflammatory process in the bowel wall
• in chronic cases of UC, a lead-pipe colon is
  often described - usually best seen on barium
  studies.

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Management of Ulcerative Colitis

• Anti-motility drugs, such as loperamide,
• should be avoided in acute attacks, as these can
  precipitate toxic megacolon
• Any acute attacks will also warrant
• aggressive fluid resuscitation
• nutritional support

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Management of Ulcerative Colitis

• for inducing remission
• Mild to Moderate (proctitis)
• Step 1 Topical mesalazine or sulfasalazine
• Step 2 Add oral prednisolone  oral tacrolimus
• Mild to Moderate (extensive inflammation)
• Step 1 High oral dose mesalazine or
  sulfasalazine
• Step 2 Add oral prednisolone  oral tacrolimus
• Severe (all spread of disease)
• Step 1 I.V Corticosteroids and assess need for
  surgery
• Step 2 Step 2 Add infliximab if no short-term
  response

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Management of Ulcerative Colitis

• Maintaining Remission
• Immunomodulators
• Mesalazine or Sulfasalazine.
• Infliximab
• monoclonal antibody therapy
• can be used as next line therapies to maintain
  remission patients with recurrent symptoms.

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Management of Ulcerative Colitis

• Colonoscopic surveillance
• Due to increased risk of colorectal malignancy
• to people who have had the disease for gt 10 years
  with gt1 segment of bowel affected
• follow-up time frame depends on risk
  stratification of disease following initial
  endoscopy

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Surgical Management

• Approximately 30 patients with ulcerative
  colitis will at some point require surgery.
• Indications for acute surgical treatment
• disease refractory to medical management,
• toxic megacolon, or
• bowel perforation.
• Surgery may also be undertaken to reduce the risk
  of colonic carcinoma, if dysplastic cells are
  detected on routine monitoring.
• Total proctocolectomy is curative

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Complications of UC

• Short term complication
• Toxic megacolon
• Hemorrhage
• Perforation
• Long term complication
• Stricture leading to obstruction
• Dysplasia leading to cancer.

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Complications of Ulcerative Colitis

• Toxic megacolon
• present with severe abdominal pain and
  distension, pyrexia, and systemic toxicity
• Pouchitis - inflammation of an ileal pouch,
• Abdominal pain, bloody diarrhoea, and nausea
• treated with Metronidazole and ciprofloxacin
• Hemorrhage
• Perforation
• Stricture leading to obstruction
• Dysplasia leading to Colorectal carcinoma
• Osteoporosis ? fracture risk

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Toxic megacolon
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Toxic megacolon
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COMPARISON OF CROHNS DISEASE vs ULCERATIVE COLITIS COMPARISON OF CROHNS DISEASE vs ULCERATIVE COLITIS COMPARISON OF CROHNS DISEASE vs ULCERATIVE COLITIS
Crohns Disease Ulcerative Colitis
Site of origin Terminal Ileum Rectum
Progression pattern Skip" lesions/irregular Proximally contiguous
Symptoms Crampy abdominal pain Bloody diarrhea
Complications Fistula, Abscess, Obstruction Haemorrhage, Toxic Megacolon
Radiographic findings String sign on Barium X-ray Lead pipe colon on Barium X-ray
Risk of Colon cancer Slight increase Marked increase
Surgery For complications such as stricture Curative
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Colon Cancer
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Colon Cancer

• Also called Colorectal cancer
• Uncontrolled, abnormal cell growth which starts
  in the colon or rectum
• These abnormal cells can form a mass of tissue
• Usually begins as a noncancerous polyp, that can,
  over time, become a cancerous tumor.

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Colon Cancer

• Although like most cancers, the occurrence
  is strongly associated with age
• can occur in patients as young as 20yrs (with the
  incidence in patients in their 40s is rising),
• particularly in patients with inherited cancer
  syndromes

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Aetiology

• Colorectal cancers originate from the epithelial
  cells lining the colon or rectum, most commonly
  an adenocarcinoma.
• Rarer types include
• lymphoma (1),
• carcinoid (lt1), and
• sarcoma (lt1).
• Most colorectal cancers develop via a progression
  of normal mucosa to colonic adenoma (colorectal
  polyps) to invasive adenocarcinoma (termed the
  adenoma-carcinoma sequence).
• Adenomas may be present for 10 years or more
  before becoming malignant and progression to
  adenocarcinoma occurs in approximately 10 of
  adenomas.

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Aetiology

• Certain genetic mutations have been implicated in
  predisposing individuals to colorectal cancer,
  most notably
• Adenomatous polyposis coli (APC)
• A tumour suppressor gene, mutation of the APC
  gene results in growth of adenomatous tissue
  associated with Familial Adenomatous Polyposis
  (FAP)
• Hereditary nonpolyposis colorectal cancer (HNPCC)
  
• A DNA mismatch repair gene, mutation to HNPCC
  leads to defects in DNA repair associated with
  Lynch syndrome

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Risk Factors

• Approximately 75 of colorectal cancers are
  sporadic, developing with no specific risk
  factors
• Potential risk factors include
• increasing age 
• family history 
• inflammatory bowel disease 
• low fibre diet
• high processed meat intake
• smoking
• high alcohol intake.

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Clinical Features

• Common clinical features
• change in bowel habit
• rectal bleeding
• weight loss
• abdominal pain
• iron-deficiency anemia.

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Clinical Features

• Classically, clinical features vary slightly
  depending on the location of the cancer
• Right-sided colon cancers
• abdominal pain,
• occult bleeding / anaemia,
• mass in right iliac fossa
• often present late
• Left-sided colon cancers
• rectal bleeding, change in bowel habit, tenesmus,
  mass in left iliac fossa or on PR exam

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Clinical Features

• Patients should be referred for urgent
  investigation of suspected bowel cancer if
• 40yrs with unexplained weight loss and
  abdominal pain
• 50yrs with unexplained rectal bleeding
• 60yrs with iron deficiency anemia or change in
  bowel habit
• Positive occult blood screening test
• As opposed to upper GI malignancies,
  progressive weight loss is usually only present
  in colorectal cancer cases with associated
  metastasis (or rarely in sub-acute bowel
  obstruction)

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Differential Diagnosis

• Inflammatory bowel disease
• The average age of onset of inflammatory bowel
  disease is younger (20-40yrs) than with
  colorectal cancer
• typically presents with diarrhoea containing
  blood and mucus
• Haemorrhoids
• Bright red rectal bleeding on the pan or surface
  of the stool
• rarely presents with abdominal discomfort or
  pain, altered bowel habits, or weight loss

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Colorectal Cancer Screening

• About 80 colorectal cancers arise from
  adenomatous polyps that progress from small to
  large (gt1.0 cm) polyps and then to dysplasia and
  cancer.
• The progression from adenoma to carcinoma is
  believed to take at least 10 years on average
• Screening
• has the potential to reduce colorectal cancer
  deaths by 60
• starting from the age of 50 to 75 is effective
  for preventing and decreasing deaths from
  colorectal cancer.

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Colorectal Cancer Screening - Risk assessment

• Screening at an earlier age
• (at 40 or 10 years younger than the age at which
  the youngest relative was diagnosed with
  colorectal cancer) and
• Done more frequently if there is Family history
  of
• colorectal cancer, or
• Polyps (Familial adenomatous polyposis
• inherited as an autosomal dominant gene,has 100
  risk to turn malignant.)
• Personal history of
• colorectal cancer or chronic inflammatory bowel
  disease

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Colorectal Cancer Screening

• Tests for adenomatous polyps and cancer, and
  their recommended frequency
• Flexible sigmoidoscopy every 5 years
• Colonoscopy every 10 years
• Double-contrast barium enema every 5 years
• CT - Colonography every 5 years

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Colorectal Cancer Screening

• Tests that primarily detect cancer, and their
  recommended frequency are
• Annual guaiac-based fecal occult blood test with
  high test sensitivity for cancer
• Annual fecal immunochemical test (FIT) with high
  test sensitivity for cancer
• Stool DNA test with high sensitivity for cancer,
  interval uncertain

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Investigations

• Laboratory tests
• FBP - microcytic anaemia (iron-deficiency
  anaemia)
• LFTs and clotting
• The tumor marker 
• Carcinoembryonic Antigen (CEA)
• Colonoscopy with biopsy
• Gold standard for diagnosis of colorectal cancer

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Investigations

• for staging
• CT scan (Chest/Abdomen/Pelvis) 
• for distant metastases and local invasion
• MRI rectum (for rectal cancers only)
• to assess the depth of invasion and potential
  need for pre-operative chemotherapy
• Endo-anal ultrasound (for early rectal cancers,
  T1 or T2 only)
• to assess suitability for trans-anal resection

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Management

• Multidisciplinary approach
• Surgery
• The only definitive curative option 
• Chemotherapy and Radiotherapy
• Neoadjuvant and adjuvant treatments
• Palliation treatment

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Management

• Chemotherapy
• Indicated typically in patients with advanced
  disease
• (adjuvant chemotherapy in Dukes C colorectal
  cancer has been found to reduce mortality by
  25).
• An example chemotherapy regime for patients with
  metastatic colorectal cancer is FOLFOX
• comprised of Folinic acid, Fluorouracil (5-FU),
  and Oxaliplatin,
• has been demonstrated to significantly
  improvement in 3-year disease-free survival for
  patients with advanced colon cancer

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Management

• Radiotherapy
• can be used in rectal cancer most often as
  neo-adjuvant treatment
• rarely given in colon cancer due to the risk of
  damage to the small bowel
• is of particular use in rectal cancers which look
  on MRI to have a threatened circumferential
  resection (i.e. within 1mm)
• pre-operative long-course chemo-radiotherapy to
  shrink the tumour, thereby increasing the chance
  of complete resection and cure

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Palliative Care

• For very advanced colorectal cancers
• focusing on reducing cancer growth and
• ensuring adequate symptom control
• Surgical options
• Endoluminal stenting 
• to relieve acute bowel obstruction in patients
  with left-sided tumours
• The main side-effects of stents are perforation,
  migration, and incontinence
• Stoma formation
• for patients with acute obstruction, usually with
  either a defunctioning stoma or palliative bypass
• Stenting cannot be used in low rectal tumours
  due to the unpleasant side-effect of intractable
  tenesmus

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REMEMBER

• More than one-third of colorectal cancer deaths
  could be avoided if people over the age of 50 had
  regular screening tests
• 92 of cases occur in people 50 and older.
• Most colorectal cancers begin as polyps.
• People who have polyps or colorectal cancer do
  not always have symptoms, so its possible to
  have either and not know it.

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REMEMBER

• Colorectal cancer is one of the most preventable
  cancers.
• Screening tests can help prevent colorectal
  cancer by finding pre-cancerous polyps so they
  can be removed before they turn into cancer.
• Screening tests can find colorectal cancer early,
  when treatment works best.
• When colorectal cancer is detected in the
  earliest stage of the disease, the survival rate
  is 96.
• Both men and women are at risk.
• Some people think that women are not at risk for
  colorectal cancer this isnt true.
• Anyone may develop it.

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Reference