Colon Tumours Cengiz Pata, M.D Gastroenterology Department, Yeditepe University Istanbul
“ Colon Tumours” ß Benign%.....Malign
Pathogenesis of Progression from Adenoma to Carcinoma Adenoma Neoplastic transformation of one cell ! Mutation APC, DCC, k, RAS Deletion 5q, 17b Activation c, myc MILD MODERATE SEVERE DYSPLASIA > 2 cm – Villous components Malignancy
Road of carcinoma
Benign Tumours = POLYPS (mostly) but may be malign ! Mucosal protrusions (= projections) into the lumen of the GI – tract.
Premalign disease of the colon Polyps Hereditary and nonhereditary polyposis syndrome Hereditary nonpolyposis syndrome İnflamatuar bowel disease
The Polyposis Syndrom’s Ú Rarely single Ú Often multiple Ú > 100 Polyps = Polyposis
Classification “ There is no unique classification “ FORM SIZE HISTOLOGY DYSPLASIA (Degree !) Hereditary X Non-hereditary NEOPLASTIC X NON-NEOPLASTIC
FORM Sessile (broad based) Pedunculated (stalk) Semi-pedunculated
SIZE + (correlation to Ca-Risk) < 1 cm ( 1 - 2 %) 1-2 cm ( 10 %) > 2 cm ( 40 - 50 %)
HISTOLOGY Tubular : inf. > 75 % in Histology is from a complex network of branching adenomatous architecture Villous : > 75 % in Histology front like surface Tubulo-villous : 50 : 50 % (not easy to distinguish)
Tubulo-adenoma
DYSPLASIA (= DEGREE) Mild: 5 % Moderate: 20% Severe: > 30 %
Polyposis Syndrome Hereditary Non-hereditary FAP · Gardner Syndrome · Turcot Syndrome PEUTZ-JEGHERS Syndrome JUVENILE (Fam) POLYPOSİS COWDEN Syndrome Non-hereditary CRONKHITE – CANADA Syndrome HYPERPLASTIC (= METAPLASTIC) INFLAMMATORY
EASY – SIMPLIFIED CLASSIFICATION NEOPLASTIC Adenomas Carcinomas NON-NEOPLASTIC Hamartomatous Hyperplastic Juvenile Inflammatory
More Simplified Classification · Four main types A ) Adenomas B ) Hamartomatous C ) Hyperplastic D ) Inflammatory · Rare Types Lipoma Fibroma Neurofibroma Leiomyoma Nodular Lymphoid Hyperplasia
Symptoms Most cases are asymptomatic Bleeding (increases with increased polyp size) Abdominal discomfort (rare) Obstruction
Diagnosis Barium-studies Endoscopically (Endoscopy is preferred polypectomy histologic examination
Hereditary Polyposis Syndromes
TYP LOCATION GENE TICS HISTO ASSOC. FINDINGS Ca-Risk Familial Juvenile TYP LOCATION GENE TICS HISTO ASSOC. FINDINGS Ca-Risk Familial Juvenile Polyposis Colon rectum AD Ham. ( - ) 8-10 % Peutz-Jeghers Syndrome Stomach, small bowel Pigmen tation 2-3% Adenoma -tous Stomach CHRP > 90 %
TYPES OF FAP GARDNER S. + Osteoma, Fibroma, Lipoma +Epidermoid-cysts TURCOT S. + Glio-, and Medulloblastoma AAPL (= before hereditary flat Adenomas) = (Attenuated Adenomatous P.) High Grade Dysplasia 5. Deka Ca Risk > 100% !
FAP ve Gardner S
Peutz-Jeghers Syndrome Recent findings GIT + Pigmentation Mouth Hands Feet Tumours : ovarian testis
Peutz Jeghers S.
Peutz Jeghers S.
Cronkhite-Canada Syndrome Acquired, nonfamilial Middle aged adults Hamartomas + Adenomas Stomach, small bowel, colon Associated findings : Alopecia cutaneous pigmentation dystrophic nails Diarrhoea Weight loss Abdominal pain Ca-Risk 5%
MANAGEMENT Tubular or Villous Other Colorectal polyp Tubular or Villous Other Tubulovillous < 1 cm > 1 cm no investigation < 5 polyps > 5 polyps in total Repeat in 1 year Repeat in 3 years All clear Repeat in 5 years
Polypectomy Operation Size < 1 cm < 2-3 cm Total < 5 polyps FAP : Prophylactic Colectomy !
Colorectal Cancer POLYP DYSPLASIA CANCER sequence is now generally accepted
Colorectal Cancer Second most common cancer in USA , Germany, UK, France ! After age 40 to age 80 the incidence doubles !!!
Colon Ca
RISC FACTORS Low-fiber, high fat diet Age > 40 Personal History : Colorectal adenomas Family History : Polyps Syndromes Inflammatory Bowel Disease ( CD, UC) Genital tract cancer in women Lynch Syndrome : Hereditary Nonpolypose Colon Carcinoma (HNPCC)
Lynch Syndrome : Hereditary Nonpolyposis Colon Carcinoma (HNPCC) Autosomal dominant Amsterdam criteria:3,2,1 rules (3 relative, 2 generation,1 person<50 DNA mismatch repair 6% of colorectal carcinoma Typ 2:Endometrium, stomach, hepatobiliary Ca HMSA %60 (+)
Symptoms Bleeding (Gross or occult) Change in bowel habit ; constipation, diarrhoea, decreased caliber of stool Anemia Weight loss Anorexia
Classification/Localization Rectum 60% Sigma 20% Rest colon 20%
Most Common Presentation Left sided : Bleeding Obstruction Diarrhoea Right sided : Fatique Weakness Occult blood loss Obstruction (late)
Staging - Systems TNM : Tumor / Nodes / Metastasis UICC : Union Internationale Contra Le Cancer ASTLER-COLLER : DEPTH OF İNVASİON DUKE + Lymph node metastasis
T1s No Mo Carcinoma in situ (Basal membrane intact) I a Dukes A T1 No Mo Tumor involves mucosa+submucosa I b T2 No Mo Tumor invades to muscularis propria (but not true it !!!) II Dukes B1 T3No Mo Tumor penetrates through the bowel wall Dukes B2 T4 No Mo Tumor involves viscerales peritoneum III Dukes C Tany N1-2 Mo + Regional positive lymph nodes IV Dukes D Tany Nany M1 Distant metastatic spread
Colon Ca-Survi
Prognosis by DUKE’s Staging 5 year survival rate : A : 80% B1 : 65% B2 : 43% C1 : 53% C2 : 15% D : 0%
Negative Prognostic Factors High-grade tumor Obstruction Perforation
Diagnostic Procedures and Presurgical Evaluation Laboratory : CEA, CA 19-9 TBC, Liver profile Colonoscopy Radiographs Detailed History (including family history) Physical examination (including breast+pelvic ovary+endometrium)
Therapy For cure in Duke’s A, B, C For palliation in Duke’s D Surgical Adjuvant Chemotherapy ( 5-FU / Folinasid) Palliative ( Stenosis anus-praeterminalis)
SURGİCAL Radical tumor-resection + regional lymph node extripation Colon Hemicolectomy Sigma Transversum > resection Rectum Distance “Linea ANOCUTANEA “ cure + maintanence of fecal continence
SCREENING of Patients After age 40 annual rectal examination Annual fecal occult blood test every year after age 50 After age 50 Sigmoidoscopy every 5 years, colonoscopy every ten years Today: colonoscopy every 5 year after 50 years
Follow up in patients with positive family history
HNPCC’ da İzlem
Ulcerative colitis following