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Colorectal Carcinoma- An Overview

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1 Colorectal Carcinoma- An Overview
Dr C. L Chaw ST4, Clinical Oncology Tayside

2 Colorectal Cancer (CRC)
3rd most common form of cancer and the 3rd leading cause of death in the Western World. Annual incidence in UK -54/ , and new cases per year,>16000 deaths per year, making it the 2nd most common cause of cancer death in UK Peak incidence ages: yrs old ♂:♀ ratio for colonic and rectal cancer is 2:3 and 2:1 Colonic cancer ( 60%) is more common> than rectal cancer (40%)

3 Risk Factors & Aetioloy
Environmental Factors Genetic The aetiology is complex, involving interplay of environmental and genetic factors. These factors conspire to change the normal mucosa to a premalignant adenomatous polyp to a frank colorectal cancer over the course of many years

4 Environmental Factors
Diet Total calories – obesity and ↑ BMI (25-30kg/m2 )↑risk of CRC ↑ consumption of Meat (red meat) /Fat (saturated) /Protein - ↑ risk of CRC High Fiber - ↓ risk of CRC Vegetables/ Fruits – Protective effects due to presence of antioxidants Lifestyles Physical inactivity -↑ risk of CRC Cigarette smoking -↑ risk of CRC ↑ alcohol consumption -↑ risk of CRC

5 Genetics/Inherited predisposition
+ve family history of CRC, esp in 1st degree relative ≤ 40 yrs old --↑ risk of CRC 15% of CRC are familial in origins FAP (Familial Adenomatous Polyposis) HNPCC (Hereditary Nonpolyposis Colorectal Cancer) /Lynch Syndrome

6 FAP Autosomal Dominant, mutation of APC gene (5q21) 1% of all CRC
Development of hundred to thousands of polyps in patients in their teen-30s, almost 100% progress to CRC if not surgically resected Extracolonic features: benign or malignant Benign:mandibular osteoma, epidermal cyst Gardner’s syndrome- desmoid tumour, osteoma and adematous polyps Malignant: thyroid CA, brain tumours (Turcot’s Syndrome), duodenal and ampullary CA.

7 HNPCC Autosomal Dominant, mutation of mismatch repair genes – hMLH1,hMLH2, hMSH6, hPMS1 3% of all CRC Presence of up 100 colonic polyps ( hence nonpolyposis), preferentially in right or proximal colon Type I and Type II (distinguished by extracolonic tumours originating in stomach, small bowel, bile duct. Pelvis, ureter, uterus, bladder, ovary, skin) Mean age of developing Ca ≈40 yrs old Lifetime risk of Ca in HNPCC is ≈80% for CRC, 40% for endometrial Ca.

8 HNPCC (Amsterdam Criteria)
≥ 3 family members with CRC, one of whom is 1st degree of the other 2 2 successive affected generations 1 or more cancer diagnosed < 50 years old FAP excluded Criteria 2: ≥ 3 family members with HNPCC related cancer, one of whom is the 1st degree of the other 2 2 successive affected generation 1 or more cancer diagnosed < 50yrs old Lab testing of MSH 1&2 and PMS 1&2

9 Pathogenesis Vogelstein model Multistep to carcinoma formation
Mutation of APC gene –polyposis K-RAS (40-50%), P53, SMAD mutation DCC gene helps to initiate metastatic potential Other pathway through MSI (DNA microsatellite instability) - HNPCC

10 Features of tumour

11 Spread Adjacent organs – small/ large bowel, bladder, uterus
Transcoelomic spread- peritoneal disease Regional lymph node involvement ( 40-70%) at presentation – usually follows the supplying blood vessels– pararectal, hypogastric, pre-sacral) Haematogenous – liver ≥ lung ≥ bone and brain 25-30% patients at presentations, the tumour will have spread either locally or distant sites, and will be unsuitable for radical treatment

12 Assessment & Management:
History Presenting complaints Family history Systemic enquiries Physical examination (PR examination) Investigations Treatments

13 Signs & Symptoms Symptoms Lower GI bleeding Altered bowel habits
Abdominal pain Weight loss Loss of appetite Obstructive symptoms – vomiting, unable to pass wind, severe abdo pain

14 Signs Inspection: Jaundice, pallor , (freckles around the lip, buccal mucosal –Peutze Jeghers) Palpable abdominal / rectal mass–don’t forget about the liver –hepatomegaly – distant mets PR bleeding – fresh red ( left-sided colon/ rectum), malena (right-sided colon) Alarming signs –Abdominal distension, peritonism, rebound tenderness, tingling bowel sound – bowel obstruction, perforation. Pulmonary signs and neurological signs can sometime present if the disease is advanced.

15 Signs

16 Investigations FBC ( Iron –deficiency anaemia ) U+E
LFT ( metastatic disease ) CEA (carcinoembryonic antigen), is raised in 85% of patients with CRC, higher value associated with worse prognosis

17 Investigations AXR ( if suspicious of SBO/ BO)
Double contrast barium enema Colonoscopy with biopsy, Flexi/ rigid sigmodoscopy CT scan –Thorax, abdo USS liver - liver metastasis Pelvic MRI –particularly for rectal Ca – To asses CRM (Circumferential resection margin) Endo-anal USS to asses nodal involvement in rectal Ca

18 Investigations

19 Investigations

20 Investigations

21 Screening 50-75 years old FOB; higher false positive rate
Colonoscopy; more specific and better at picking proximal lesion.

22 Staging (TMN & Dukes ) Dukes’Stage Description Stage (AJCC) TNM A
In situ Cancer confined to submucosa or muscularis propria but not through it I Tis N0M0 T1N0M0 T2N0M0 B(1) Into but not beyond muscularis propria;no LN spread II T3N0M0 T4N0M0 B(2) Through the muscularis propria with no nodes involved C(1) Nodes positive but not apical node III Any T, N1-2, M0 C(2) Apical node positive D Metastatic IV Any T, Any N, M1

23 Prognosis ( 5-yr survival)
Stage I (Dukes A): 95% Stage II (Dukes B1/2): 70-80% Stage III (Dukes C1/2): 40% Stage IV (Dukes D): 5%

24 Management Radical/Curative Palliative Non-metastatic disease
Multimodality approaches Surgery, chemotherapy, radiotherapy Palliative Metastatic disease, inoperable disease Symptoms control

25 Management (Surgery- Curative)
Depending on site of lesions: Caecum, ascending colon, hepatic flexure – right hemicolectomy Transverse colon – extended hemicolectomy Splenic flexure, descending colon –left hemicolectomy Sigmoid colon – high anterior resection Upper rectum- anterior resection Defunctioning loop ileostomy is anastomosis <12cm from anal margin Lower rectum- Abdominal –perineal resection Total mesorectal resection- high rectum

26 Management (Chemothrapy)
Adjuvant Chemotherapy T3 disease or node positive tumours (Dukes C disease, selective in Dukes B) – 4-13% survival benefits Serosal involvement, perforated tumours, extramural vascular invasion or involvement of circumferential margin 5- Flourouracil based chemo, platinum based chemo Side effects: nausea, myelosuppression, diarrhoea, neuropathy

27 Management ( Radiotherapy )
Rectal cancer – reduce rate of local recurrence, downstaging of inoperable disease Pre-operatively or post-operatively 25Gy in 5#, 45Gy in 25# Side effects: erythema (local skin reaction), cystitis, diarrhoea, sterility, urge incotinence, bowel dysfunction

28 Management ( Palliative )
Inoperable disease, medically unfit patients Defunctiong Colostomy, Surgical/ endoscopic stenting – for obstructing lesions, aiming to improve quality of life Resection for isolated liver and pulmonary metastasis if patients are fit. Radiotherapy – palliation of local symtoms, bony pain, rectal bleeding

29 Management ( palliative )
Chemotherapy Patients selection- performance status 1-2 Aiming to improve quality of life and control of disease Improves survival by 3-6 months 5-FU based chemo, platinum based.

30 References: SIGN Guidelines no 67
Practical Clinical Oncology – Louise Hanna Cancer, Principle & Practice of Oncology – DeVita, Hellman et al

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