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home - Colon - Colorectal and Anal Cancer - Colon Cancer Prognosis Written by Dr Sebastian Zeki

Knows the pathology of benign and malignant tumours of the colon
and rectum
Has awareness of the molecular genetics of colorectal
carcinogenesis and the adenoma-carcinoma sequence
Knows the range of predisposing conditions including inherited
syndromes and acquired colonic diseases
Knows the range of clinical presentation and the means of
diagnosis, investigation, management and follow-up
Knows the strategy for prevention including procedures for

Uses clinical assessment and selects investigations to reach a rapid
conclusion as to whether a patient might have colorectal cancer and
arranges timely investigation.
Refers the patient to the multi-disciplinary team CbD, mini-CEX,

Shows ability to react to possible diagnosis of malignancy in a timely

Communicates with patient and family in a sympathetic and
understanding manner, explains next steps, involves other health
professionals (including the GP) as appropriate

Colon Cancer Prognosis

Cell surface moleculesClass I or II HLA molecules ;CA 19-9 and CA 72-4 Sialyl Lex or sialosyl-Tn; Urokinase-type plasminogen activator (uPA) and plasminogen activator inhibitor 2 (PAI-2); Glycoprotein 72; P-glycoprotein (MDR gene product); MUC-1 mucin; E-cadherin, integrins, type IV collagen, gelatinase B (MMP-9), laminin, and tenascin All other molecular markers : Tumour suppressor genes (eg TP53) Oncogenes (K-ras; c-myc) Apoptosis/cell suicide-related genes (bcl-2;BAX;Apoptosis protease activating factor-1) DNA synthesis-related genes (thymidylate synthetase; thymi-dine phosphorylase) Growth factors/growth factor receptor genes (TGFa; TGFb; HER2 [c-erbB-2]; EGF-R) Cyclins/cyclin dependent kinase inhibitor genes (p27; p21) Angiogenesis-related genes (vascular endothelial growth factor [VEGF]) Adhesion molecule/glycoprotein genes (CD44; E-cadherin [CDH1]; sialo-Tn antigen) Matrix metalloproteinases and their inhibitors (MMPs; urokinase-type plasminogen activator) Metastasis suppressor genes (nm23-H1) MicroRNA overexpression Epigenetic aberrations eg meth-ylation levels Category III factors DNA content.All other molecular markers.Microvessel density.Cell surface molecules.Peritumoural fibrosis and inflammatory response.Focal neuroendo differentiation.Proliferative activity. Category IIA factors:Tumour grade.Circumferential (radial) margins.Residual tumour following neoadjuvant Category IIB factors: Histologic type.Microsatellite instability.18q deletions.Tumour border. CEA (CEA) Ways to detect serosal (peritoneal) involve-ment by tumour:-The presence of a mesothelial inflammatory and/or hyperplastic reaction with tumour close to the serosal surface.-The tumour is present at the serosal surface with an inflammatory reaction, mesothelial hyperplasia, and/or erosion or ulceration.There are free tumour cells on the serosal surface within the peritoneum with ulceration of the visceral perito-neum Regional nodesNeed to have 12 nodes retrieved.>4 positive nodes are >2x likely to die from CRC than those with1-3.Fat clearing can increase detection of nodal micro-metastases. Nodal micrometastasesMicrometastases are histologically confirmed tumour focus ≤0.2 mm and >0.02 mm =pN0.Isolated tumour cells (ITCs) are single tumour cells/small clusters of tumour of ≤0.02mm =pNo(i+).Tumour that is detected only by special molecular techniques is described as pN0 (mol+).Micrometastases detection may result in upstaging of up to 50 % of patients with CRC who have histologically negative nodes, depending upon the pT category . Vascular invasionTumour invasion into veins or small non-muscularized vessels that may represent either post-capillary lymphatics or venules is an important prognostic determi-nant. Residual tumour It is an adverse prognostic factor. Serum CEA Category I factors:Local extent of tumour.Regional nodes.Nodal micrometastases.Vascular invasion.Residual tumour.Serum CEA. Colorectal Cancer Prognosis Neuroendocrine Neuroendocrine Incidence of CRCThe lifetime CRC incidence average is 5% (90 % > 50yrs old).Right sided CRC is becoming more common (esp caecal).The highest rate is in the developed world. I IIA IIB IIIA IIIB IIIC IV 93 % 85 % 72 % 83 % 64 % 44 % 8 % Stage vs 5 year survival MortalityOverall 5 yr survival: 61 %. Written by Dr Sebastian Zeki : Preoperative CEA >5.0 ng/mL

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