pierluigi pilati chirurgia generale padova
TRANSCRIPT
I TUMORI DI INTERESSE ASSICURATIVO
I TUMORI DEL COLON RETTO
Pierluigi PilatiChirurgia Generale
ULSS 16Padova
Siegal, CA Cancer J Clin 2014
Colorectal cancer
EPIDEMIOLOGY
→ 1,2 million new cancer cases per year (413.000 cases/year in Europe)
→ Median incidence in Italy: 88/100.000 (males); 70/100.000 (females); that value increases consensually with age, particularly in 50-60 years old patients
Colorectal cancer
EPIDEMIOLOGY
Colorectal cancer
EPIDEMIOLOGY
• > in Industrialized countries, but rapidly in less-developed nations that adopt features of a Western lifestyle
• Immigrants in Industrialized countries have an higher incidence compared to residents remaining in their native countries
DeVita, Cancer 2011
Colorectal cancer
EPIDEMIOLOGY
Colorectal cancer
BIOLOGY
The genetic basis of CRC is best appreciated in light of the adenoma-carcinoma sequence and the premise that CRCs arise from benign precursor polyps
The progression is slow (5-10 yrs)
Most frequent molecular alterations in multiple genes that cause colorectal cancer
POLYP
Macroscopic protrusion of the colonic mucosa into the bowel lumen
NEOPLASTIC POLYPS
BENIGN MALIGNANT
Adenomatous polyp Carcinoma in situ
-tubular Invasive carcinoma
-tubular-villous Polypoid carcinoma
-villous
NON NEOPLASTIC POLYPS
Hyperplastic polyps
Juvenile polyps
Peutz-Jeghers
Infiammatory polyps
RISK OF MALIGNANT DEGENERATION
HISTOLOGICAL PATTERN DIMENSION
Adenomatous polyp <1 CM 1%
-tubular 5% 1-2 CM 10%
-tubular-villous 20% >2 CM 20%
-villous 40%
Colorectal cancer
BIOLOGY
Pedunculated (with stalk) polyps can be resected with application of cautery through a snare localized around the polyp stalk.
Endoscopic polypectomy
Colorectal cancer
Some sessile polyps require special techniques. Saline is injected into the submucosa area in order to elevate the polyp and facilitate removal by snare.
Colorectal cancer
Endoscopic polypectomy
Colorectal cancer
ENDOSCOPIC TREATEMENT
• Polypectomy is radical if
• pTIS
• T1
• Free margin
• No lymphovascular invasion
• G1
• Endoscopic follow-up is necessary
Colorectal cancer
ETIOLOGY
DeVita, Cancer 2011
Colorectal cancer
ETIOLOGY
DeVita, Cancer 2011
INCREASED RISK DECREASED RISK
Inflammatory bowel disease Antioxidant vitaminconsumption
Diabetes Consumption of fresh fruit and vegetables
Obesity Use of nonsteroidal antiinflammatory drugs
High red meat consumption High calcium diet
Overcooked red meat consumption
High fiber diet
High saturated fat consumption
Excess alchol consumption
Sedentary lifestyle
Cigarette smoking
Colorectal cancer
ETIOLOGY
DeVita, Cancer 2011
Colorectal cancer
COLO RECTAL CANCER RISK: FAMILIAL HISTORY
DeVita, Cancer 2011
5%
Colorectal cancer
COLO RECTAL CANCER RISK
DeVita, Cancer 2011
5%5%
INFLAMMATORY BOWEL DISEASEPersonal history
Colorectal cancer
the risk of CRC begins to increase 8 or 10 years after the establishment of diagnosis
screening starting 8-10 yr after onset of symptoms of pancolitis
Colonscopy every 1-2 yrs If low grade or high grade dysplasia: surgical consultation for
resection
Colorectal cancer
ETIOLOGY
DeVita, Cancer 2011
Colorectal cancer
COLO RECTAL CANCER RISK: FAMILIAL HISTORY
DeVita, Cancer 2011
5%
Is the most common of the recognized inherited colorectal cancer syndromes
Autosomal dominant disorder, involved mutation of DNA mismatch repair genes (MMR): MSH2, MLH1, MSH6, PMS1 e PMS2
The lifetime risk of cancer in HNPCC is 80% for colorectal cancer (usually in the third and fourth decades of life)
Familial Colorectal cancer
Hereditary Non-Polyposys Colorectal Cancer (HNPCC)
Familial Colorectal cancer
Hereditary Non-Polyposys Colorectal Cancer (HNPCC)
Mutation of MMR genes → MSI (mycrosatellite instability)
Approximately 60% of germline mutations in HNPCC are found
Clinical diagnosis
HNPCC is defined classically by the modified Amsterdam Criteria
Familial Colorectal cancer
Hereditary Non-Polyposys Colorectal Cancer (HNPCC)
Clinical diagnosis
Familial Colorectal cancer
Hereditary Non-Polyposys Colon Cancer (HNPCC)
Patients with CRC who should undergo testing for MSI
(Bethesda criteria):
Individuals with CRC Cancer in families that meet Amsterdam criteria
Individuals with two HNPCC-related cancers
Individuals with CRC cancer and a first degree relative with colorectal cancer and/or HNPCC-related extracolonic cancer and/or colorectal adenoma: one cancer before age 45 and adenoma before age 40
Individuals with CRC cancer or endometrial cancer before age 50
Individuals with Right-sided CRC cancer with an undifferentiated pattern on histopathology before age 45
Individuals with Signet-ring cell type colorectal cancer before age 45
Individuals with Adenomas diagnosed at age < 40 years
• HNPCC pts with CCR: colectomy (ileo-rectal anastomosis )
• HNPCC mutation found: colonscopy every 1-3 yrs (starting 20-25 yrs)
• Female mutation found: pelvic ultrasound annually (starting 25-35 yrs)
Familial Colorectal cancer
Hereditary Non-Polyposys Colon Cancer (HNPCC)
Patient management
• Men and women at risk for HNPCC need examinations of the entire colon (colonscopy).
• Women at risk should also have yearly endometrial and ovarian screening.
Colorectal cancer
COLO RECTAL CANCER RISK
De Vita, Cancer 2011
Familial Adenomatous Polyposis (FAP)
• FAP is an inherited condition that primarily affects the gastrointestinal tract.
• Is caused by a mutation on chromosome 5 gene APC (“Adenomatous Polyposis Coli”)
• This disorder leads to hundreds or thousands of colonic polyps that develop in patients in their teens to 30s
• If the colon is not surgically removed 100% of patients progress to colorectal cancer
Familial Colorectal cancer
• Benign conditions (congenital hypertrophy of the retinal pigment epithelium, mandibular osteomas, supernumerary teeth, epidermal cysts, adrenal cortical adenomas, desmoid tumors)
• Malignant conditions (thyroid tumors, gastric-small intestinal polyps with a 5% to 10% risk of duodenal and/or ampullary adenocarcinoma, and brain tumors)
EXTRACOLONIC MANIFESTATIONS
Familial Colorectal cancer
Familial Adenomatous Polyposis (FAP)
Genetic counseling is available and recommended for individuals with suspected
FAP and for their family members.
Familial Colorectal cancer
Familial Adenomatous Polyposis (FAP)PATIENT MANAGEMENT
ASCO guidelines 2012
APC GENE TEST AT 10-12 YEARS
How identificate a persons at high genetic risk of CRC who should undergo genetic testing??
1- history who satisfied Bethesda Criteria (HNPCC ?)
2- patient with suspected or diagnosed intestinal polyposis (FAP?)
Clinical criteria
Familial Colorectal cancer
Right colon
Growing and ulcerated neoplasia
Anemia
Palpable mass
Left colon
Infiltrating neoplasia
Bowel habit alteration
Blood in the stool
Obstruction
Colorectal cancer
LOCATION AND SYMPTOMS
Occult bleeding 75%
Rectal bleeding 55%
Anemia 55%
Abdominal pain 50%
Weight loss 40%
Constipation and anorexia 25%
Diarrhea 20%
Nausea and vomiting 20%
Tenesmus 10%
Colorectal cancer
SYMPTOMS AT DIAGNOSIS
• Massive bleeding rare
• Obstruction left colon
• Perforation
– neoplasia
– caecum diastatic perforation
• Invasion or compression of adjacent structures
Colorectal cancer
COMPLICATIONS
Colorectal cancer
DIAGNOSIS
Personal history
Colorectal cancer
DIAGNOSIS
Personal history
Colorectal cancer
DIAGNOSISPersonal history
Colonoscopy
Ca in situ
Ca ulcerato
Carcinoma vegetante
Colorectal cancer
DIAGNOSIS
Growing neoplasia
Stenotic neoplasia
Double contrast barium enema
Colorectal cancer
DIAGNOSIS
→ 15 - 50% of patients will develop metastatic disease by these
pathways:
Loco-regional
Blood circulation
Colorectal cancer
DISSEMINATION
CONTIGUITY LIMPHATIC BLOOD
Eco
Thorax-abdominal CT scan
Pelvi MRI
CEA (Prognostic value )
Colorectal cancer
STAGING
INTRAOPERATIVE ULTRASOUND
Colorectal cancer
STAGING
10-20%:identify liver undiagnosed liver mts change the surgical strategy
1. to remove en block the neoplastic mass and the involved structure, with at least 5 cm of “neoplastic-free” colon before and after the tumor
2. to remove locoregional lymph nodes (> 12 lymph nodes)
Principles of Oncologic Surgery
Colorectal cancer
TREATEMENT
Right Hemicolectomy
Right Hemicolectomy Extended Right Hemicolectomy
Resection of transverseLeft Hemicolectomy and sigmoid
colon resection
Colorectal cancer
SURGERY
Rectosigmoid resection combined with hepatic resection (segment III) for metastasis
SURGERYColorectal cancer
LAPAROSCOPIC SURGERY FOR COLORECTAL CANCER
Colorectal cancer
N Engl J Med 2004;350:2050-9
Randomized Trial on 872 patients
N Engl J Med 2004;350,2050-2059
Comparison of laparoscopically assisted and open colectomy for COLON cancer: randomized trial on 872 pts (COST trial).
Colorectal cancer
TREATEMENT
N Engl J Med. 2004;350;2050-2059
Outcomes: morbility and mortality
Colorectal cancer
TREATEMENT
Outcomes pain and hospital stay
N Engl J Med. 2004;350,2050-2059
Colorectal cancer
TREATEMENT
Colorectal cancer
TNM STAGE
The TNM system is one of the most widely used cancer staging systems. This system has been accepted by the Union for International Cancer Control (UICC) and the American Joint Committee on Cancer (AJCC).
The TNM system is based on the size and/or extent (reach) of the primary tumor (T), the amount of spread to nearby lymph nodes (N), and the presence of metastasis (M)
Extended primary tumor (T3/4)
Regional lymph nodes involved (N+)
Presence of metastases (M+)
Colorectal cancer
TNM STAGE
WORSE PROGNOSISINCREASED RECURRENCE
DeVita, Cancer 2011
Colorectal cancer
Survival and Recurrence rate
DUKES TNM 5 - years Survival (%) Recurrence(%)Local Distant
A I 90% 5 10
B II 70-90% 10-20 20-25
C III 70-90% per T1-T2, N1 60-80% per T1-T2, N230-50% per T3-T4, N1-2
10-20 20-2530 25
35-50 40-60
D IV 10%-
DeVita, Cancer 2011
Stage
5-y
ear
Su
rviv
al
10
20
30
40
5060
70
80
90
100Localized(stage I-II)
Regional(stage III)
Distant metastases(stage IV)
Manfredi Ann Surg 2008
LIVER FAILURE DUE TO LIVER METASTASES IS THE MAJOR DETERMINANT OF SURVIVAL
Colorectal cancer
DISSEMINATION
PROGNOSTIC FACTORS
Age More advanced stage if age >40 yrs
Sympthoms More advanced stage if sympthoms
Complications Worse prognosis
Tumor morphology Advanced stage: growing > ulcerated
Vascular invasion Worse prognosis if present
Lymphatic invasion Worse prognosis if present
Perineural invasion Worse prognosis if present
Lymphocyte infiltration
Better prognosis if present
CEA Poor prognosis if preoperative > 5ng/ml
Aneuploidy Worse prognosis if present
Site Sigmoid and rectal cancer
Colorectal cancer
PROGNOSTIC FACTORS
Colorectal cancer
Dukes C: survival related number lymphonodes involved
T3…
Colorectal cancer
EPIDEMIOLOGY
Colorectal cancer
TREATEMENT
Primary prevention: preventing the developments of cancer
Secondary prevention (SCREENING):early detection of cancer
Tertiary prevention: preventing the cancer recurrence
Colorectal cancer
PREVENTION
Primary prevention:
Colorectal cancer
PREVENTION
Three categories:
1. Avoidance of noxious substances
2. Chemoprevention: ingestion of natural o synthetic substances
3. Prophylactic colectomy (genetic syndromes)
Colorectal cancer
PRIMARY PREVENTIONAvoidance of noxious substances
Red meat: eating beaf, pork o lamb > 5 times/week--> 3-fold increase RR colon cancer
Red meat
stimulates secretion of endogenous insulin
is a > source of saturated fats
Heavily browned surface or prolonged frying or grilling --> mutagenic heterocyclic amine formed from creatinine
Colorectal cancer
PRIMARY PREVENTIONAvoidance of noxious substances
Alcohol: men who drink > 2 drinks (30g) per day 2-fold increase RR colon cancer
Alcohol:
Reduce folate levels
Antagonize metabolism of metyl groups, contributing to abnormal DNA repair
Suppress tumor immune surveillance
Alter composition of bile acids
Induce cit P450 to activate hepatic carcinogenesis
Colorectal cancer
PRIMARY PREVENTIONAvoidance of noxious substances
Tobacco:
+ 38% RR for > 40 cigarettes/day
+ 20% RR for > 40 yrs duration
+ 51% RR for increment > 60 pack-yrs
- 4% RR for delay of 10 yrs in smoking initiation
- Association stronger for rectal than colon cancer
Mechanism → Release carcinogenic compounds: aromatic amines, nitrosamines, heterocyclic amines, polynuclear aromatic hydrocarbons
Colorectal cancer
PRIMARY PREVENTIONAvoidance of noxious substances
Obesity:
BMI <23 Kg/m2 RR1
BMI 23-24.9 RR +14%
BMI 25-27.4 RR +19%
BMI 27.5-29.9 RR +24%
BMI 30 RR +41%
Ning, Obes Rev 2009
Increase in insulin resistance → stimulation of insulin secretion → mitogenic properties of hyperinsulinemia
Central adiposity appears to more affect the risk of colorectal cancer
Fiber:
European population (EPIC study): -40%
relative risck (RR) for individuals
USA population: no significant
Since 1998 mandatory in USA fortification
with folate of flour and breakfast cereals Bingham, Lancet 2003
Park, JAMA 2005
Colorectal cancer
PRIMARY PREVENTIONChemoprevention
Colorectal cancer
PRIMARY PREVENTIONChemoprevention
Fish and poultry:
reduced risk of colon cancer and adenoma
good sources of methionine, that improve the regulation of DNA methylation
High in n-3 fatty acids (specially fish), that reduce inflammation, disrupt acitivity of nf-kB and COX-2
Calcium:
22% risk reduction of CRC
Most of risk reduction with intakes of 700 to 800 mg/day
Mechanism:
Binding to toxic secondary bile acids and ionized fatty acids → form insoluble soaps in colon lumen
Directly reducing proliferation and inducing apoptosis in the colonic mucosa
Colorectal cancer
PRIMARY PREVENTIONChemoprevention
Folate:
Folate deficiency induce p53 mutations
Low dietary folate associated with RR CRC
RCT: folic acid supplementation not significative, because 10 yrs required for any preventative effects
Colorectal cancer
PRIMARY PREVENTIONChemoprevention
Aspirin and NSAID:
Short term use of aspirine reduce risk af adenoma recurrence
Cole, JNCI 2009
Colorectal cancer
PRIMARY PREVENTIONChemoprevention
Age-specific incidence of CRC per 100.000/yrs according to modificable risk factors
Chan, Gastroenterology 2010Brenner, Lancet 2014
Colorectal cancer
PRIMARY PREVENTION
Primary prevention: preventing the developments of cancer
Secondary prevention: early detection of cancer
Tertiary prevention: preventing the cancer recurrence
Colorectal cancer
PREVENTION
Colorectal cancer
SECONDARY PREVENTION SCREENING
National Comprehensive Cancer Network (NCCN) FOBT or colonoscopy or sigmoidoscopy +/-FOBT
starting at 50 yrs
European Society of Medical Oncology (ESMO) Faecal occult blood test (FOBT) annual for people aged 50-74 yrs
Associazione italiana di Oncologia Medica (AIOM) Faecal occult blood test (FOBT) annual or sigmoidoscopy every 5
yrs or colonoscopy every 10yrs for people starting at 50 yrs
Colorectal cancer
SECONDARY PREVENTIONGUIDELINES
FOBT (Fecal Occult BloodTest)
meta-analysis of RCTs demonstrated a reduction in mortality of the intervention group of 16% (RR 0.84)
Sensibility for adenomas 1 cm 16-33%
Specificity for adenomas 1 cm 94-98%
Sensibility for CRC 6-46%
Specificity for CRC 80-89%
Mandek, NEJM 2000
Burch, J Med Scren 2007
Whitlock, Ann Int Med 2008
Colorectal cancer
SECONDARY PREVENTION
It also may not detect precancerouslesions or early stage adenomas as bleeding may not bereadily detectable in the presence of these conditions
- RCT: reduction in CRC incidence and mortality of the intervention group of 31% and 38%
- Sensibility for CRC 58-86%--> These variations are likely accounted for by the differences in examiners’experience and skills, and by the risk of proximal lesions in the unexplored colon.
- When sigmoidoscopy detects a carcinoma or an adenoma of >10 mm, conducting a complete study of the colon is mandatory given the major incidence of synchronic lesions proximal to the tract explored. It has been estimated that 5–16% of colonoscopies are performed after sigmoidoscopy
Segnan, JNCI 2011Weissfiled, JNCI 2005
Colorectal cancer
SECONDARY PREVENTIONSigmoidoscopy: examination of the mucous surface with a flexible endoscope uP to 60 cm from the anal verge
Colonoscopy:
this test not only favors CRC detection in early stages but also reduces the incidence of CRC as it identifies and resects polyps
For each 1% in colonoscopies → 3% reduction in mortality rates
A colonoscopy in the previous 10 yrs is associated with a 59% reduction CRC incidence
Several cohort studies demonstrate that polyp removal lower incidence of CRC by 76-90%
Rex. Gastr Endoscop 2013
Tarraga Lopez, Clin Med Ins Gastro 2014
Colorectal cancer
SECONDARY PREVENTION
Colonoscopy 0.01-0.05 % hemorrhages
0.01-0.05% perforations
0.03% deaths
low-residue diet on the days before the test
lassative
Examination takes 20-40 min, most people fully recovered afterone hour
Baxter, Ann Int Med 2009
Tarraga Lopez, Clin Med Ins Gastro 2014
Colorectal cancer
SECONDARY PREVENTION
Other screnning tools:
FOBT + sigmoidoscopy: 2 RCTs concluded that not better than sigmoidoscopy Colongraphy CT:
No RCT to assess the efficacy Similar rate in detecting polyps 10 mm and advanced CRC than colonoscopy If positive, colonoscopy mandatory 0.05% symptomatic colon perforations
Fecal DNA detection: Higher sensitivity than FOBT to detect CRC and adenomas High cost and cost-effective ratio No RCT to evaluate the efficacy in terms of incidence and mortality
Sosna, Am J Roentgenol 2008
Colorectal cancer
SECONDARY PREVENTION
All these screening tolls have been demostrated not equivalent to colonoscopy
COST/EFFECTIVENESS
All studies consistently found that CRC screening is cost-effective compared with no screening, for each of the screening strategies
The incremental CE ratios for the different strategies ranged from $1200 per life-year saved (SIG once at 55 years of age) to $92,900 per life-year saved
(RFOBT plus SIG every 5 years).
Frazier, JAMA 2000
Lansdorp-Vogelaar, Epid Reviews 2011
Cruzado, Best Pract Res Clin Gastr 2013
Colorectal cancer
SECONDARY PREVENTION
Lansdorp-Vogelaar, Epid Reviews 2011
Colorectal cancer
SECONDARY PREVENTION
Colorectal cancer
SECONDARY PREVENTION
Among the 1-time screening alternatives,
COLONOSCOPY was the most effective
option with a lifetime reduction in CRC
mortality of 31% and an incremental CE
ratio of $22,400 per life-year saved-
Frazier, JAMA 2000
Colorectal cancer
SECONDARY PREVENTION
Colorectal cancer
SECONDARY PREVENTION
→ As of 2008, the basic screening modalities remain remarkably similar to those used in 1980 when the original guideline was issued, even when taking into account the development of newer technology in subsequent years
→ In an ideal world, the first line screening should be performed to identify a high risk segment of the population and then use a more extensive test (colonoscopy) on this sub group to reduce incidence of advanced diseases
Colorectal cancer
SECONDARY PREVENTION
Primary prevention: preventing the developments of cancer
Secondary prevention: halting the progression from polyp to cancer
Tertiary prevention: preventing the cancer
recurrence
Colorectal cancer
PREVENTION
NCCN 2014
PE, CEA every 3-6 mo for 2yrs, than 6 mo for 5 yrs
CT total body annually for 5 yrs
Colonoscopy: after 1 yr, if no preop for obstrucing lesions in 3-6 mo
If no polyp > 1 cm, no HG dysplasia : repeat in 3yrs, than every 5 yrs
If advanced adenoma: repeat in 1 yr
Colorectal cancer
TERTIARY PREVENTION
MULTIDISCIPLINARY TEAM MEETING (MDT)
• Surgeon
• Medical oncologist
• Radiation oncologist
• Radiologist
• Pathologist
• Internal medicine
AIM
improve patient outcome and guidelines adherence
Meagher, ANZ J Surg 2013
MacDermid, Col Dis 2009
MDT status is an indipendent predictor of SV (P=0.044)
PRIMARY PREVENTION
SECONDARYPREVENTION
MULTIDISCIPLINARY TEAM
i
INCIDENCE
MORTALITYIMPROVE SURGICAL
TECHNIQUE
Pilli’s group
THE WAR IS NOT WIN YETBUT THE WAY IS RIGHT
Virtual colonoscopy
Colorectal cancer
DIAGNOSIS
Chan, Gastroenterology 2010
Colorectal cancer
SECONDARY PREVENTION
Colorectal cancer
ETIOLOGY
DeVita, Cancer 2011
Colorectal cancer
ETIOLOGY
DeVita, Cancer 2011
Colorectal cancer
TNM STAGE
DUKES TNM 5-YEAR SURVIVAL RECURRENCEL D
A I 90% 5 10
B II 70-90% 10-20 20-25
C III 70-90% se T1/2 N160-80% se T1/2 N230-50% se T3/4 N1
10-20 20-25• 2535-50 40-60
D IV 10%
Which surgeon?
Nathan, Ann Surg Oncol 2012
Which center?
Goyer, Clinics and Research in Hepatology and Gastroenterology 2013
Colorectal cancer
TREATMENT
51 PATIENTS CURED!!!
Personal history of IBD
Colorectal cancerPersonal history of IBD
(Crohn's disease, ulcerative colitis)
SCRRENING• Can prevent many deaths• More treatable stage• Can detect and remove nonmalignant
precuros lesion
Colorectal cancer
SECONDARY PREVENTIONGUIDELINES
Tumor residual (R)
Colorectal cancer
TREATEMENT
TUMORAL RESIDUAL
R0 Absence of tumor
R1 Microscopic residual
Sigmoidoscopy
0.03 % hemorrhages
0.015% perforations
0.0025% deaths
Case-control studies estimate a protector effect over a period of 9-10 yrs
Screening every 5yrs because sensitivity < colonscopy, less preparation and variability in examiners’experience
The results of an RCT indicate that 14% of individuals complain of pain (which is strong in 1%) after having been submitted to sigmoidoscopy. If we compare it to colonoscopy, lack of sedation is associated with more discomfort and less adhesion to future sigmoidoscopies
Senore, Dis Colon Rectum 2004Tarraga Lopez, Clin Med Ins Gastro 2014
Colorectal cancer
SECONDARY PREVENTION
MULTIDISCIPLINARY TEAM MEETING
Meagher, ANZ J Surg 2013
MacDermid, Col Dis 2009
• Second review radiology investigation: incorrect reports and new findings in 2-20%
• 105 papers in literature that confirm MDT decrease the rate of Circumferential Resection Margins in rectal cancer (1% vs 25%)
• MDT status is an indipendent predictor of SV (P=0.044)
• More patients were given CT in the MDT group (p=0.0023)
Colorectal cancer
Survival e recurrence rate
DUKES TNM 5 Years survival(%) Recurrence (%)L D
A I 90% 5 10
B II 70-90% 10-20 20-25
C III 70-90% per T1-T2, N1 60-80% per T1-T2, N230-50% per T3-T4, N1-2
10-20 20-2530 25
35-50 40-60
PRIMARY PREVENTION
SECONDARYPREVENTION
MULTIDISCIPLINARY TEAM
i
INCIDENCE
MORTALITY
→ 15 - 50% of patients will develop metastatic disease by these
pathways:
Loco-regional
Blood circulation
Colorectal cancer
DISSEMINATION
CONTIGUITY LIMPHATIC BLOOD
Colorectal cancer
ETIOLOGY
DeVita, Cancer 2011
INCREASED RISK DECREASED RISK
Inflammatory bowel disease Antioxidant vitamin consumption
Diabetes Consumption of fresh fruit and vegetables
Obesity Use of nonsteroidal antiinflammatory drugs
High red meat consumption High calcium diet
Overcooked red meat consumption High fiber diet
High saturated fat consumption
Excess alchol consumption
Sedentary lifestyle
Cigarette smoking