Colorectal Cancer: Basic Information

ALG Colorectal Cancer 393
cases of CRC; Criteria for diagnosis of sided cancers because the clinical presentation
BASIC INFORMATION HNPCC are summarized in Table 2
14. Previous endometrial or ovarian cancer,
can vary with the location.
• Right side of colon:
C
DEFINITION particularly when diagnosed at an early 1. Anemia (from chronic blood loss).
Colorectal cancer (CRC) is a neoplasm arising age 2. Abdominal pain may be present, or the
from the luminal surface of the large bowel; patient may be completely asymptomatic.
PHYSICAL FINDINGS & CLINICAL 3. Rectal bleeding is often missed because
locations include descending colon (40% to
PRESENTATION blood is mixed with feces.
42%), rectosigmoid and rectum (30% to 33%),
cecum and ascending colon (25% to 30%), and • Physical examination may be completely 4. Obstruction and constipation are unusual
transverse colon (10% to 13%). unremarkable. because of large lumen and more liquid
• Digital rectal examination can detect approxi- stools.
mately 50% of rectal cancers. • Left side of colon:
ICD-10CM CODES • Palpable abdominal masses may indicate 1. Change in bowel habits (constipation,
and Disorders
Diseases
C18 Malignant neoplasm of colon metastasis or complications of colorectal car- diarrhea, tenesmus, pencil-thin stools).
C18.2 Malignant neoplasm of colon, cinoma (abscess, intussusception, volvulus). 2. Rectal bleeding (bright red blood coating
ascending colon • Abdominal distention and tenderness are the surface of the stool).
C18.4 Malignant neoplasm of colon, suggestive of colonic obstruction. 3. Intestinal obstruction is frequent because
transverse colon • Hepatomegaly is indicative of hepatic of small lumen.
C18.6 Malignant neoplasm of colon,
descending colon
metastasis.
CLASSIFICATION (TABLE 3) AND I
C18.7 Malignant neoplasm of colon, ETIOLOGY STAGING
sigmoid colon CRC can arise through either of two mutational AJCC 8th edition classification for CRC:
C19 Malignant neoplasm of rectosigmoid pathways: Microsatellite instability or chromo- A. Confined to the mucosa-submucosa (stage I)
junction somal instability. Germline genetic mutations B. Invasion of muscularis propria (stage II)
are the basis of inherited colon cancer syn- C. Local node involvement (stage III)
EPIDEMIOLOGY & dromes; an accumulation of somatic mutations D. Distant metastasis (stage IV)
DEMOGRAPHICS in a cell is the basis of sporadic colon cancer. TNM Classification:
• Worldwide, CRC accounts for about 1.4 mil- Fig. 1 illustrates the molecular carcinogenesis
lion new cases and 700,000 deaths annually. of colon cancer. Approximately 15% of CRC lack Stage TNM Classification
The highest incidence is in North America, one or more mismatch repair enzymes (mis- I T1-2, N0, M0
Australasia, Europe, and South Korea match repair deficient [dMMR]-CRC).
IIA T3, N0, M0
• CRC is the fourth most common cancer and
IIB T4a, N0, M0
the second leading cause of cancer deaths
in the U.S. (145,600 new cases and 51,020
DIAGNOSIS IIC T4b, N0, M0
deaths for 2019). Distant metastatic disease IIIA T1-2, N1, M0;
DIFFERENTIAL DIAGNOSIS
is present in 18% to 22% of patients at time T1, N2a, M0
of diagnosis • Diverticular disease
• Strictures or adhesions IIIB T3-4a, N1, M0
• The peak incidence is in the seventh decade T2-3, N2a, M0
of life. The lifetime risk for development of • Inflammatory bowel disease (IBD)
• Infectious or inflammatory lesions T1-2, N2b, M0
CRC is 1 in 17, with 90% of cases occurring
• Arteriovenous malformations IIIC T4a, N2a, M0
after age 50 yr
• Metastatic carcinoma T3-4a, N2b, M0
• Risk factors (Table 1):
• Extrinsic masses (cysts, abscesses) T4b, N1-2, M0
1. Hereditary polyposis syndromes
2. Familial polyposis (high risk) IVA T(any), N(any), M1a
WORKUP IVB T(any), N(any), M1b
3. Gardner syndrome (high risk)
4. Turcot syndrome (high risk) The clinical presentation of colorectal malig- IVC T(any), N(any), M1c
5. Peutz-Jeghers syndrome (low to moder- nancies may consist of nonspecific symptoms
ate risk) (weight loss, anorexia, malaise) or of specific
symptoms related to mass effect or bleeding. It LABORATORY TESTS
6. Inflammatory bowel disease (IBD), both
is useful to divide colon cancer symptoms into • Positive fecal occult blood test (FOBT): Many
ulcerative colitis and Crohn disease
those usually associated with the right- or left- primary care physicians use single digital
7. Family history of “cancer family syn-
drome”
8. Heredofamilial breast cancer and colon TABLE 1 Recognized Risk Factors for Colorectal Cancer
carcinoma
Family History
9. Pelvic irradiation history
10. First-degree relatives with colorectal • Colorectal cancer (CRC)
• Inherited syndromes (e.g., familial adenomatous polyposis [FAP])
carcinoma • Racial and ethnic background (e.g., African American, Ashkenazi Jews)
11. Age >50 yr
Personal History
12. Dietary factors (diet high in fat or red
meat, alcohol use, low vegetable intake) • Age
• Male sex
13. Hereditary nonpolyposis colon cancer • Previous colonic polyps or CRC
(HNPCC): Autosomal dominant disorder • History of inflammatory bowel disease
characterized by early age of onset • Diabetes mellitus
(mean age, 44 yr) and right-sided or Lifestyle
proximal colon cancers, synchronous • Obesity
and metachronous colon cancers, muci- • High consumption of alcohol
nous and poorly differentiated colon • Diet high in red meat and fat, low in fiber
cancers; accounts for 1% to 5% of all
From Niederhuber JE: Abeloff’s clinical oncology, ed 6, Philadelphia, 2020, Elsevier.
Descargado para Diego Andres Vasquez Bracho (davb.8877@gmail.com) en Pontifical Catholic University of Ecuador de ClinicalKey.es por Elsevier en noviembre 17, 2020.
Para uso personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2020. Elsevier Inc. Todos los derechos reservados.
These proofs may contain color figures. Those figures may print black and white in the final printed book if a color print product has not been planned. The color figures will appear in color
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394 Colorectal Cancer ALG
TABLE 2 Criteria for Diagnosis of Hereditary Nonpolyposis Colon Cancer TABLE 3 World Health
(HNPCC) Organization Classification of
Colorectal Carcinoma
Amsterdam Criteria1
• At least three relatives have colorectal cancer, and all of the following are present: • Adenocarcinoma
• One is a first-degree relative (parent, sibling, or child) of the other two • Cribriform comedo-type adenocarcinoma
• At least two successive generations are involved • Medullary carcinoma
• At least one relative had colorectal cancer when he or she was younger than 50 • Micropapillary carcinoma
• Familial adenomatous polyposis has been excluded • Mucinous adenocarcinoma
• Serrated adenocarcinoma
Revised Bethesda Guidelines2
• Signet ring cell carcinoma
(Indicates tumors to select for microsatellite instability testing) • Adenosquamous carcinoma
• Colorectal cancer in a patient younger than 50 yr • Spindle cell carcinoma
• A second synchronous or metachronous colorectal cancer or cancer associated with HNPCC • Squamous cell carcinoma
• Presence of high-level microsatellite instability histologically in a patient younger than 60 yr • Undifferentiated carcinoma
• One or more first-degree relatives with either colorectal cancer or HNPCC-associated tumor diagnosed at • Neuroendocrine carcinoma (NEC):
younger than 50 yr • Large NEC
• Colorectal cancer in two or more first- or second-degree relatives with HNPCC-related tumors at any age • Small NEC
Either all of the Amsterdam criteria or one of the Bethesda criteria is used to identify an individual • Mixed adenoneuroendocrine carcinoma
at risk of HNPCC
From Niederhuber JE: Abeloff’s clinical oncology, ed 6, Phila-
• HNPCC-associated tumors include endometrial, gastric, ovarian, pancreatic, ureter, renal pelvis, biliary tract, delphia, 2020, Elsevier.
small bowel, and brain
1Vasen HF, Watson P, Mecklin JP et al: New clinical criteria for hereditary nonpolyposis colorectal cancer (HNPCC, Lynch syn- asymptomatic persons at average risk for
drome) proposed by the International Collaborative group on HNPCC. Gastroenterology 116:1453-1456, 1999.
2Umar
colorectal cancer, multitarget stool DNA test-
A, Boland CR, Terdiman JP et al: Revised Bethesda Guidelines for hereditary nonpolyposis colorectal cancer (Lynch syn-
drome) and microsatellite instability. J Natl Cancer Inst 96:261-268, 2004.
ing detects significantly more cancers than
From Niederhuber JE: Abeloff’s clinical oncology, ed 6, Philadelphia, 2020, Elsevier. FIT but has more false-positive results. High
cost and rate of false positives are the main
obstacles inhibiting broader adoption of fecal
Molecular Carcinogenesis, Colon DNA testing.
• M olecular markers including abnormal
MGMT, APC, WNT P16, KRAS, BRAF P53, DCC DNA from cancerous cells can be detected
Mutation/ Mutation/ Mutation/ in stool. FIT combined with stool DNA test
methylation/ methylation/ methylation/
rearrangement rearrangement rearrangement (FIT-DNA) has been approved by the FDA
for colorectal screening. One study showed
Low-grade High-grade that one-time FIT-DNA had a higher sen-
Wild type sitivity for detection of colorectal can-
polyps polyps
cer than one-time FIT alone (92.3% vs.
73.8%), but specificity was lower (86.6%
vs. 94.9%).1
MMR mutation MSI Lynch syndrome • Circulating methylated SEPT9 DNA: Does
CRC not reliably detect precancerous neopla-
APC mutation FAP
sia. Studies showing mortality benefit are
MUTYH mutation MAP lacking.
STK11 mutation PJS “Second hit”: • Plasma carcinoembryonic antigen (CEA) level
SMAD4 mutation JPS, HHT • Methylation is not useful for screening because it can be
• Deletion increased in nonmalignant conditions (smok-
BMPR1 mutation JPS
• Mutation, etc. ing, IBD, alcoholic liver disease). A normal
Other/unknown ??
CEA result does not exclude the diagnosis of
CRC.
Age/years IMAGING STUDIES
FIG. 1 Accumulation of molecular changes that precede colorectal carcinoma (CRC). Sporadic tumors are • Colonoscopy with biopsy (primary assess-
initiated by a serial accumulation of somatic mutations that may eventuate in CRC. The initiating event in these ment tool): The American College of
polyposes is the mutation present at birth. Second hits may include a variety of molecular changes, such as Physicians (ACP) recommends that patients
tumor suppressor gene promoter methylation, mutations, and copy number changes. Mismatch repair (MMR) should be offered a colonoscopy beginning
includes hMLH1, hMLH2, hMSH2, hPMS2, and EpCAMP genes. FAP, Familial adenomatous polyposis; HHT, at age 50, and it should be repeated every
hereditary hemorrhagic telangiectasia; JPS, juvenile polyposis syndrome; MAP, MUTYH-associated polyposis; 10 yr in average-risk patients. Screening is
MSI, microsatellite instability; PJS, Peutz-Jeghers syndrome. (From Niederhuber JE: Abeloff’s clinical oncology, recommended in African Americans begin-
ed 6, Philadelphia, 2020, Elsevier.) ning at age 45 yr. Persons with only one
first-degree relative with CRC or advanced
FOBT as their primary screening test for CRC. intact human globin protein (as opposed adenomas diagnosed at 60 yr or older may
Single FOBT has low specificity for detect- to heme) in the stool and detects more be screened as at average risk. The U.S.
ing human hemoglobin, is a poor screen- advanced adenomas than FOBT. Preventive Services Task Force guidelines
ing method for CRC (sensitivity, 4.9%), and • Fecal DNA testing is a newer screening state that screening should not be routinely
is inappropriate as the only test because method that detects colonic cells shed into recommended in persons older than 75
negative results do not decrease the odds of the fecal stream that possess specific genet- yr, and it should not be recommended at
advanced neoplasia. The American College ic or epigenetic changes. The technique has
of Gastroenterology recommends the fecal a reported sensitivity of 97% and a specificity 1Inadomi JM: Screening for colorectal neoplasia, N
immunochemical test (FIT), which measures of 90% for CRC stages I-III. In trials involving Engl J Med 376:149-156, 2017.
ALG Colorectal Cancer 395
TABLE 4 Colorectal Cancer (CRC) Screening and Surveillance Recommendations*

Indication Recommendations
C
Average risk Beginning at age 50 yr: Colonoscopy every 10 yr; Computed tomographic colonography every 5 yr; Flexible sigmoid-
oscopy every 5 yr; Double-contrast barium enema every 5 yr; Stool blood testing annually or stool; DNA testing
acceptable but not preferred
One or two first-degree relatives with CRC at Colonoscopy every 5 yr beginning at age 40 yr, or 10 yr younger than earliest diagnosis, whichever comes first
any age or adenoma at age <60 yr
Hereditary nonpolyposis CRC Genetic counseling and screening†
Colonoscopy every 1 to 2 yr beginning at age 25 yr and then yearly after age 40 yr‡
Familial adenomatous polyposis and variants Genetic counseling and testing†
Flexible sigmoidoscopy yearly beginning at puberty‡
and Disorders
Diseases
Personal history of CRC Colonoscopy within 1 yr of curative resection; repeat at 3 yr and then every 5 yr if normal
Personal history of colorectal adenoma Colonoscopy every 3 to 5 yr after removal of all index polyps
Inflammatory bowel disease Colonoscopy every 1 to 2 yr beginning after 8 yr of pancolitis or after 15 yr if only left-sided disease
*Recommendations proposed by the American Cancer Society and U.S. Multi-Society Task Force on Colorectal Cancer; recommendations for average-risk patients also endorsed by the American
College of Radiology.
†Whenever possible, affected relatives should be tested first because of potential false-negative results.
‡Screening recommendation for individuals with positive or indeterminate tests as well as for those who refuse genetic testing. I
From Andreoli TE et al: Andreoli and Carpenter’s Cecil essentials of medicine, ed 8, Philadelphia, 2010, Saunders.
all in persons older than 85 yr. If persons now expected in the 30-mo range with mod-
between the ages of 75 and 85 yr have TREATMENT ern chemotherapeutic regimens. In patients
never undergone screening, the decision with limited, resectable metastases in sites
about screening should be individualized GENERAL Rx such as the liver, the 5-yr median overall
according to health status. The ACP recom- • Surgical resection is the definitive and cura- survival is in the 50% range.
mends that clinicians stop screening for tive upfront treatment for stages I-III colon • Chemotherapy agents used in the meta-
colorectal cancer in adults over age 75 yr cancers. Selected patients (high-risk stage static setting include 5-fluorouracil (5-FU),
or in adults with a life expectancy of <10 II, all stage III) are recommended to receive capecitabine, irinotecan, oxaliplatin, and
yr. Table 4 describes CRC screening and adjuvant chemotherapy. Microsatellite insta- mitomycin. Chemotherapy regimens using
surveillance recommendations. bility can be used alongside clinicopathologic a combination of antimetabolite (5-FU or
• Computed tomography colonoscopy (CTC) factors in stage II and III colorectal cancer to capecitabine) in combination with either
virtual colonoscopy (VC) uses helical (spi- guide therapy (Fig. 5). oxaliplatin or irinotecan form the backbone
ral) CT scanning to generate a two- or • The standard chemotherapy regimen for of systemic chemotherapy.
three-dimensional virtual colorectal image adjuvant therapy of resected CRC is the com- • Molecularly targeted therapy against the
(Fig. E2). CTC does not require sedation, bination of oxaliplatin with a fluoropyrimidine epidermal growth factor receptor (EGFR) and
but, like optical colonoscopy, it requires (5-fluorouracil or capecitabine) for a period the angiogenesis pathway are used in com-
some bowel preparation (either bowel of 3 to 6 mo. Older patients and patients with bination with the chemotherapy backbone
cathartics or ingestion of iodinated con- significant comorbidities have more toxicity in metastatic CRC. Antiangiogenic agents
trast medium with meals during the 48 with combination chemotherapy; treatment include monoclonal antibodies bevacizumab,
hr before CT) and air insufflation. It also with single-agent fluoropyrimidine therapy aflibercept, and ramucirumab. Cetuximab
involves substantial exposure to radiation. only is recommended. and panitumumab are EGFR receptor block-
In addition, patients with lesions detected • Neoadjuvant chemotherapy and radiation ers that are active in metastatic CRC patients
by VC will require traditional colonoscopy. therapy are used to downsize and downstage whose tumors do not harbor mutated RAS
Compared with colonoscopy, CTC sen- rectal cancers before definitive resection and oncogenes.
sitivity for detection of polyps >10 mm improve overall survival and local disease • The liver is generally the initial and most
ranges from 70% to 96%, and specific- control in stage II-III cancers. common site of CRC metastases. Resection
ity ranges from 72% to 96%. CTC has • Adjuvant chemotherapy in stage II disease of liver-limited metastases followed by sys-
replaced double-contrast barium enema provides a modest improvement in overall temic combination chemotherapy is cura-
as the radiographic screening alternative survival by 3% to 4%, with current 5-yr sur- tive in more than 30% of selected patients.
when patients decline colonoscopy. vival rates in the 80% range. As such, current Metastasectomy of limited pulmonary metas-
• Capsule endoscopy allows visualization of guidelines recommend consideration of adju- tases can also be considered in selected
the colonic mucosa but is not recommended vant chemotherapy only in high-risk stage II cases.
as a screening procedure because its sen- patients. The magnitude of survival benefit • Unresectable multiple liver metastases are
sitivity for detecting colonic lesions is low is significantly higher in stage III patients, often approached by locoregional therapeu-
compared with colonoscopy. and combination chemotherapy is associated tic approaches such as transarterial che-
• CT scanning of the abdomen (Fig. E3), pelvis, with 5-yr overall survival rate in the 70% moembolization (TACE), selective internal
and chest assists in preoperative staging. range with wide variation in the subgroups. radiation therapy (SIRT) using yttrium-90
• PET scanning (Fig. E4) can display func- More recent data have revealed that low-risk brachytherapy, or hepatic arterial infusional
tional information and is accurate in the stage III colon cancer patients may have chemotherapy.
detection of CRC and its distant metas- equivalent survival with adjuvant multiagent • The oral multitargeted kinase inhibitor rego-
tases. Colonography composed of a com- chemotherapy of only 3 mo in duration. rafenib and the oral antimetabolite drug
bined modality of PET and CT is a newer • The outlook for patients with metastatic and TAS-102 provide modest survival benefit in
diagnostic modality that can provide relapsed CRC has improved dramatically in patients who have failed standard chemo-
whole-body tumor staging in a single the past few yr. Median overall survival in therapy approaches.
session. patients with unresectable metastases is
Colorectal Cancer 395.e1
Surgical resection
Stage II Stage III
MSI-H tumor MSI-L/MSS tumor
High-risk clinical Low-risk clinical

pathologic pathologic
indicators indicators
No adjuvant Consider adjuvant No adjuvant Adjuvant

chemotherapy chemotherapy chemotherapy chemotherapy
FIG. 5 Proposed algorithm for using microsatellite instability (MSI) alongside clinicopathologic factors in stages
II and III colorectal cancer. ASCO guidelines: Inadequate samples nodes, T4 lesions, perforation, poorly differ-
entiated histology. MSI-H, High-level microsatellite instability; MSI-L/MSS, low-level microsatellite instability/
microsatellite stability. (From Niederhuber JE: Abeloff’s clinical oncology, ed 6, Philadelphia, 2020, Elsevier.)
• Patients with tumors harboring BRAF muta- • Overall 5-yr disease-free survival rate has • Decreased fat intake to 30% of total energy
tions can now have improved survival with increased from 50% to 63% during the past intake, increased fiber through fruit and veg-
the use of combination molecularly tar- two decades. etable consumption may reduce CRC risk.
geted therapy consisting of encorafenib, bin- • High-frequency microsatellite instability in • Chemoprophylaxis with aspirin (81 mg/day)
imetinib, and cetuximab. CRC is independently predictive of a relatively reduces the incidence of colorectal adeno-
• In patients with pathologically confirmed favorable outcome and reduces the likelihood mas in persons at risk.
microsatellite instability in their cancers (Fig. of metastases. • The National Cancer Institute has published
5), the checkpoint inhibitors (pembrolizumab, • In patients with high-risk stage II and with stage consensus guidelines for universal screen-
nivolumab) are effective options after failure III CRC, there is improved 5-yr survival among ing for HNPCC in patients with newly diag-
of standard therapies and have been recently patients treated with adjuvant chemotherapy. nosed CRC. Tumors in mutation carriers of
approved in this setting. • Expression patterns of microRNA are sys- HNPCC typically exhibit microsatellite insta-
• Reviews of randomized trials in metastatic temically altered in colon adenocarcinomas. bility, a characteristic phenotype caused by
CRC have demonstrated that right-sided can- High miR-21 expression is associated with expansion or contraction of short nucle-
cers are associated with shorter overall sur- poor survival and poor therapeutic outcome. otide repeat sequences. These guidelines
vival when compared with left-sided cancers. • The optimal timing from surgery to initiation of (Bethesda Guidelines) are useful for selective
adjuvant chemotherapy is 4 to 8 wk. A longer patients for microsatellite instability testing.
CHRONIC Rx time to initiation of adjuvant chemotherapy is Screening patients with newly diagnosed
Follow-up is indicated with: associated with worse survival rates. CRC for HNPCC is cost effective, especially if
• Physician visits with a focus on clinical and • Regular aspirin use after the diagnosis of CRC the benefits to their immediate relatives are
disease-related history, directed physical has been reported to be associated with lower considered.
examination, coordination of follow-up, and risk for CRC-specific and overall mortality, espe- • The use of either annual or biennial FOBT
counseling every 3 to 4 mo for the first 3 yr cially among individuals with tumors that over- significantly reduces the incidence of CRC.
and then every 6 mo for 2 yr. express cyclooxygenase-2. Regular aspirin use is • The detection of mutations in the APC gene
• Colonoscopy at end of first yr, then after 3 yr, associated with lower BRAF-wild type colorectal from stool samples is a promising new
and subsequently every 5 yr. cancer but not with BRAF-mutated cancer risk. modality for early detection of colorectal
• Baseline CEA level, if elevated, can be used All aspirin doses starting with 75 mg daily had neoplasms.
after surgery as a measure of completeness similar effects on CRC incidence and mortality.
of tumor resection. It is used to monitor
tumor recurrence and is obtained every 3 to REFERRAL SUGGESTED READINGS
6 mo for up to 5 yr. • Multidisciplinary referral to colorectal sur- Available at ExpertConsult.com
gery or surgical oncology, medical oncology,
DISPOSITION radiation oncology RELATED CONTENT
The 5-yr survival rate varies with the stage of
the carcinoma: Colon Cancer (Patient Information)
PEARLS & Familial Adenomatous Polyposis and Gardner
TNM Stage 5-yr Survival Rate (%) CONSIDERATIONS Syndrome (Related Key Topic)
Lynch Syndrome (Related Key Topic)
I >90 COMMENTS Peutz-Jeghers Syndrome and Other Polyposis
IIA-C 60-85 Syndromes (Related Key Topic)
• Metastases of tumor cells to regional lymph
IIIA-C 25-65 nodes is the single most important prognostic AUTHOR: Ritesh Rathore, MD
IV 5-10 factor in patients with colon cancer.
Ai
FIG. E3 Colon carcinoma: Wall thickening.

A carcinoma of the descending colon near the
splenic flexure causes thickening of the colon wall
(arrowhead) and narrowing of the lumen. Stranding
densities (arrow) extending into the pericolonic fat
Aii suggest tumor extension through the bowel wall.
(From Webb WR, Brant WE, Major NM: Fundamentals
of body CT, ed 4, Philadelphia, 2015, Saunders.)
Aiii B
FIG. E2 Colon polyps seen at (Ai-iii) colonoscopy and (B) computed tomography (CT) colonography. Aii,
After endoscopic resection of the polyps in Ai. (From Ballinger A: Kumar & Clark’s essentials of medicine, ed
5, Edinburgh, 2012, Saunders.)
A B
FIG. E4 Colon cancer. A, Positron emission tomography (PET) and computed tomography (CT) image display of a patient with two fluorine-18 (18F)-fluorodeoxyglucose
(FDG)–avid lesions in the liver. These are seen on the CT scan (upper left), the attenuation-corrected PET scan (upper right), the non–attenuation-corrected PET scan
(lower right), and fused images (lower left). B, PET and CT images of the pelvis, oriented as in A, show increased FDG uptake in a left external iliac lymph node metastasis.
(From Niederhuber JE: Abeloff’s clinical oncology, ed 6, Philadelphia, 2020, Elsevier.)
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Bagshaw PF et al: The Australasian Laparoscopic Colon Cancer Study Group: long- 2017.
term outcomes of the Australasian randomized clinical trial comparing laparoscop- Kopetz S et al: BEACON CRC: a randomized, 3-Arm, phase 3 study of encorafenib
ic and conventional open surgical treatments for colon cancer: the Australasian and cetuximab with or without binimetinib vs. choice of either irinotecan or
Laparoscopic Colon Cancer Study Trial, Ann Surg 256:915-919, 2012. FOLFIRI plus cetuximab in BRAF V600E–mutant metastatic colorectal cancer,
Biaggi JJ et al: Association between time to initiation of adjuvant chemotherapy Annals of Oncology 30(Supplement 4):iv137-iv151, 2019.
and survival in colorectal cancer, JAMA 305(22):2335-2342, 2011. Lieberman D: Screening for colorectal cancer and evolving issues for physicians
Chuba KJ et al: Aspirin for the prevention of cancer: incidences and mortality: and patients, a review, JAMA 316(20):2135-2145, 2016.
systemic evidence reviews for the U.S. Preventive Services Task Force, Ann Nishihara R et al: Aspirin use and risk of colorectal cancer according to BRAF
Intern Med 164:814-815, 2016. mutation status, JAMA 309(24):2563-2571, 2013.
Dalerba P et al: CDX2 as a prognostic biomarker in stage II and stage III colon Primrose JN et al: Effect of 3 to 5 years of scheduled CEA and CT follow-up to
cancer, N Engl J Med 374:211-222, 2016. detect recurrence of colorectal cancer, JAMA 311:263, 2014.
Friis S et al: Low-dose aspirin or nonsteroidal anti-inflammatory drug use and Qaseem A et al: Screening for colorectal cancer: a guidance statement for the
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Garcia-Albeniz X et al: Effectiveness of screening colonoscopy to prevent colorec- Rothwell PM et al: Long-term effect of aspirin on colorectal cancer inci-
tal cancer among Medicare beneficiaries aged 70 to 79 years, Ann Intern Med dence and mortality: 20-year follow-up of five randomized trials, Lancet
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Grothey A et al: Duration of adjuvant chemotherapy for stage III colon cancer, N Schetter AJ et al: MicroRNA expression profiles associated with prognosis and
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ALG Colorectal Cancer 393

TABLE 4 Colorectal Cancer (CRC) Screening and Surveillance Recommendations*

Stage II Stage III

MSI-H tumor MSI-L/MSS tumor

High-risk clinical Low-risk clinical

No adjuvant Consider adjuvant No adjuvant Adjuvant

FIG. E3 Colon carcinoma: Wall thickening.

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