adenocarcinoma of the colon &/or rectum

Introduction

The second leading cause of death due to cancer in the US, in men after lung cancer & in women after breast cancer.

Etiology

diet: proposed predisposing factors include
- consumption of red meat & processed meat increases risk^[2]
- low-fiber diets^[18]^[40]
  - whole grain & cereal fibers linked with lower risk for colorectal cancer
  - fruits, vegetables reduce risk, but less so
  - legumes with largest risk reduction (RR=0.62), but risk reduction highly variable (RR=0.27-1.42)^[40]
  - ultra-processed foods are associated with an increased risk of colorectal cancer^[134]
- low Ca+2 & low Mg+2^[16] diets (low dairy intake)^[2]
- low vitamin 25-OH vitamin D^[32]^[103], low vitamin B6^[31]
- diet of fat & sweets associated with recurrence^[24]
- coffee & soda not risk factors; tea maybe^[33]
- proinflammatory foods associated with increased risk^[93]
  - overabundance of certain omega-6 fatty acids, perhaps from ultraprocessed foods, may hinder anti-inflammatory & anti-neoplastic properties of omega-3 fatty acids^[148]
lifestyle
- alcohol compsumption increases risk^[2]
- smoking increases risk^[2]
- excess body weight increases risk^[2]
  - obesity in adolescent males^[68]
  - obesity in women < 50 years^[106]
- sedentary lifestyle associated with increased risk
- physical fitness in midlife associated with reduced risk of colorectal cancer after age 65 (RR=0.5)^[65]
genetics
- intestinal polyposis syndromes confer highest risk
- inflammatory bowel disease
  - ulcerative colitis
    - patients with pancolitis at highest risk^[2]
    - risk is negigible with proctitis^[2]
    - risk further increased with comorbid primary sclerosing cholangitis^[2]
  - Crohn's disease
- first degree relatives: 2-3 fold increased risk in the absence of other associated syndromes
adenomatous polyps; serrated, tubular, villous;
- not hyperplastic polyps^[29]
history of other cancer
other etiologic &/or risk factors:
- ureterosigmoidostomy
- bacteremia
  - bacteremia in hospitalized patients^[99], especially B fragilis & S gallolyticus
  - Streptococcus bovis bacteremia
  - bacteria may enter the bloodstream due to a perturbed intestinal barrier^[99]
- alterations in the gut microbiome^[127]
  - Fusobacterium species, particularly F. nucleatum, may play a role^[39]
- peridiodontal disease^[130]
- cholecystectomy
- acromegaly
- diabetes mellitus type 2^[2]
- radiation injury to colon
- black ethnicity
- taller height is a risk factor; RR=1.06 for each 10 cm increase in height^[132]
- maternal overweight & obesity during pregnancy increased the risk for colorectal cancer in offspring later on in life (RR=2.12 & 2.51)^[126]
- appendicitis increases risk within 1 year 4-fold^[141]
older age (> 50 years) & male sex are risk factors^[44]
antibiotic use
- linked to early-onset colon cancer (RR=1.5)^[125]
  - oral penicillin use (RR=1.03%)^[116]
- linked to colon cancer; risk was highest in proximal colon (RR=1.2 high use)^[128]
- inversely associated with rectal cancer (RR=0.91)^[128]

Epidemiology

11% of solid tumors in men
14% of solid tumors in women
2nd most common cause of death from cancer in men
2nd most common cause of death from cancer in women^[2]
incidence race-dependent 31-57/100,000, blacks > non-Hispanic > whites > Hispanic > Asian/Pacific Islanders > American Indian/Alaska Natives^[30]
- survival disparity between blacks & whites largely due to later diagnosis & comorbid conditions^[64]
75% of colorectal cancers diagnosed in average-risk persons^[2]
15% of colorectal cancer diagnosed before age 50^[82]
incidence rates for colon cancer & rectal cancer in young persons (age 20-34) may increase 90% & 124%, respectively by 2030^[62]*
- obesity may play a role^[88]
colorectal cancer mortality among U.S. adults 20-54 years of age
- 6.3/100,000 in 1970; 3.9/100,000 in 2004; 4.3/100,000 in 2014
  - only white adults saw an increase 2004-2014^[90]
metastatic colorectal cancer increased 3% 1995-2015 in persons 40-49%^[115]
10% of colon cancers & 25% of rectal cancers will occur in adults < 50 years^[127]
- younger patients tend to present with advanced disease & unfavorable histopathological features
- distal colon & rectum most commonly involved in younger patients^[127]
- genetic predisposition plays a role in early-onset colorectal cancer, but most cases are sporadic^[127]

* absolute risk of non-hereditary colon cancer in young persons still quite low^[62]

Pathology

the majority of colorectal carcinomas begin as adenomatous polyps
prevalence of adenomatous polyps increases with age to > 25% in patients over the age of 50 years
most lesions are left sided, but not all right-sided lesions have synchronous left-sided lesions^[5]
42% of all tumors were located in the proximal colon^[30]
- tumors arising in the proximal colon have & different pathology & worse prognosis than tumors in the distal colon^[2]
metastases
- regional lymph nodes (53)
  - rectal carcinomas metastasize early because of extensive lymphatic drainage
- liver via the portal venous circulation (44%)
- lungs (16%)
  - rectal carcinoma may metastasize via the paravertebral venous plexus to the lungs & supraclavicular nodes
- bone (27%)
- brain (11%)
- skin (5%)
- adrenal (31%)
- kidney (16%)
37% diagnosed as localized disease, 55% as regional or distant disease, 7% unstaged
increased abundance of Fusobacterium (odds ratio = 4.11); & Porphyromonas species (odds ratio = 5.7); decreased abundance of Clostridium species (69 vs 78%) in patients with colorectal cancer^[56]
fusobacterial DNA in 50%^[92] majority^[143] of colorectal cancers
- fusobacterial DNA found primarily within malignant cells
- fusobacterial DNA also found colorectal cancer metastases
- Fusobacterium nucleatum animalis C2 contains a unique adhesion antigen (FadA) on its surface that binds to cell surface E-cadherin, activating beta-catenin signaling & stimulating both inflammation & carcinogenesis^[39]^[143]
western-style diet is associated with higher incidence of colorectal cancer containing abundant pks+ E coli, linking diet, intestinal microbiota, & colorectal cancer^[133]

* images^[136]

* seen low power histopathology & high power histopathology

Genetics

chromosomal instability in 85% of colorectal cancers
- familial adenomatous polyposis coli (APC-gene)
- deleted in colon carcinoma (DCC) gene
- mutated in colon carcinoma (MCC) gene
- mutation in KRAS proto-oncogene^[147] & NRAS proto-oncogene
- V600E BRAF mutation associated with poorest prognosis in patients with liver metastases^[100]
- P53 tumor suppressor gene
- defects in PDGFRL are associated with colorectal cancer
- mutations in PIK3CA (aspirin-sensitive)
- mutations in PTEN gene (MMAC1 gene)
- mismatch repair genes
  - MLH1 (hereditary non-polyposis coli)
  - MLH3, MSH2, MSH6, PMS1, PMS2^[83] (case report)
  - AXIN2
- base excision repair genes: MYH
microsatellite instability
- occurs in the germline of patients with hereditary nonpolyposis colorectal cancer & in 15% of sporadic colorectal cancers
- may be associated with defects in mismatch repair genes
- may be associated with defects in AIM2
hypermethylation of CpG islands of promoter regions associated with tumor suppressor genes
- precursor lesions are serrated polyps^[2]
other genetic predispositions
- oncogenes involved in sporadic colon cancer
  - c-myc, c-src, ras, erbB2^[2]
- susceptibility to colorectal cancer
  - SMAP7 (type 3)
- abnormal transcripts of FHIT found in ~50%
- overexpression of SMYD3, TPBG, AAMP, NAV2, PLXNB1, TNFRSF6B, ADAMTS20, BIRC5, ARHGEF4, TDGF1
- underexpression of LLGL1, PDCD4, B3GNT6, CEACAM1
other implicated genes ACRBP, WFDC2, SPECC1, ATAD2, GCNT3, KAAG1, RNF43, CHRDL2, HES2, PHF20, REG4, RET, ANLN, PRAF2, ARID4B, LEMD1, TAK1L, B3GNT8, ARHGAP8, PRR5, LRRC26, VWA2, LETMD1, OLFM4, MINA, PRAP1, SFRS19, MTUS1, TTYH2, TKT2, MAP2K3, MAP1D, BCL9L, KRT24, NF1, PHF19, XRRA1, PTPRH, CTNNB1, CCNDBP1, CASC2, CLCA1, CLCA2, PCNXL2, SLC5A8, UCHL3, PTPN12, PPAP2A, RUNX1T1, TP63, LEF1, EED, ZNF146, CCKBR, CD97, PPARG, EPHA3, WRN, MMP25, RAC1, EREG, WISP1, TSPAN8, AgSK1, SMAD2, SMAD3, SMAD7, MT-CO1, MTHFD1, DYRK1B, ENPP7, ZNF306, TCF7L2
increased risk of colon cancer in first degree relatives of patient with colon cancer, especially if diagnosis at an early age &/or other 1st degree relative affected^[80]
- risk conferred by affected half-sibling is similar to that conferred by first-degree relatives^[114]

Clinical manifestations

often asymptomatic until late stages
bowel-specific manifestations
- changes in bowel habits - tenesmus
- hematochezia (rectal bleeding)
- abdominal pain, abdominal distension, pelvic pain
- palpable abdominal mass, rectal mass
- fistulas are rare
- right-sided lesions may not cause obstruction until late due to liquid nature of stool entering cecum
- digital rectal exam
  - guaiac positive stool
  - rectal may be felt, 30% of colorectal carcinomas arise from rectosigmoid area
hepatomegaly
systemic manifestations
- anemia
- fatigue
- weight loss
- fever may occur with metastasis to the liver
early red flags beginning as early as 2 years prior to diagnosis
- abdominal pain
- persistent diarrhea
- rectal bleeding
- iron-deficiency anemia^[139]

Laboratory

complete blood count (CBC) may show microcytic anemia
iron studies may show iron-deficiency anemia
- serum iron, TIBC
- serum ferritin
test all patients for Lynch syndrome^[73]
- DNA mismatch repair gene mutations^[2]
- microsatellite instability^[2]
metastatic workup
- liver function tests
- serum carcinoembryonic antigen (CEA)
  - direct relationship between CEA & Duke's stage
  - CEA > 50 ng/mL is associated with poor prognosis
  - elevated CEA is associated with greater likelihood of recurrence
  - do not institute therapy for metastatic disease based upon elevated serum CEA alone^[2]
- genetic testing for metastatic colon cancer
  - DNA mismatch repair gene mutations
  - microsatellite instability
  - NRAS gene mutation in colorectal cancer
  - KRAS gene mutation in colorectal cancer
    - Kras gene mutation & Nras gene mutation for cetuximab & panitumumab eligibility ^[2]^[60]^[76]^[78]
    - cancers that carry these mutations will not respond to anti-EGFR agents cetuximab or panitumumab (50%)^[2]
  - BRAF gene mutation^[2]
    - BRAF V600E mutation for prognosis (NGC, weak evidence)
  - PIK3CA gene mutation in colorectal cancer
  - PTEN gene mutation in colorectal cancer
elevated levels of serum lactate dehydrogenase, serum AST, serum ALT, & neutrophil count predict 60 day mortality in patients presenting with metastatic colorectal cancer who undergo primary tumor resection^[129]
monitoring response to therapy
- liver function tests every 6 months
- serum carcinoembryonic antigen (CEA) every 6 months for 1st 3 years, then annually therafter (see Management)
- stool guaiac every 6 months
loincs for pathology reports
investigational:
- chromosome region 8q23.3-24.13 deletion (DCC)
- no benefit in tumor expression of thymidylate synthetase or TP53^[21]
- VWA2 may be serologic marker
- increased micro RNA expression associated with poor prognosis^[26]
- colon cancer 12 mRNA expression analysis (CPT)
- fusobacterium DNA
see ARUP consult^[41]

Diagnostic procedures

colonoscopy with polypectomy
- diagnostic procedure of choice
- staging of colorectal carcinoma
- screening & yearly monitoring response to therapy
- colonoscopy 1 & 3 years after colectomy, then at 5 year intervals^[2]^[48]^[81]
- colonoscopy 3-6 months after polypectomy of > 2 cm well- differentiated adenocarcinoma with clean margins^[2]
sigmoidoscopy every 6 months for rectal carcinoma monitoring response to therapy

* images^[136]

Radiology

screening (see screening for colon cancer)
staging of colorectal cancer
- contrast-enhanced CT of abdomen & pelvis^[2]
- contrast-enhanced CT of thorax
- CT staging not needed if surgical margins are clear
- rectal cancers require MRI of rectum^[2]
follow-up of treated colorectal cancer
- CT of chest & abdomen annually for 1st 3-5 years if patient would be eligible for surgical resection of metastases^[2]^[19]^[72]
- include pelvis if rectal cancer^[2]^[72]
- of no benefit in follow-up over serum CEA alone to identify curable recurrences^[58]
chest X-ray (metastatic workup) & every 6 months monitoring response to therapy
preoperative PET scan does not improve staging^[2]
- do not obtain PET scan for initial staging^[2]
postoperative PET scan not routinely indicated^[2]
- do not obtain PET scan to follow patient for recurrent disease^[2]

* images^[136]

Staging

see staging of colorectal carcinoma

Complications

Streptococcus bovis bacteremia
Clostridium septicum sepsis, gas gangrene^[63]
60 day mortality highest in patients presenting with metastatic colorectal cancer undergoing resection of primary right-sided tumor prior to chemotherapy^[129]

disease interaction(s) of renal transplantation with colorectal cancer

Differential diagnosis

Management

treatment: surgery, chemotherapy, radiation

surgery
- surgical resection for cure stage 1 & 2
- metastatic workup prior to surgery (see laboratory)
  - neoadjuvant chemotherapy + radiation therapy prior to surgery in patients presenting with stage 3 or stage 4 (metastases)^[129]
  - 4-week course of neoadjuvant ipilimumab (Yervoy) + nivolumab (Opdivo) prior to surgery in patients with DNA mismatch repair deficient colon cancer shows 95% of patients with major pathologic response & 67% with complete response^[135]
- surgical resection (colectomy) generally indicated unless
  - well-differentiated adenocarcinoma with clean margins on examination of polypectomy specimen^[2]
  - preoperative evidence of metastatic disease^[124]
- metastases precludes surgical cure, but surgery may
  - relieve obstruction
  - prevent bleeding^[2]
  - some patients with metastatic colon cancer confined to a single organ may be cured by resecting both the primary tumor & the metastases^[2]
  - tumor debulking does not improve survival in metastatic colorectal cancer^[145]
- RT-PCR for guanylate cyclase-C (intestinal-specific) in lymph nodes during surgery may predict metastases
- surgical resection of primary tumor & regional lymph nodes
- laparoscopic-assisted resection may be an option^[17]
- limited distant recurrence may be amenable to for a second attempt at surgical cure in 25% of patients
- heated chemotherapy during surgery of no benefit^[102]
- surgery almost never results in a need for permanent colostomy^[2]

* see prognosis after surgical resection of colorectal carcinoma

chemotherapy
- stage 1 without benefit from chemotherapy (surgery alone)
- stage 2 without microsatellite instability or high risk features unlikely to benefit from adjuvant chemotherapy
- stage 2 with high risk of recurrence is treated similarly to stage 3^[2]
- neoadjuvant chemotherapy + radiation therapy prior to surgery & adjuvant chemotherapy following surgery for stage 3 & stage 4 (metastases)
  - role is primarily palliative
  - neoadjuvant chemotherapy may obviate need for adjuvant chemotherapy for stage 3
  - 4-week course of neoadjuvant ipilimumab (Yervoy) + nivolumab (Opdivo) prior to surgery effective in patients with DNA mismatch repair deficient colon cancer^[135]
- stage 3 colon cancer
  - neoadjuvant ipilimumab (Yervoy) + nivolumab (Opdivo) effective in stage 3 colon cancer with minimal disease recurrence at 1 year^[135] (see above)
  - prolongs disease-free survival (Stage 3)^[2]^[11]
  - standard of care (Stage 3)^[2]^[11]
  - 5-fluorouracil, leucovorin & oxaliplatin (FOLFOX)^[2]^[46] for 3 months (low-risk)^[6]
  - in the elderly, no added benefit of oxaliplatin^[66]
  - capecitabine/oxaliplatin (CAPOX, CAPEOX, XELOX) for 3 months^[38]^[96]
  - high-risk stage III: treat for 6 months with CAPEOX or FOLFOX (risk of neurotoxicity < 1/2 for 3 vs 6 months of therapy)^[96]
  - levamisole (Ergamisole) has immunomodulatory activity
  - irinotecan (CPT-11) for 5-FU refractory disease
  - hyperthermic intraperitoneal chemotherapy with mitomycin C plus complete cytoreduction may improve locoregional control in patients with locally advanced colorectal cancer^[142]
- metastatic colon cancer
  - combination chemotherapy consisting of 5-fluorouracil & oxaliplatin^[2]
  - combination chemotherapy consisting of 5-fluorouracil & leucovorin with addition of irinotecan (FOLFIRI) or oxaliplatin (FOLFOX) in combination with bevacizumabor, cetuximab or panitumumab if the tumor contains a wild-type RAS gene is the standard of care^[67]
  - 5-FU + leucovorin + irinotecan (CPT-11) (FOLFIRI)^[11]
  - fluorouracil + leucovorin + irinotecan + bevacizumab^[51]
    - bevacizumab potentiates efficacy of 5-FU combined with leucovorin or irinotecan at a cost of increasing risk for hypertension, arterial thrombosis, poor wound healing, gastrointestinal perforation & fistulas^[2]
  - capecitabine is an alternative to 5-fluorouracil^[2]
  - bevacizumab & cetuximab in combination with standard therapy improves survival^[2]
  - bevacizumab in combination with oxaliplatin-based chemotherapy^[2]^[52]
  - cetuximab as single agent
    - increases survival^[25] 6.1 vs 4.6 months for supportive care; no benefit in survival^[51]
    - benefit only in KRAS mutation negative tumors^[27]^[51]
  - no benefit of bevacizumab maintenance monotherapy^[95]
  - panitumumab & cetuximab (EGFR monoclonal Abs) of benefit only in the absence of KRAS, NRAS & BRAF mutations^[22]^[76]^[78]
  - panitumumab-FOLFOX4 useful for metastatic colorectal cancer without RAS mutations^[78]
  - ramucirumab in combination with FOLFIRI (after ramucirumab) improves survival (13.3 vs. 11.7 months)^[70]
  - tipiracil/trifluridine (Lonsurf) improves overall & progression-free survival in patients with disease progression after treatment with fluorouracil-containing combination chemotherapy^[67]
  - fruquintinib may improve survival in refractory metastatic colorectal cancer^[104]
  - treatment of asymptomatic patients with small volume, metastatic cancer discovered incidentally does not improve outcomes^[2]
  - an oligometastatic lesion confined to a single organ may be cured with surgical resection of the primary tumor & the metastasis^[2]
  - metastatic DNA mismatch repair-deficient colorectal cancer
    - checkpoint inhibitor may benefit patients; nivolumab + ipilimumab^[94]; pembrolizumab may be alternative^[2]
- not recommended^[2]^[11]
  - aflibercept in combination with irinotecan & fluorouracil is not recommended [NGC]
  - do not use anti-VEGF & anti-EGFR Ab together^[2]
- benefits of chemotherapy became much less marked for progressively older patients, particularly >= 70 years of age^[113]
- frail elderly may not benefit from chemotherapy^[38]
radiation therapy
- useful in conjunction with neoadjuvant chemotherapy & surgical excision of Dukes'stage B2 & C (stage 3) colorectal carcinoma
- inhibits metastasis to regional lymph nodes
- especially useful for rectal carcinoma^[11]
  - rectum lacks peritoneal covering
  - local recurrence rate is high
  - see rectal cancer

follow-up, prognosis, prevention, screening

follow-up
- colonoscopy 1 & 3 years after surgical resection, then at 5 year intervals^[2]^[48] (non-metastatic colon cancer)
- air-contrast barium enema along with sigmoidoscopy may be an alternative to colonoscopy^[2]
- serum carcinoembryonic antigen (CEA)^[2]^[48]
- every 6 months for 2 years^[2] (MKSAP19)
  - CEA alone inadequate because serum CEA is not elevated in all patients with recurrent colorectal cancer; imaging needed^[2]
- every 3-6 months for 2 years, then every 6 months for an additional 3 years^[72]
- if serum CEA > 10 ng/mL, colonoscopy vs abdominal CT^[11]
- CT of chest & abdomen & pelvis annually for 1st 5 years if patient would be eligible for surgical resection of metastases^[2]^[19]^[72]
  - applies to stage 2, stage 3 & stage 4^[2]
    - CT alone insufficient for stage 2 & stage 3; CEA needed^[2]
  - of no benefit over serum CEA alone in identifying curable recurrences^[58]
  - include pelvis if rectal cancer^[2]^[72]
  - liquid biopsy for circulating tumor DNA detects relapse months before CT of chest & abdomen^[120]
- serum CEA + CT of chest & abdomen at 6, 12, 18, 24, & 36 months after surgery does not confer 5 year survival advantage vs these tests at 12 & 36 months after surgery^[101]
  - editorialist suggests best evidence supports annual surveillance^[101]
- history & physical exam every 3-6 months for 2 years, then every 6 months for an additional 3 years^[72]
  - screen for cognitive problems, depression, anxiety, psychosocial stress, mucositis, loss of taste, dry mouth, fatigue, neuropathy, sexual dysfunction, constipation, diarrhea, urinary disease
- surgical resection is the treatment of choice with solitary lung metastasis^[2]^[43]
- surgical resection of a few isolated metastatic lesions may be curative^[2]
  - radiologic evidence of metastatic recurrence precludes need for needle biopsy
  - a negative needle biopsy would not change management
  - resection is 1st line therapy if feasible^[2]
  - outcomes similar for laparoscopic vs open surgery for liver metastases^[119]
- conversion chemotherapy may offer hope to patients with initially unresectable liver metastases^[2]^[77]
- monitor patients treated with pelvic radiation for chronic proctitis^[72]
- aspirin 75-160 mg QD reduces colorectal cancer-specific mortality (RR=8.85) & overall mortality (RR=0.95)^[86] -guidelines to do not yet recommend
- no benefit or Ca+2 or vitamin D in preventing recurrence of colorectal cancer^[79]
prognosis
- 5 year survival by stage (most important prognostic factor)^[2]
  - stage 1: 90-95%
  - stage 2: 70-85%
  - stage 3: 25-70%
  - stage 4: 0-10% (metastatic disease)
  - survival better for left-sided cancer vs right-sided cancer, but can be improved by removal of more lymph nodes during surgery^[2]^[105]
- median survival with metastatic colorectal cancer is < 30 months^[67]
- higher post-operative plasma 25-hydroxyvitamin D is associated with better survival^[61] & with better survival in patients with metastatic colon cancer^[69]
- a healthy lifestyle including diet, physical activity, & moderation in alcohol intake can lower risk of death or cancer recurrence by 42% during follow-up 7-10 years^[89]
- adherence to a healthy lifestyle after diagnosis of colorectal cancer may improve survival^[97]
  - includes healthy body weight, regular physical activity, & high intake of fruits, vegetables, & whole grains^[97]
- high fiber intake after diagnosis of colorectal cancer is associated with improved survival
  - fiber from cereals appear particularly effective^[91]
prophylaxis
- aspirin, NSAIDs may diminish risk of colon cancer^[13]^[14]^[34]^[35]^[71]^[84]
  - USPSTF recommends prevention of both cardiovascular disease & colorectal cancer in adults 50-59 years of age with a 10-year cardiovascular risk of >= 10%^[74]^[85]
    - adults 60-69 years of age should discuss risks & benefits with their clinicians^[74]^[85]
    - for patients < 50 or > 69 years, there is not enough evidence to make recommendations^[85]
    - starting use of aspirin to prevent colorectal cancer after age 70 years of no benefit^[123]
  - USPSTF previously recommended against the routine use of aspirin & NSAIDs to prevent colorectal cancer^[28]
  - aspirin does not reduce mortality from colon cancer^[28]^[34]^[35]
  - dose-independent reduction in mortality due to proximal colon cancer & rectal cancer, but not distal colon cancer^[37]
  - aspirin diminished mortality in patients that harbor PIK3CA mutations^[42]
  - aspirin lowers risk of colorectal cancer in patientswith wild-tyep BRAF but not mutated BRAF^[49]
  - low-dose aspirin 100 mg QOD for 10 years lowers risk of colorectal cancer in women^[53]
  - benefit of aspirin for colorectal cancer prevention is not apparent until 10 years after aspirin therapy is started^[149]
    - 53 fewer cancer cases vs 193 more GI bleeds & 214 more peptic ulcers
  - risk reduction 27% for low-dose aspirin, 35% for other NSAIDs^[71]
  - aspirin at least twice weekly for > 6 years reduces risk for colorectal cancer (RR=0.81)^[84]
  - only nonaspirin NSAIDs reduce risk of recurrent invasive colon cancer^[87] 16.3% vs 6.7%
  - also see Nurses Health Study
  - also see aspirin & colorectal polyps
- magnesium, folate, fiber, dairy products, fruits, vegetables & soy reduce risk of colorectal cancer^[118]
  - higher intakes of dietary fiber, dietary calcium, & yogurt & lower intakes of alcohol & red meat may reduce risk of colorectal cancer^[121]
- Ca+2 & vitamin D
  - may reduce risk of colorectal adenomas & colon cancer^[15]^[22]
  - no benefit in Women's Health Initiative
    - 1000 mg Ca+2 plus 400 IU of vitamin D3 per
  - no benefit &/or Ca+2 & vitamin D +/- 81 mg of aspirin in preventing recurrence of colorectal cancer^[79]
  - of no benefit it prevention of colon cancer^[118]
  - no benefit of high-dose vitamin D supplementation with standard chemotherapy plus bevacizumab^[146]
- higher intakes of dietary fiber, dietary calcium, & yogurt & lower intakes of alcohol & red meat reduce colorectal cancer risk^[122]
- vitamin B6 may reduce risk of colon cancer^[31]
- one-a-day multivitamin use after a diagnosis of nonmetastatic colorectal cancer is associated with a 45% lower colorectal cancer-specific & overall mortality^[144]
- high-fat dairy products reduce risk, speculation that linoleic acid may be protective^[20]
- high intake of marine omega-3 fatty acids & dark fish after diagnosis of colon cancer may prolong disease-free survival^[98]
- coffee may reduce risk of colorectal cancer (both caffeinated & decaffeinated) & reduces risk of mortality & disease progression in patients with colorectal cancer with a dose-response relationship^[117]
- about a quarter of <A385219>colorectal cancers</A385219> may be prevented by simple lifestyle choices^[36]^[138]
  - not smoking
  - daily physical activity (30 minutes/day)
  - no excessive drinking
  - healthy diet
    - healthy plant-based diet reduces risk of colorectal cancer in men^[137]
  - waist circumference control
    - < 40 inches men
    - < 35 inches women
- alteration in microbial flora may prove useful^[56]^[57]
  - lactic acid-producing bacteria (Bifidobacterium) appear promising in animal studes^[57]
screening, including screening of family members
- see screening for colorectal cancer

Comparative biology

when mice with colorectal tumors containing bacterial DNA were treated with metronidazole (to which Fusobacteria are sensitive), tumor growth & load decreased^[92]

Notes

Multi-omics Multi-cohort Assessment (MOMA) platform (AI technology) provides clinically actionable predictions that can inform treatment for colorectal cancer^[140]

More general terms

More specific terms

secondary colorectal carcinoma

Additional terms

References

↑ Saunders Manual of Medical Practice, Rakel (ed), WB Saunders, Philadelphia, 1996, pg 332-33
↑ ^2.00 ^2.01 ^2.02 ^2.03 ^2.04 ^2.05 ^2.06 ^2.07 ^2.08 ^2.09 ^2.10 ^2.11 ^2.12 ^2.13 ^2.14 ^2.15 ^2.16 ^2.17 ^2.18 ^2.19 ^2.20 ^2.21 ^2.22 ^2.23 ^2.24 ^2.25 ^2.26 ^2.27 ^2.28 ^2.29 ^2.30 ^2.31 ^2.32 ^2.33 ^2.34 ^2.35 ^2.36 ^2.37 ^2.38 ^2.39 ^2.40 ^2.41 ^2.42 ^2.43 ^2.44 ^2.45 ^2.46 ^2.47 ^2.48 ^2.49 ^2.50 ^2.51 ^2.52 ^2.53 ^2.54 ^2.55 ^2.56 ^2.57 ^2.58 ^2.59 ^2.60 ^2.61 ^2.62 ^2.63 Medical Knowledge Self Assessment Program (MKSAP) 11, 14, 15, 16, 17, 18, 19. American College of Physicians, Philadelphia 1998, 2006, 2009, 2012, 2015, 2018, 2021.
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022
↑ Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 670-671
↑ Journal Watch 20(23):154-55, 2000
↑ ^5.0 ^5.1 Journal Watch 20(23):182-183, 2000 Sonnenberg A et al Cost-effectiveness of colonoscopy in screening for colorectal cancer. Ann Intern Med 133:573, 2000 PMID: https://www.ncbi.nlm.nih.gov/pubmed/11033584
Frazier AL et al Cost-effectiveness of screening for colorectal cancer in the general population. JAMA 284:1954, 2000 PMID: https://www.ncbi.nlm.nih.gov/pubmed/11035892 Inciardi JF et al Incidence trends for colorectal cancer in California: implications for current screening practices. Am J Med 109:277, 2000 PMID: https://www.ncbi.nlm.nih.gov/pubmed/10996577
↑ ^6.0 ^6.1 Journal Watch 20(24):189, 2000 Ahlquist DA et al Colorectal cancer screening by detection of altered human DNA in stool: feasibility of a multitarget assay panel. Gastroenterology 119:1219, 2000 PMID: https://www.ncbi.nlm.nih.gov/pubmed/11054379
↑ Mandel JS et al The effect of fecal occult-blood screening on the incidence of colorectal cancer. N Engl J Med 343:1603, 2000 PMID: https://www.ncbi.nlm.nih.gov/pubmed/11096167
↑ Harrison's Principles of Internal Medicine, 14th ed. Fauci et al (eds), McGraw-Hill Inc. NY, 1998, pg 521, 539
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Patient information

colorectal adenocarcinoma information

Database

OMIM: https://mirror.omim.org/entry/114500
OMIM: https://mirror.omim.org/entry/612229

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adenocarcinoma of the colon &/or rectum

Contents

Introduction

Etiology

Epidemiology

Pathology

Genetics

Clinical manifestations

Laboratory

Diagnostic procedures

Radiology

Staging

Complications

Differential diagnosis

Management

treatment: surgery, chemotherapy, radiation

follow-up, prognosis, prevention, screening

Comparative biology

Notes

More general terms

More specific terms

Additional terms

References

Patient information

Database

Navigation menu

adenocarcinoma of the colon &/or rectum

Introduction

Etiology

Epidemiology

Pathology

Genetics

Clinical manifestations

Laboratory

Diagnostic procedures

Radiology

Staging

Complications

Differential diagnosis

Management

treatment: surgery, chemotherapy, radiation

follow-up, prognosis, prevention, screening

Comparative biology

Notes

More general terms

More specific terms

Additional terms

References

Patient information

Database

Navigation menu

Search