Rates of New or Missed Colorectal Cancers After Colonoscopy and Their Risk Factors: A Population-Based Analysis

Bressler, Brian; Paszat, Lawrence; Chen, Zhongliang; Rothwell, Deanna M.; Vinden, Chris; Rabeneck, Linda

doi:10.1053/j.gastro.2006.10.027

Cited by 579 publications

(429 citation statements)

References 11 publications

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“…Previous studies have focused primarily on cancers occurring within 3 to 5 years after the colonoscopic examination; rapidly progressing adenomas or cancers that were present but not detected at the time of colonoscopy would presumably account for these interval cancers. 15,21,29,30,[33][34][35][36][37][38][39][40][41] The number of cancers detected in this study is similar to or lower than the numbers observed in other studies (which often evaluated cancers over a shorter period). 29,30 Interval cancers accounted for only 8.2% of all colorectal cancers detected in our study cohort, and the absolute risk of an interval cancer was relatively low (9.8 interval cancers per 10,000 person-years of follow-up in quintile 1 of adenoma detection rates and 4.8 interval cancers per 10,000 person-years of follow-up in quintile 5).…”

Section: Discussionsupporting

confidence: 74%

Adenoma Detection Rate and Risk of Colorectal Cancer and Death

Barret¹,

Chaussade²,

Coriat³

2014

N Engl J Med

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Section: Discussionsupporting

confidence: 74%

Adenoma Detection Rate and Risk of Colorectal Cancer and Death

Barret¹,

Chaussade²,

Coriat³

2014

N Engl J Med

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“…In the clinical arena, optical colonoscopy is the gold standard for colon cancer screening, but a significant number of polyps are still missed (20). There is growing interest in the use of molecular beacon protease-activated synthetic probes for improved detection of early stage cancers including flat adenomas.…”

Section: Adeno-cre Treatment Of Apc Cko/lsl-kras Mice Results In Advamentioning

confidence: 99%

Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment

Hung

Maricevich

Richard

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

180

236

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Most genetically engineered mouse (GEM) models for colon cancer are based on tissuewide or germline gene modification, resulting in tumors predominantly of the small intestine. Several of these models involve modification of the adenomatous polyposis coli (Apc) gene and are excellent models for familial cancer predisposition syndromes. We have developed a stochastic somatic mutation model for sporadic colon cancer that presents with isolated primary tumors in the distal colon and recapitulates the entire adenoma-carcinoma-metastasis axis seen in human colon cancer. Using this model, we have analyzed tumors that are either solely mutant in the Apc gene or in combination with another colon cancer-associated mutant gene, the Kras G12D allele. Because of the restricted location in the distal colon, the natural history of the tumors can be analyzed by serial colonoscopy. As the mammalian target of rapamycin (mTOR) pathway is a critical component of the complex signaling network in colon cancer, we used this model to assess the efficacy of mTOR blockade through rapamycin treatment of mice with established tumors. After treatment, Apc mutant tumors were more than 80% smaller than control tumors. However, tumors that possessed both Apc and Kras mutations did not respond to rapamycin treatment. These studies suggest that mTOR inhibitors should be further explored as potential colorectal cancer therapies in patients whose tumors do not have activating mutations in KRAS.colon cancer | mouse model | adenovirus | colonoscopy | mammalian target of rapamycin C olon cancer continues to be one of the leading causes of cancerrelated deaths. The prognosis for patients with early stage cancers is good, but the majority of cancers are diagnosed at later stages (1). Most drug development strategies use transplantation of human tumor cells into immunocompromised mice. These models are not truly predictive of response in human patients because they are derived from tumor cell lines grown in vitro and are implanted into ectopic sites that bear no resemblance to the colonic microenvironment (2). Furthermore, these xenograft models fail to recapitulate the heterogeneous nature of cancer and the critical endogenous interplay between tumor and supporting stroma. Genetically engineered mouse (GEM) models circumvent these shortcomings, making them an attractive platform for biomarker discovery, study of cancer biology, and preclinical therapeutic trials (2, 3).Several GEMs that use germline or tissuewide modification of genes known to be mutated in human colon cancer spontaneously develop intestinal tumors (4). Depending on the gene(s) that is modified, these are reasonable models for inherited cancer predisposition syndromes, such as familial adenomatous polyposis (FAP) and hereditary nonpolyposis colon cancer (HNPCC). However, these are not models for sporadic colon cancer, which comprises 75-80% of all cases in humans (5). In these mouse models for FAP and HNPCC, the genetic mutations are present in the germline. Consequently, they are exp...

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“…The sensitivity for proximal cancers was lower, but it should be stressed that these tumours are notoriously difficult to diagnose even by colonoscopy. 33,34 Hence the sensitivity of 77.8% obtained at the DNA score cut-off point of 2.5 lg/ml (PicoGreen assay) could improve proximal tumour detection if confirmed in larger studies. It…”

Section: Discussionmentioning

confidence: 93%

A case‐control study of colorectal cancer detection by quantification of DNA isolated from directly collected exfoliated colonocytes

Loktionov

Ferrett

Gibson

et al. 2009

Intl Journal of Cancer

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This pilot study aimed to assess an original test based on the analysis of exfoliated colonocytes as a new approach to colorectal cancer (CRC) detection. DNA was isolated from exfoliated cells collected from the surface of the rectal mucosa by a standardized minimally invasive procedure in a case-control trial involving 66 patients with CRC diagnosis and 110 healthy volunteers (age 50-70). PicoGreen staining and quantitative real-time PCR (QRTPCR) were used for DNA quantification. Mean DNA scores in lg/ml obtained for the control and cancer groups were 2.1 (95% CI 1.7-2.5) and 9.0 (CI 6.7-11.2) respectively (p < 0.001) for PicoGreen and 0.8 (CI 0.6-0.9) and 3.8 (CI 1.9-5.7) respectively (p 5 0.003) for QRTPCR. The PicoGreen assay better detected CRC presence. At DNA score cut-off point of 2.5 lg/ml this assay gave sensitivities of 77.8% ) for proximal tumours, 91.4% (CI 76.9-98.2) for distal CRC and 86.8% ) for all CRC with specificity at 74.0% (CI 64.0-82.4). Increasing the cut-off point to 5.0 lg/ml resulted in sensitivities of 38.9% 3) for proximal tumours, 71.4% (CI 53.7-85.4) for distal CRC and 60.4% (CI 46.0-73.5) for all CRC. Specificity for this cut-off point increased to 94.8% 3). The new procedure of exfoliated cell collection from the surface of the rectal mucosa is a simple, safe and well-tolerated technique providing high quality cells. These early results suggest that exfoliated cell collection in combination with DNA quantification can potentially be employed as a tool for CRC early detection.Colorectal cancer (CRC) is one of the most common fatal malignancies. 1 CRC mortality can be greatly reduced by early tumour detection through population screening, 2-6 but the choice of CRC screening methods is still limited with two main categories: i) stool tests comprising different versions of faecal occult blood test (FOBT) and molecular analysis of stool DNA; ii) structural examinations including full colonoscopy, flexible sigmoidoscopy, double contrast barium enema and computed tomographic colonography. 6 Although the validity of the structural exams, especially colonoscopy, is well proven, they are either highly invasive or technically complex and expensive. 3,7 In many countries FOBT remains the most popular mass screening method due to its low cost, noninvasiveness and simplicity, however this test often produces both false-negative and false-positive results. [3][4][5][6][8][9][10] Stool DNA analysis targeting molecular markers in exfoliated colonocytes excreted with faeces is being actively developed, 12-18 but its suitability for CRC screening is still questioned. Purification of human DNA from stool is difficult, [14][15][16] and there is no unique molecular signature reliably indicating cancer presence. The latter difficulty resulted in the use of multimarker assays, 3,9,[11][12][13][14][15][16][17][18] making the cost-effectiveness of the approach a major issue. 9,[19][20][21] It has been suggested that exfoliated colonocytes collected directly from the surface of colonic mucosa could serve f...

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Rates of New or Missed Colorectal Cancers After Colonoscopy and Their Risk Factors: A Population-Based Analysis

Cited by 579 publications

References 11 publications

Adenoma Detection Rate and Risk of Colorectal Cancer and Death

Adenoma Detection Rate and Risk of Colorectal Cancer and Death

Development of a mouse model for sporadic and metastatic colon tumors and its use in assessing drug treatment

A case‐control study of colorectal cancer detection by quantification of DNA isolated from directly collected exfoliated colonocytes

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