Topic Highlight Open Access
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Oncol. Jun 15, 2016; 8(6): 481-488
Published online Jun 15, 2016. doi: 10.4251/wjgo.v8.i6.481
Colorectal cancer in the young, many questions, few answers
Kemal I Deen, Hiroshi Silva, Raeed Deen, Pramodh C Chandrasinghe
Kemal I Deen, Consultant in Colon and Rectal Surgery, The Asiri Surgical Hospital, Colombo 11600, Sri Lanka
Hiroshi Silva, Pramodh C Chandrasinghe, The University of Kelaniya Medical School, Ragama 11600, Sri Lanka
Raeed Deen, The University of Sydney Medical School, Sydney NSW 2006, Australia
Author contributions: All authors equally contributed to this paper with conception and design, literature review and analysis, drafting and critical revision and editing, and final approval of the final version.
Conflict-of-interest statement: No potential conflicts of interest relevant to this article were reported.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Kemal I Deen, MD, MS, FRCS, FACRSI, FNat, Ac Sci, Consultant in Colon and Rectal Surgery, The Asiri Surgical Hospital, No.21 Kirimandala Mawatha, Colombo 11600, Sri Lanka.
Telephone: +94-777-746158
Received: January 4, 2016
Peer-review started: January 5, 2016
First decision: January 30, 2016
Revised: February 29, 2016
Accepted: March 14, 2016
Article in press: March 16, 2016
Published online: June 15, 2016


At a time where the incidence of colorectal cancer, a disease predominantly of developed nations, is showing a decline in those 50 years of age and older, data from the West is showing a rising incidence of this cancer in young individuals. Central to this has been the 75% increase in rectal cancer incidence in the last four decades. Furthermore, predictive data based on mathematical modelling indicates a 124 percent rise in the incidence of rectal cancer by the year 2030 - a statistic that calls for collective global thought and action. While predominance of colorectal cancer (CRC) is likely to be in that part of the large bowel distal to the splenic flexure, which makes flexible sigmoidoscopic examination an ideal screening tool, the cost and benefit of mass screening in young people remain unknown. In countries where the incidence of young CRC is as high as 35% to 50%, the available data do not seem to indicate that the disease in young people is one of high red meat consuming nations only. Improvement in our understanding of genetic pathways in the aetiology of CRC, chiefly of the MSI, CIN and CIMP pathway, supports the notion that up to 30% of CRC is genetic, and may reflect a familial trait or environmentally induced changes. However, a number of other germline and somatic mutations, some of which remain unidentified, may play a role in the genesis of this cancer and stand in the way of a clear understanding of CRC in the young. Clinically, a proportion of young persons with CRC die early after curative surgery, presumably from aggressive tumour biology, compared with the majority in whom survival after operation will remain unchanged for five years or greater. The challenge in the future will be to determine, by genetic fingerprinting or otherwise, those at risk of developing CRC and the determinants of survival in those who develop CRC. Ultimately, prevention and early detection, just like for those over 50 years with CRC, will determine the outcome of CRC in young persons. At present, aside from those with an established familial tendency, there is no consensus on screening young persons who may be at risk. However, increasing awareness of this cancer in the young and the established benefit of prevention in older persons, must be a message that should be communicated with medical students, primary health care personnel and first contact doctors. The latter constitutes a formidable challenge.

Key Words: Colon cancer, Young age, Rectal cancer, Colorectal cancer, Young patients, Survival, Early onset

Core tip: This review of colorectal cancer in the young focuses on new data that reveal CRC to be more a left sided cancer than previously thought and the predicted rise by the year 2030. The article outlines the genetics of colorectal cancer (CRC) and discusses limitation in current knowledge in establishing a fingerprint for sporadic CRC. Aside from diet in its aetiology, luminal alkalinity and the colonic microbiome may be contributory and require further research. The review discusses the need for increased awareness of CRC in the young and the need for global consensus on screening young people at risk.


Colorectal cancer (CRC) is now the fourth most common cause of cancer deaths, with 600000 deaths reported worldwide annually - about 8% of all cancer deaths[1,2]. It is the third most common cancer in men and the second most common cancer in women. The sporadic form, known to affect individuals in their fifth and sixth decades of life[3], arises from a pre-existing polyp which progresses to cancer through the adenoma-dysplasia-carcinoma sequence; a pathological process which, in general, takes five to ten years[4], and lends itself to prevention by screening[5,6]. CRC is a disease of developed nations, and screening by faecal occult blood testing and colonoscopy has stemmed its incidence in those over 50 years[6]. By contrast, CRC in the young, was a disease prevalent in the developing world[7-14] compared with Australia, New Zealand and the West, where its prevalence in young individuals was low[11,15,16]. However, more recently, there has been an increase in the number of reports of CRC in the young from the developed world[17-19]. This is of concern because the incidence of rectal cancer has risen by 75% in the last 40 years[20-22], contributing chiefly to the overall rise in cancer prevalence. Furthermore, this disease affects people in the prime of their life, and unlike cancer in older individuals, there is limited knowledge about the aetiology and pathogenesis of CRC in the young. The aim of this review is to present the current status of CRC in the young and to highlight areas for future research.


Historically, CRC in young patients was highest in proportional prevalence from the Asian region. Studies have reported a high young cancer prevalence of 38% in Egypt[7], 18% in Turkey[8], 39% in India[9], 29% in Nepal[10], 23% from Saudi Arabia[11], 19.7% from Sri Lanka[12], 52% from a single institution in Pakistan[13] and 10.1% from Taiwan[14]. Most significantly, a recent study from the United States[19], where the authors evaluated the records of 393241 patients over a 15-years period, revealed an overall decline in CRC by 0.92% - the effect attributed to screening. While this was true for those over 50 years old with CRC, the study observed an alarming increase in CRC in those less than 50 years, specifically, in young patients less than 35 years. Using statistical modelling, the authors predicted an increase in colon cancer by 90% in patients aged 20 to 34 years and 27.7% in those 35 to 49 years old by the year 2030. For rectal cancer, the predicted percentage increase in cancer prevalence for these two age groups was 124.2% and 46% respectively. Gender based analysis of CRC in young patients revealed an equal prevalence in young men and women[22] contradicting the theory that female hormones are protective of colon and rectal cancer. Furthermore, a 1991 study of young patients in North America showed that the disease occurred in 34% more black men and 45% more black women compared with white Caucasian counterparts[23]. Most young patients did not report a family history of CRC; O’Connell et al[22] revealed that only 23% of young patients with CRC reported the presence of cancer in a family member.


Contrary to previous knowledge, a current estimate of the proportion of CRC likely to have a major hereditary component is between 15% and 30%[24]. The common heritable syndromes in CRC are either familial adenomatous polyposis (FAP) or hereditary non-polyposis colorectal cancer (HNPCC)[25-27] known to be found in 2 to 5 percent of all patients with CRC. Familial adenomatous polyposis is defined by phenotype if an individual has multiple colonic polyps, usually over 100, in association with loss of the tumour suppressor gene -the adenomatous polyposis coli-APC gene-located on the long arm of chromosome 5 (5q21)[25]. Most FAP patients will develop CRC by age 40 years, while in a minority, cancer will manifest in the fifth decade or after, due to the presence of the attenuated FAP gene. In contrast to FAP, HNPCC, first described by Henry Lynch, is characterised by the presence of fewer colonic polyps or cancer that is indistinguishable from sporadic CRC. In both conditions, which are of autosomal dominant inheritance, family history is of prime importance. For HNPCC, an affected member or members of a family should have had either CRC (Lynch type 1-site specific) or other extra-intestinal cancers (Lynch type 2), in association with an index patient with CRC. In the absence of definitive genetic testing, a detailed family history was essential and formed the core of the Amsterdam and Bethesda criteria to make a diagnosis of HNPCC[28,29]. Currently, we know that young patients with an underlying genetic syndrome are more likely to have a family history of cancer and present earlier compared with those with no known genetic syndrome, who presented with late stage metastatic disease[30]. Thus, family history must continue to remain an essential component of clinical evaluation in patients with CRC, while it is essential to note that up to 20 percent of patients with a germline mutation in the study reported by Mork et al[30] had no family history of CRC.


Several studies have reported that CRC in the young is a condition mostly confined to the left colon and rectum; in a retrospective study of young patients, Leff et al[31] revealed that 65% of cancers were in the rectum and that 83% of all colon and rectal cancers were distal to the splenic flexure. Kumar et al[32] reported that CRC was confined to the left colon and rectum in 67% of their study population Furthermore, O’Connell et al[22] in a structured review of 55 studies comprising 6425 patients with young CRC, reported that cancer of the rectum was most frequent (54%). In the most recent publication of the Surveillance Epidemiology and End Result (SEER) study from the United States, dominance of cancer in the left colon and rectum was again mirrored[19].


Studies have shown that CRC in young patients presents with three cardinal features of rectal bleeding, abdominal pain and alteration in bowel habit - constipation, altered stool diameter, mucoid rectal discharge[33,34]. In general, CRC diagnosis in young patients was associated with a delay of approximately 6 mo[33]. Physician related delay in diagnosis was chiefly because of a lack of understanding and suspicion of this disease in the young, where symptoms in young patients were considered due to such benign causes as haemorrhoidal disease by first contact physicians and patients alike. Some other factors that may contribute to delay are patients’ preference in seeking non-traditional methods of symptom relief, such as Ayurvedha and Chinese medical treatment, in Asia, and because practitioners of allopathic medicine fail to perform a focused rectal examination at the point of first contact. With current worldwide reports of increasing prevalence of young CRC, it is important that we offer young symptomatic patients flexible sigmoidoscopy early, after comprehensive clinical examination, including focused digital rectal examination.


In young patients, CRC is likely to be found in those with a heritable syndrome[28-30] such as FAP and HNPCC. In the Lynch Syndrome, tumours have been known to be predominant in the proximal colon[35,36], but recent research revealed contradictory data where the most frequent site among early onset CRC patients was the distal colon[37]. Of these, between 40 and 60 percent were in the rectum[38,39]. In the WHO classification of tumours[40], HNPCC and sporadic CRC with microsatellite instability have been classified based on the site and microscopic criteria. These are (1) proximally located mucinous adenocarcinomas which are commonly well circumscribed and are moderate-to-well differentiated; (2) proximally located poorly differentiated adenocarcinomas which show failure of gland formation with malignant epithelium arranged in small clusters, irregular trabeculae or large aggregates in well circumscribed tumours; and (3) adenomas in HNPCC indicating features of high cancer risk including villous and high grade intraepithelial neoplasia which display good circumscription and present as polypoid growths, plaques, bulky masses or ulcers rather than diffuse growths or strictures[40]. In a single centre study, mucinous and signet-ring histological subtypes and poor to non-differentiated tumours were frequently seen among the young[38,41,42], and accounted for 41.5% of all tumours[38]. The incidence of tumour in situ (Tis) was lower in young patients compared with older patients and may indicate either failure of early detection or rapid progression from adenoma to carcinoma in the young compared with older patients[43]. Other features that suggest more aggressive tumour biology in the young compared with older patients are the higher percentages of patients with lymph node metastasis (≥ 4 lymph nodes), distance metastasis and stage IV disease[41,42].


All colorectal cancers occur from genetic mutations, which are part of a familial syndrome, hereditary syndrome or as sporadic cancer[44]. Frequent among young patients are either FAP, variants of FAP or HNPCC. Historically, in the sporadic subtype, the origin of CRC was attributed to various common or rare genetic alterations that displayed variable penetrance, and remained largely unidentified[45]. It is now estimated that up to 30% of CRC may have a hereditary component, with identifiable genetic aberration, especially if cancer occurs in the young[23,24,30,46]. Next generation sequencing (NGS) is likely to further increase our knowledge of hitherto unidentified chromosome aberrations in association with cancer[47] resulting in such diagnoses as the Li-Fraumeni syndrome, Cowden’s disease, Juvenile polyposis and Peutz-Jegher syndrome[46].

Different from germline mutations, somatic mutation, that may be spontaneous or follow contact with luminal carcinogens, may result in genetic alteration of a colonocyte in which control of apoptosis is lost in conjunction with a series of chromosomal changes that create microsatellite instability[43]. In fact, the aetiology and range of hitherto unidentified germline and early onset somatic mutations is likely to be more extensive than previously understood, which makes our understanding of the pathology in young patients with sporadic cancer even more complex. Essential to our understanding of tumourigenesis is knowledge of preservation of DNA integrity in the intestinal epithelial cell; deep within the base of the intestinal crypt lies the colonocyte stem cell that is covered in a thick layer of mucus. Each stem cell is designed to replicate into a transit amplifier stem cell and an inert stem cell that remains in the protected crypt base, remote from contact with carcinogens that may be present in the lumen of large bowel, thus preserving its DNA intact. In health, upward migration of the amplifier cell will give rise to a functional colonocyte that will shed in 5 to 7 d by genetically determined apoptosis, controlled by the p53 gene located on chromosome 17 and the mitogen-activated protein kinase pathway (MAPK)[43]. The MAPK pathway, of which KRAS and BRAF proteins are part, regulates cell proliferation, cell differentiation, cellular aging and apoptosis[48]. Programmed colonocyte death prevents the propagation of mutagenic change, and constitutes yet another strategy of preserving intestinal cell DNA integrity[43]. In the adenoma-carcinoma sequence, initialisation of neoplastic change occurs with silencing of the tumour suppressor genes located on chromosome 5 (APC gene), followed by serial changes in chromosome 17 (p53 gene-mutated in colorectal cancer) and chromosome 18 (long arm deletion)[49]. Furthermore, simultaneous activation of the proto-oncogene K-Ras will lead to uncontrolled cell growth[49]. Hence, both germline mutations and somatic mutations may drive colorectal cancer in the young.

Currently, the genetic mechanisms that trigger CRC are grounded in three major pathways; chromosomal instability (CIN), microsatellite instability (MSI) and the cytosine-phosphate-guanine island methylator phenotype pathway (CIMP) pathway[50,51] - mechanisms that create genomic instability, which together with a process that will selectively support mutagenic driver cells, produce colorectal cancer. It is essential in our understanding of this process that none of these pathways is mutually exclusive. However, CIN aberrations, by far, constitute the most common pathway in the development of CRC[52].

CIN pathway

This describes the classical adenoma-dysplasia-carcinoma sequence in which it is thought that tumour formation is a result of progressive and sequential inactivation of tumour suppressor genes and, correspondingly, activation of tumour promoting oncogenes - mutation in the adenomatous polyposis coli (APC) gene being an important initial step in this pathway[52]. Likewise, it is known that mutation of the KRAS oncogene contributes to CIN-associated sporadic CRC in up to a half of such sporadic cancer[53]. Since RAS proteins control signaling in cell differentiation and apoptosis, disruption of such pathways will lead to neoplastic transformation. CIN-associated tumours comprise 75% to 80% of all tumours found in Western populations[54].

MSI pathway

It is known that formation of new strands of DNA may be interrupted by base pair mismatches, i.e., mutations which may be either deletions or insertions. In health, the role of mismatch repair proteins is to bind, remove and repair the region of the mismatch error. In cells with malfunction of mismatch repair proteins, these mutations will tend to accumulate within areas of DNA coding called microsatellites. Such areas of microsatellite instability are the cause of sporadic CRC[55].

CIMP pathway

This pathway of CRC differs fundamentally from CIN and MSI, in that, it causes mutation and epigenetic silencing of genes that control the cell cycle outside the APC control system. This pathway is chiefly associated with a group of protein kinases known as BRAF proteins, and usually occurs due to promoter methylation and silencing of the mut-L homologue 1 gene (MLH-1- short arm of chromosome 3), resulting in microsatellite instability. CIMP associated cancer is frequently found in patients of older age, has a slight female preponderance and is associated with right sided colon cancer, similar to the Lynch syndrome. However, it is rare for patients with Lynch syndrome-associated CRC to have BRAF mutations, which helps differentiate Lynch syndrome associated CRC from sporadic CRC[56]. Thus, it becomes evident that no two colorectal cancers are likely to be the same, and that each will have its own unique characteristic genetic “fingerprint”. It is also known that each cancer may have more than one of the aforementioned carcinogenic pathways[57,58], which makes genetic imprinting of sporadic CRC all that more challenging. Furthermore, since CIN and MSI associated CRC is known to respond differently to chemotherapeutic agents and impact on cancer related survival, to enable tumour specific personalized treatments, future standard pathological tumour work-up may have to include such genetic “fingerprinting”.


A historic study of tumour genesis in the colon shed light on the alkaline environment in the lumen of the colon which, combined with secondary bile acids, is a promoter of tumour formation[59]. N-nitroso compounds and ammonia, produced from bacterial action upon undigested protein products, and secondary bile acids alter the luminal environment, which affect colonocyte function and deplete oxygen levels in the colonic mucosa, thus favouring tumourigenesis. Furthermore, rapid urbanization with environmental pollution, lifestyle alterations such as reduction in physical activity and change in dietary patterns in young individuals[9,60], may have also contributed to the rising incidence of CRC, although this alone does not explain its disproportionate rise in incidence in previously low incidence parts of the world[61].


Multiple studies of young patients with CRC from cancer registries have shown that, in young patients, 5-year survival did not differ from older patients despite a greater proportion of locally advanced cancer, regional lymph node involvement and less favourable histological types in the young[61-63]. Ruiz et al[64] showed an overall survival rate of 69.4% and 67.4% at 5 years for colon and rectal cancer respectively from a cancer registry database in Peru. Likewise, Parc et al[63], reporting survival data from the central South Korean cancer registry, revealed a 5-year survival of 66% for young patients with cancer of the proximal colon, 70% for patients with distal colon cancer and 66% in patients with rectal cancer. However, if young patients with CRC present with concomitant metastasis, or in the case of a small proportion of patients with unfavourable histological features (poorly differentiated cancer, signet ring cancer), survival may be poor[65]. Chan et al[66] have shown that survival in young patients with a poor prognosis is predictable, and that maximum survival in this group of young patients after surgical intervention is no more than 20 mo.


CRC screening guidelines currently recommend routine screening of individuals from the age of 50 years. The screening tests range from invasive procedures such as flexible sigmoidoscopy and colonoscopy, through imaging investigations such as virtual colonoscopy, to minimally invasive procedures such as faecal occult tests[67].

Although each test has its own different advantages and limitations, colonoscopy - widely regarded as the gold standard - has shown to decrease the incidence of CRC up to 80%. However, it is essential to note that colonoscopy is not a perfect test - studies have shown a miss rate of 6%-12% of adenomas > 1 cm and 5% for CRC[67]. Faecal occult tests have shown promise too; an example being, the faecal immunochemical test which has shown high rates of detection of prevalent CRC in an asymptomatic population[68].

With the rising incidence and mortality of CRC in young patients, effective screening methods must be able to detect these tumours early. Current guidelines suggest that individuals with a family history of CRC or adenomatous polyps, other than FAP, undergo screening earlier than at 50 years. That is, from the age of 40 or 10 years before the youngest cancer affected family member, while those with a family history of FAP undergo screening in adolescence[68]. Population based early-onset CRC screening has not been justified due to low prevalence, cost and potential adverse procedural outcomes outweighing the benefits[17]. To detect early onset CRC, suggestions have been to undertake routine screening from 40 years, instead of 50 years - however, decision analysis models have shown no significant life-year gains for this change[37].

To combat the rising incidence by screening of potential early onset CRC patients, awareness among physicians, primary healthcare workers and the lay public must increase. For the physician, this should begin at the stage of medical school by integration of preventive medicine and longitudinal cancer prevention modules into medical school curriculums - which have shown positive results[69], and will improve the future physician’s ability to identify young individuals at high risk.

In terms of young patient awareness, it is imperative that young adults are aware of screening for early onset CRC. A study revealed that university students had very poor knowledge of CRC screening, indicating the necessity for early-onset cancer awareness campaigns[70]. Another feasible plan to improve screening rates is the employment of a well-trained lay cancer-screening navigator; this person’s role would involve contacting individuals, discussing the importance of screening for CRC and implementing screening procedures such as faecal tests sent by mail. Although this was a feasible strategy for older patients aged 50 to 74 years[71], it has yet to be determined how effective this strategy would be in younger individuals.

To avoid low screening rates, patients’ screening method preferences require consideration. Studies have shown faecal aversion to be one of the chief hindrances to screening participation, and a survey revealed that 78% of participants would prefer to provide a blood sample instead[72]. One such blood test to detect CRC, which requires further development, is the assessment of circulating methylated SEPT9 DNA, and although it is able to detect CRC in an asymptomatic individual, improved sensitivity is required for population screening[73]. A highly sensitive and specific blood test for CRC could very well become the gold standard in the future, and thereby decrease incidence and mortality rates.


An epidemic of colorectal cancer in young patients is imminent. Based on better understanding of genetic mechanisms, currently it is estimated that genetic predisposition to colorectal cancer is 30% of all CRC. The figure is likely to be higher in young patients if all young patients with CRC were to have genetic assessment by NGS testing. While the MSI, CIN and CIMP pathways have been isolated and well defined, a number of germline and somatic mutations in CRC are likely to manifest from widespread use of NGS, multiple panel genetic tests. Furthermore, multiple permutations of genetic alterations are likely to show up in individual CRCs, with overlap of previously known syndrome based genetic changes, which will make individual genetic fingerprinting of CRC more complex and perhaps the age of onset of CRC, that is, whether young or older, irrelevant. In lifestyle assessment, populations, such as in Egypt, where consumption of red meat is high seem to have similar proportions of young patients with CRC compared with predominantly non-meat eating populations, such as is found in India, which further complicates the search for a common lifestyle aetiology. What is common across the world in lifestyle is the growing fast food industry and childhood obesity; more thought and research needs to focus on its contributory role. For the present, the majority of cases of CRC remains sporadic and of multifactorial origin: Diet and nutrition, obesity, the colonic microbiome, smoking, alcohol consumption and hitherto unknown germline or somatic mutation. The role of screening for CRC in young patients is not likely to follow a “one test fits all” policy until we have worldwide genetic data in this group of patients. At present, mass screening by flexible sigmoidoscopy is expensive and may yield low productive rates. However, better education of medical students, primary healthcare personnel and first contact doctors, about the benefit of prevention and early detection of CRC in the young is likely to improve early detection rates in young persons. Whether early detection influences lead-time in such young patients with cancer remains unresolved, as some studies have shown a clear cut-off in survival at around 2 years. It is a formidable challenge to fight the rising incidence and mortality in early onset CRC patients, an effort that will require global co-operation and consensus.


P- Reviewer: Martinez JD, Park JH, Yaeger R S- Editor: Qi Y L- Editor: A E- Editor: Lu YJ

1.  Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer. 2010;127:2893-2917.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10555]  [Cited by in F6Publishing: 9791]  [Article Influence: 1055.5]  [Reference Citation Analysis (3)]
2.  American Cancer Society Global Cancer Facts and Figures. 2nd ed. Atlanta: American Cancer Society 2011; .  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Siegel R, Ward E, Brawley O, Jemal A. Cancer statistics, 2011: the impact of eliminating socioeconomic and racial disparities on premature cancer deaths. CA Cancer J Clin. 2011;61:212-236.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2864]  [Cited by in F6Publishing: 2647]  [Article Influence: 286.4]  [Reference Citation Analysis (0)]
4.  Vogelstein B, Fearon ER, Hamilton SR, Kern SE, Preisinger AC, Leppert M, Nakamura Y, White R, Smits AM, Bos JL. Genetic alterations during colorectal-tumor development. N Engl J Med. 1988;319:525-532.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4353]  [Cited by in F6Publishing: 1457]  [Article Influence: 131.9]  [Reference Citation Analysis (0)]
5.  Scholefield JH, Moss S, Sufi F, Mangham CM, Hardcastle JD. Effect of faecal occult blood screening on mortality from colorectal cancer: results from a randomised controlled trial. Gut. 2002;50:840-844.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 181]  [Cited by in F6Publishing: 138]  [Article Influence: 9.5]  [Reference Citation Analysis (0)]
6.  Bond JH. Fecal occult blood test screening for colorectal cancer. Gastrointest Endosc Clin N Am. 2002;12:11-21.  [PubMed]  [DOI]  [Cited in This Article: ]
7.  Abou-Zeid AA, Khafagy W, Marzouk DM, Alaa A, Mostafa I, Ela MA. Colorectal cancer in Egypt. Dis Colon Rectum. 2002;45:1255-1260.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 42]  [Cited by in F6Publishing: 31]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
8.  Alici S, Aykan NF, Sakar B, Bulutlar G, Kaytan E, Topuz E. Colorectal cancer in young patients: characteristics and outcome. Tohoku J Exp Med. 2003;199:85-93.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 30]  [Cited by in F6Publishing: 26]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
9.  Gupta S, Bhattacharya D, Acharya AN, Majumdar S, Ranjan P, Das S. Colorectal carcinoma in young adults: a retrospective study on Indian patients: 2000-2008. Colorectal Dis. 2010;12:e182-e189.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 24]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
10.  Singh Y, Vaidya P, Hemandas AK, Singh KP, Khakurel M. Colorectal carcinoma in Nepalese young adults: presentation and outcome. Gan To Kagaku Ryoho. 2002;29 Suppl 1:223-229.  [PubMed]  [DOI]  [Cited in This Article: ]
11.  Isbister WH. Colorectal cancer Below Age 40 in The Kingdom of Saudi Arabia. Aust N Z J Surg. 1992;62:468-472.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 52]  [Cited by in F6Publishing: 43]  [Article Influence: 1.8]  [Reference Citation Analysis (0)]
12.  de Silva MV, Fernando MS, Fernando D. Comparison of some clinical and histological features of colorectal carcinoma occurring in patients below and above 40 years. Ceylon Med J. 2000;45:166-168.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 9]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
13.  Amini AQ, Samo KA, Memon AS. Colorectal cancer in younger population: our experience. J Pak Med Assoc. 2013;63:1275-1277.  [PubMed]  [DOI]  [Cited in This Article: ]
14.  Han-Shiang C. Curative resection of colorectal adenocarcinoma: multivariate analysis of 5-year follow-up. World J Surg. 1999;23:1301-1306.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 12]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
15.  Adloff M, Arnaud JP, Schloegel M, Thibaud D, Bergamaschi R. Colorectal cancer in patients under 40 years of age. Dis Colon Rectum. 1986;29:322-325.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 61]  [Cited by in F6Publishing: 19]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
16.  Keating J, Yong D, Cutler G, Johnston J. Multidisciplinary treatment of colorectal cancer in New Zealand: survival rates from 1997-2002. N Z Med J. 2006;119:U2238.  [PubMed]  [DOI]  [Cited in This Article: ]
17.  Young JP, Win AK, Rosty C, Flight I, Roder D, Young GP, Frank O, Suthers GK, Hewett PJ, Ruszkiewicz A. Rising incidence of early-onset colorectal cancer in Australia over two decades: report and review. J Gastroenterol Hepatol. 2015;30:6-13.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 83]  [Cited by in F6Publishing: 69]  [Article Influence: 13.8]  [Reference Citation Analysis (0)]
18.  Steliarova-Foucher E, Stiller C, Kaatsch P, Berrino F, Coebergh JW, Lacour B, Parkin M. Geographical patterns and time trends of cancer incidence and survival among children and adolescents in Europe since the 1970s (the ACCISproject): an epidemiological study. Lancet. 2004;364:2097-2105.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 369]  [Cited by in F6Publishing: 94]  [Article Influence: 23.1]  [Reference Citation Analysis (0)]
19.  Bailey CE, Hu CY, You YN, Bednarski BK, Rodriguez-Bigas MA, Skibber JM, Cantor SB, Chang GJ. Increasing disparities in the age-related incidences of colon and rectal cancers in the United States, 1975-2010. JAMA Surg. 2015;150:17-22.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 394]  [Cited by in F6Publishing: 361]  [Article Influence: 65.7]  [Reference Citation Analysis (0)]
20.  Merrill RM, Anderson AE. Risk-adjusted colon and rectal cancer incidence rates in the United States. Dis Colon Rectum. 2011;54:1301-1306.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 10]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
21.  O’Connell JB, Maggard MA, Liu JH, Etzioni DA, Livingston EH, Ko CY. Rates of colon and rectal cancers are increasing in young adults. Am Surg. 2003;69:866-872.  [PubMed]  [DOI]  [Cited in This Article: ]
22.  O’Connell JB, Maggard MA, Livingston EH, Yo CK. Colorectal cancer in the young. Am J Surg. 2004;187:343-348.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 181]  [Cited by in F6Publishing: 167]  [Article Influence: 10.6]  [Reference Citation Analysis (0)]
23.  Griffin PM, Liff JM, Greenberg RS, Clark WS. Adenocarcinomas of the colon and rectum in persons under 40 years old. A population-based study. Gastroenterology. 1991;100:1033-1040.  [PubMed]  [DOI]  [Cited in This Article: ]
24.  Slattery ML. Diet, lifestyle, and colon cancer. Semin Gastrointest Dis. 2000;11:142-146.  [PubMed]  [DOI]  [Cited in This Article: ]
25.  Fearnhead NS, Britton MP, Bodmer WF. The ABC of APC. Hum Mol Genet. 2001;10:721-733.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 591]  [Cited by in F6Publishing: 520]  [Article Influence: 29.6]  [Reference Citation Analysis (0)]
26.  Jass JR. Hereditary Non-Polyposis Colorectal Cancer: the rise and fall of a confusing term. World J Gastroenterol. 2006;12:4943-4950.  [PubMed]  [DOI]  [Cited in This Article: ]
27.  Lynch HT, Lynch JF. Hereditary nonpolyposis colorectal cancer (Lynch syndromes I and II): a common genotype linked to oncogenes? Med Hypotheses. 1985;18:19-28.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 1]  [Reference Citation Analysis (0)]
28.  Vasen HF, Watson P, Mecklin JP, Lynch HT. New clinical criteria for hereditary nonpolyposis colorectal cancer (HNPCC, Lynch syndrome) proposed by the International Collaborative group on HNPCC. Gastroenterology. 1999;116:1453-1456.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1664]  [Cited by in F6Publishing: 577]  [Article Influence: 75.6]  [Reference Citation Analysis (0)]
29.  Umar A, Boland CR, Terdiman JP, Syngal S, de la Chapelle A, Rüschoff J, Fishel R, Lindor NM, Burgart LJ, Hamelin R. Revised Bethesda Guidelines for hereditary nonpolyposis colorectal cancer (Lynch syndrome) and microsatellite instability. J Natl Cancer Inst. 2004;96:261-268.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2011]  [Cited by in F6Publishing: 1644]  [Article Influence: 118.3]  [Reference Citation Analysis (0)]
30.  Mork ME, You YN, Ying J, Bannon SA, Lynch PM, Rodriguez-Bigas MA, Vilar E. High Prevalence of Hereditary Cancer Syndromes in Adolescents and Young Adults With Colorectal Cancer. J Clin Oncol. 2015;33:3544-3549.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 1]  [Reference Citation Analysis (0)]
31.  Leff DR, Chen A, Roberts D, Grant K, Western C, Windsor AC, Cohen CR. Colorectal cancer in the young patient. Am Surg. 2007;73:42-47.  [PubMed]  [DOI]  [Cited in This Article: ]
32.  Kumar RR, King J, Holt A, Huynh R, Mittal R, Deen R, Kim J. Prevalence of left-sided colorectal cancer and benefit of flexible sigmoidoscopy: a county hospital experience. Am Surg. 2007;73:994-997.  [PubMed]  [DOI]  [Cited in This Article: ]
33.  Dozois EJ, Boardman LA, Suwanthanma W, Limburg PJ, Cima RR, Bakken JL, Vierkant RA, Aakre JA, Larson DW. Young-onset colorectal cancer in patients with no known genetic predisposition: can we increase early recognition and improve outcome? Medicine (Baltimore). 2008;87:259-263.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 106]  [Cited by in F6Publishing: 51]  [Article Influence: 8.2]  [Reference Citation Analysis (0)]
34.  Taggarshe D, Rehil N, Sharma S, Flynn JC, Damadi A. Colorectal cancer: are the “young” being overlooked? Am J Surg. 2013;205:312-316; discussion 316.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 29]  [Cited by in F6Publishing: 31]  [Article Influence: 3.6]  [Reference Citation Analysis (0)]
35.  Lynch HT, Lynch PM, Lanspa SJ, Snyder CL, Lynch JF, Boland CR. Review of the Lynch syndrome: history, molecular genetics, screening, differential diagnosis, and medicolegal ramifications. Clin Genet. 2009;76:1-18.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 506]  [Cited by in F6Publishing: 423]  [Article Influence: 42.2]  [Reference Citation Analysis (0)]
36.  da Silva FC, de Oliveira LP, Santos EM, Nakagawa WT, Aguiar Junior S, Valentin MD, Rossi BM, de Oliveira Ferreira F. Frequency of extracolonic tumors in Brazilian families with Lynch syndrome: analysis of a hereditary colorectal cancer institutional registry. Fam Cancer. 2010;9:563-570.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 22]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
37.  Ahnen DJ, Wade SW, Jones WF, Sifri R, Mendoza Silveiras J, Greenamyer J, Guiffre S, Axilbund J, Spiegel A, You YN. The increasing incidence of young-onset colorectal cancer: a call to action. Mayo Clin Proc. 2014;89:216-224.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 218]  [Cited by in F6Publishing: 193]  [Article Influence: 31.1]  [Reference Citation Analysis (0)]
38.  You YN, Xing Y, Feig BW, Chang GJ, Cormier JN. Young-onset colorectal cancer: is it time to pay attention? Arch Intern Med. 2012;172:287-289.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 1]  [Reference Citation Analysis (0)]
39.  Zahir MN, Azhar EM, Rafiq S, Ghias K, Shabbir-Moosajee M. Clinical features and outcome of sporadic colorectal carcinoma in young patients: a cross-sectional analysis from a developing country. ISRN Oncol. 2014;2014:461570.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 12]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
40.  Hamilton SR, Aaltonen LA.  Pathology and genetics of tumours of the digestive system. Lyon: IARC press 2000; 103-126.  [PubMed]  [DOI]  [Cited in This Article: ]
41.  Fu JF, Huang YQ, Yang J, Yi CH, Chen HL, Zheng S. Clinical characteristics and prognosis of young patients with colorectal cancer in Eastern China. World J Gastroenterol. 2013;19:8078-8084.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 19]  [Cited by in F6Publishing: 19]  [Article Influence: 2.4]  [Reference Citation Analysis (0)]
42.  Domergue J, Ismail M, Astre C, Saint-Aubert B, Joyeux H, Solassol C, Pujol H. Colorectal carcinoma in patients younger than 40 years of age. Montpellier Cancer Institute experience with 78 patients. Cancer. 1988;61:835-840.  [PubMed]  [DOI]  [Cited in This Article: ]
43.  Armaghany T, Wilson JD, Chu Q, Mills G. Genetic alterations in colorectal cancer. Gastrointest Cancer Res. 2012;5:19-27.  [PubMed]  [DOI]  [Cited in This Article: ]
44.  Stigliano V, Sanchez-Mete L, Martayan A, Anti M. Early-onset colorectal cancer: a sporadic or inherited disease? World J Gastroenterol. 2014;20:12420-12430.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 63]  [Cited by in F6Publishing: 58]  [Article Influence: 9.0]  [Reference Citation Analysis (0)]
45.  Taylor DP, Burt RW, Williams MS, Haug PJ, Cannon-Albright LA. Population-based family history-specific risks for colorectal cancer: a constellation approach. Gastroenterology. 2010;138:877-885.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 139]  [Cited by in F6Publishing: 116]  [Article Influence: 11.6]  [Reference Citation Analysis (0)]
46.  Stoffel EM. Colorectal Cancer in Young Individuals: Opportunities for Prevention. J Clin Oncol. 2015;33:3525-3527.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 103]  [Cited by in F6Publishing: 47]  [Article Influence: 17.2]  [Reference Citation Analysis (0)]
47.  Frampton GM, Fichtenholtz A, Otto GA, Wang K, Downing SR, He J, Schnall-Levin M, White J, Sanford EM, An P. Development and validation of a clinical cancer genomic profiling test based on massively parallel DNA sequencing. Nat Biotechnol. 2013;31:1023-1031.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1178]  [Cited by in F6Publishing: 1075]  [Article Influence: 147.3]  [Reference Citation Analysis (0)]
48.  Fang JY, Richardson BC. The MAPK signaling pathways and colorectal cancer. Lancet Oncol. 2005;6:322-327.  [PubMed]  [DOI]  [Cited in This Article: ]
49.  Weinberg RA The Biology of Cancer. Baltimore, MD: Garland Science 2006; .  [PubMed]  [DOI]  [Cited in This Article: ]
50.  Grady WM, Pritchard CC. Molecular alterations and biomarkers in colorectal cancer. Toxicol Pathol. 2014;42:124-139.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 53]  [Cited by in F6Publishing: 48]  [Article Influence: 6.6]  [Reference Citation Analysis (0)]
51.  Lengauer C, Kinzler KW, Vogelstein B. Genetic instabilities in human cancers. Nature. 1998;396:643-649.  [PubMed]  [DOI]  [Cited in This Article: ]
52.  Powell SM, Zilz N, Beazer-Barclay Y, Bryan TM, Hamilton SR, Thibodeau SN, Vogelstein B, Kinzler KW. APC mutations occur early during colorectal tumorigenesis. Nature. 1992;359:235-237.  [PubMed]  [DOI]  [Cited in This Article: ]
53.  Tan C, Du X. KRAS mutation testing in metastatic colorectal cancer. World J Gastroenterol. 2012;18:5171-5180.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 73]  [Reference Citation Analysis (0)]
54.  Bardhan K, Liu K. Epigenetics and colorectal cancer pathogenesis. Cancers (Basel). 2013;5:676-713.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 142]  [Cited by in F6Publishing: 140]  [Article Influence: 17.8]  [Reference Citation Analysis (0)]
55.  Geiersbach KB, Samowitz WS. Microsatellite instability and colorectal cancer. Arch Pathol Lab Med. 2011;135:1269-1277.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 76]  [Cited by in F6Publishing: 42]  [Article Influence: 7.6]  [Reference Citation Analysis (0)]
56.  Iacopetta B, Li WQ, Grieu F, Ruszkiewicz A, Kawakami K. BRAF mutation and gene methylation frequencies of colorectal tumours with microsatellite instability increase markedly with patient age. Gut. 2006;55:1213-1214.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 10]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
57.  Kinzler KW, Vogelstein B. Landscaping the cancer terrain. Science. 1998;280:1036-1037.  [PubMed]  [DOI]  [Cited in This Article: ]
58.  Raskov H, Pommergaard HC, Burcharth J, Rosenberg J. Colorectal carcinogenesis--update and perspectives. World J Gastroenterol. 2014;20:18151-18164.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in CrossRef: 90]  [Cited by in F6Publishing: 90]  [Article Influence: 12.9]  [Reference Citation Analysis (0)]
59.  Newmark HL, Lupton JR. Determinants and consequences of colonic luminal pH: implications for colon cancer. Nutr Cancer. 1990;14:161-173.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 64]  [Cited by in F6Publishing: 52]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]
60.  Aune D, Chan DS, Lau R, Vieira R, Greenwood DC, Kampman E, Norat T. Dietary fibre, whole grains, and risk of colorectal cancer: systematic review and dose-response meta-analysis of prospective studies. BMJ. 2011;343:d6617.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 580]  [Cited by in F6Publishing: 490]  [Article Influence: 58.0]  [Reference Citation Analysis (0)]
61.  McKay A, Donaleshen J, Helewa RM, Park J, Wirtzfeld D, Hochman D, Singh H, Turner D. Does young age influence the prognosis of colorectal cancer: a population-based analysis. World J Surg Oncol. 2014;12:370.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 41]  [Cited by in F6Publishing: 47]  [Article Influence: 5.9]  [Reference Citation Analysis (0)]
62.  Schellerer VS, Merkel S, Schumann SC, Schlabrakowski A, Förtsch T, Schildberg C, Hohenberger W, Croner RS. Despite aggressive histopathology survival is not impaired in young patients with colorectal cancer: CRC in patients under 50 years of age. Int J Colorectal Dis. 2012;27:71-79.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 56]  [Cited by in F6Publishing: 57]  [Article Influence: 5.6]  [Reference Citation Analysis (0)]
63.  Park HC, Shin A, Kim BW, Jung KW, Won YJ, Oh JH, Jeong SY, Yu CS, Lee BH. Data on the characteristics and the survival of korean patients with colorectal cancer from the Korea central cancer registry. Ann Coloproctol. 2013;29:144-149.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 26]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
64.  Ruiz R, Taxa L, Casanova L, Ruiz E, Montenegro P. Clinicopathologic features and survival outcomes of colorectal cancer in young patients: Experience from a cancer institute in Peru. Ann Oncol. 2015;26:70-71.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 2]  [Article Influence: 0.2]  [Reference Citation Analysis (0)]
65.  Wang MJ, Ping J, Li Y, Adell G, Arbman G, Nodin B, Meng WJ, Zhang H, Yu YY, Wang C. The prognostic factors and multiple biomarkers in young patients with colorectal cancer. Sci Rep. 2015;5:10645.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 35]  [Article Influence: 5.2]  [Reference Citation Analysis (0)]
66.  Chan KK, Dassanayake B, Deen R, Wickramarachchi RE, Kumarage SK, Samita S, Deen KI. Young patients with colorectal cancer have poor survival in the first twenty months after operation and predictable survival in the medium and long-term: analysis of survival and prognostic markers. World J Surg Oncol. 2010;8:82.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 30]  [Article Influence: 2.5]  [Reference Citation Analysis (0)]
67.  Geiger TM, Ricciardi R. Screening options and recommendations for colorectal cancer. Clin Colon Rectal Surg. 2009;22:209-217.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 27]  [Cited by in F6Publishing: 28]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
68.  Levin B, Lieberman DA, McFarland B, Smith RA, Brooks D, Andrews KS, Dash C, Giardiello FM, Glick S, Levin TR. Screening and surveillance for the early detection of colorectal cancer and adenomatous polyps, 2008: a joint guideline from the American Cancer Society, the US Multi-Society Task Force on Colorectal Cancer, and the American College of Radiology. CA Cancer J Clin. 2008;58:130-160.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1114]  [Cited by in F6Publishing: 556]  [Article Influence: 85.7]  [Reference Citation Analysis (0)]
69.  Geller AC, Prout MN, Miller DR, Siegel B, Sun T, Ockene J, Koh HK. Evaluation of a cancer prevention and detection curriculum for medical students. Prev Med. 2002;35:78-86.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 33]  [Cited by in F6Publishing: 29]  [Article Influence: 1.7]  [Reference Citation Analysis (0)]
70.  Al-Naggar RA, Bobryshev YV. Knowledge of colorectal cancer screening among young Malaysians. Asian Pac J Cancer Prev. 2013;14:1969-1974.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 5]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
71.  Liu G, Perkins A. Using a lay cancer screening navigator to increase colorectal cancer screening rates. J Am Board Fam Med. 2015;28:280-282.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 5]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
72.  Osborne JM, Wilson C, Moore V, Gregory T, Flight I, Young GP. Sample preference for colorectal cancer screening tests: Blood or stool? Open J Preventat Med. 2012;2:326-331.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 23]  [Cited by in F6Publishing: 8]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
73.  Church TR, Wandell M, Lofton-Day C, Mongin SJ, Burger M, Payne SR, Castaños-Vélez E, Blumenstein BA, Rösch T, Osborn N. Prospective evaluation of methylated SEPT9 in plasma for detection of asymptomatic colorectal cancer. Gut. 2014;63:317-325.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 403]  [Cited by in F6Publishing: 364]  [Article Influence: 50.4]  [Reference Citation Analysis (0)]