scholarly journals 96P Early-onset colorectal cancer prognosis, conflict resolution, review of literature and meta-analysis

2020 ◽  
Vol 31 ◽  
pp. S1279
Author(s):  
E.S. Poles ◽  
D. Barakat ◽  
S. Abdel-Karim ◽  
S. Eid ◽  
D. El-Sers ◽  
...  
2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Hengjing Li ◽  
Daniel Boakye ◽  
Xuechen Chen ◽  
Michael Hoffmeister ◽  
Hermann Brenner

2020 ◽  
Vol 1 (3) ◽  
Author(s):  
Hytham K. S. Hamid ◽  
Artur Marc-Hernández ◽  
Javier Hernández-Losa ◽  
Jaime Ruiz-Tovar

Background: Several studies have investigated the possible role of John Cunningham virus (JCV) in colorectal carcinogenesis, however the results were conflicting. The aim of this meta-analysis was to examine the association between JCV and colorectal tumors with special reference to early-onset colorectal cancer (EO-CRC).Methods: A systematic search was conducted through the Embase, Cochrane Collaboration, and PubMed databases for studies comparing the presence of JCV DNA in colorectal cancerous and non-cancerous tissues. Countries where the studies were conducted were categorized into high and low prevalence settings for EO-CRC, and according to the incidence rates of EO-CRC into rising-trend, stable-trend, and decreasing-trend settings. The strength of association was estimated by Peto odds ratio and 95% confidence interval.Results: The meta-analysis showed that JCV increased the odds for colorectal cancer by 4.1-fold, and for colorectal adenoma by 6-fold in comparison to controls. Compared with adjacent and non-adjacent colorectal tissues, JCV increased the odds for colorectal cancer by 4-fold and 4.2-fold, and for colorectal adenoma by 6.6-fold and 5.6-fold, respectively. The odds for colorectal tumor development with JCV infection were significantly higher in the high-prevalence settings than in the low-prevalence settings when compared with controls (P = 0.01) and matched adjacent colorectal tissues (P = 0.0002). Similarly, the odds for colorectal tumor development trended to be higher in the rising-trend settings than in the stable-trend settings when compared with controls (P = 0.05); no JCV DNA was detected in the decreasing-trend settings in both cancerous and non-cancerous colorectal tissues.   Conclusion: JCV infection is associated with increased risk of both colorectal cancer and adenoma, and is likely involved in early stage of carcinogenesis. The higher odds for colorectal tumor development in the high-prevalence and rising-trend settings for EO-CRC indicate that JCV may play a role in the international variations and temporal trends of EO-CRC in several parts of the world. 


Author(s):  
Dylan E. O’Sullivan ◽  
R. Liam Sutherland ◽  
Susanna Town ◽  
Kristian Chow ◽  
Jeremy Fan ◽  
...  

2020 ◽  
Vol 158 (6) ◽  
pp. S-496
Author(s):  
Arif A. Arif ◽  
Daljeet Chahal ◽  
Caroline Speers ◽  
Mary A. De Vera ◽  
Sharlene Gill ◽  
...  

Author(s):  
Jeong Eun Kim ◽  
Jaeyong Choi ◽  
Chang-Ohk Sung ◽  
Yong Sang Hong ◽  
Sun Young Kim ◽  
...  

AbstractThe global incidence of early-onset colorectal cancer (EO-CRC) is rapidly rising. However, the reason for this rise in incidence as well as the genomic characteristics of EO-CRC remain largely unknown. We performed whole-exome sequencing in 47 cases of EO-CRC and targeted deep sequencing in 833 cases of CRC. Mutational profiles of EO-CRC were compared with previously published large-scale studies. EO-CRC and The Cancer Genome Atlas (TCGA) data were further investigated according to copy number profiles and mutation timing. We classified colorectal cancer into three subgroups: the hypermutated group consisted of mutations in POLE and mismatch repair genes; the whole-genome doubling group had early functional loss of TP53 that led to whole-genome doubling and focal oncogene amplification; the genome-stable group had mutations in APC and KRAS, similar to conventional colon cancer. Among non-hypermutated samples, whole-genome doubling was more prevalent in early-onset than in late-onset disease (54% vs 38%, Fisher’s exact P = 0.04). More than half of non-hypermutated EO-CRC cases involved early TP53 mutation and whole-genome doubling, which led to notable differences in mutation frequencies between age groups. Alternative carcinogenesis involving genomic instability via loss of TP53 may be related to the rise in EO-CRC.


Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3857
Author(s):  
Pilar Mur ◽  
Nuria Bonifaci ◽  
Anna Díez-Villanueva ◽  
Elisabet Munté ◽  
Maria Henar Alonso ◽  
...  

A large proportion of familial and/or early-onset cancer patients do not carry pathogenic variants in known cancer predisposing genes. We aimed to assess the contribution of previously validated low-risk colorectal cancer (CRC) alleles to familial/early-onset CRC (fCRC) and to serrated polyposis. We estimated the association of CRC with a 92-variant-based weighted polygenic risk score (wPRS) using 417 fCRC patients, 80 serrated polyposis patients, 1077 hospital-based incident CRC patients, and 1642 controls. The mean wPRS was significantly higher in fCRC than in controls or sporadic CRC patients. fCRC patients in the highest (20th) wPRS quantile were at four-fold greater CRC risk than those in the middle quantile (10th). Compared to low-wPRS fCRC, a higher number of high-wPRS fCRC patients had developed multiple primary CRCs, had CRC family history, and were diagnosed at age ≥50. No association with wPRS was observed for serrated polyposis. In conclusion, a relevant proportion of mismatch repair (MMR)-proficient fCRC cases might be explained by the accumulation of low-risk CRC alleles. Validation in independent cohorts and development of predictive models that include polygenic risk score (PRS) data and other CRC predisposing factors will determine the implementation of PRS into genetic testing and counselling in familial and early-onset CRC.


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