sporadic colorectal cancer
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Diseases ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 86
Author(s):  
Emily Reznicek ◽  
Mohammad Arfeen ◽  
Bo Shen ◽  
Yezaz Ghouri

Ulcerative colitis (UC) is a risk factor for the development of inflammation-associated dysplasia or colitis-associated neoplasia (CAN). This transformation results from chronic inflammation, which induces changes in epithelial proliferation, survival, and migration via the induction of chemokines and cytokines. There are notable differences in genetic mutation profiles between CAN in UC patients and sporadic colorectal cancer in the general population. Colonoscopy is the cornerstone for surveillance and management of dysplasia in these patients. There are several modalities to augment the quality of endoscopy for the better detection of dysplastic or neoplastic lesions, including the use of high-definition white-light exam and image-enhanced colonoscopy, which are described in this review. Clinical practice guidelines regarding surveillance strategies in UC have been put forth by various GI societies, and overall, there is agreement between them except for some differences, which we highlight in this article. These guidelines recommend that endoscopically detected dysplasia, if feasible, should be resected endoscopically. Advanced newer techniques, such as endoscopic mucosal resection and endoscopic submucosal dissection, have been utilized in the treatment of CAN. Surgery has traditionally been the mainstay of treating such advanced lesions, and in cases where endoscopic resection is not feasible, a proctocolectomy, followed by ileal pouch-anal anastomosis, is generally recommended. In this review we summarize the approach to surveillance for cancer and dysplasia in UC. We also highlight management strategies if dysplasia is detected.


2021 ◽  
Vol 116 (1) ◽  
pp. S1441-S1441
Author(s):  
Vihitha Thota ◽  
Sudheer Konduru ◽  
Manaswitha Thota

2021 ◽  
Vol 60 (2) ◽  
pp. 9-21
Author(s):  
G. A. Afonin ◽  
N. A. Baltayev ◽  
D. R. Kaidarova ◽  
А. К. Ababakriyev ◽  
P. B. Kalmenova

Relevance: In the Republic of Kazakhstan, colorectal cancer (CRC) ranks third in the structure of oncological pathology. In 2008-2019, the CRC incidence in the Republic was growing each year. There is an upward trend in CRC incidence among young people. Cohort studies show that, in young patients, CRC is characterized by distal localization of the tumor process, advanced stages of the disease, an aggressive course, and low tumor differentiation. The known association of phenotypic signs with clinical characteristics of the disease, such as the response to therapy and survival rates, urges addressing this problem. The phenotypic and molecular genetic aspects of CRC in young people have not been systematically studied in Kazakhstan. The purpose of the study was to compare the phenotypic features of hereditary and sporadic colorectal cancer in young patients and patients over 65 years. Results: The study involved 185 patients aged 17 to 50 years (Group 1) and 112 patients aged 65 to 85 (Group 2). In Group 1, a locally advanced process (stage III) was 14.8% more often than in Group 2; stage IV was 1.23 times more common in men; and multiple primary tumors were 3.1% more often, with a prevailing metachronous course. In Groups 1 & 2, most tumors were localized in the rectum; 84.8% and 78.6% of tumors, respectively, occurred in the left half of the colon. The frequency of right-sided tumors increased with age modified by gender (in Group 2). Hereditary burdened anamnesis was detected in 14.6% patients before 50 (6.57% more than in Group 2); family history of CRC – in 4.8% patients. The latter is consistent with published data. The studied syndromic variants met the diagnostic criteria for familial adenomatous polyposis, Lynch syndrome, Peutz-Jeghers syndrome, and familial type X colorectal cancer. Conclusion: The increase in CRC incidence at the age of 50-70 years is explained by the effectiveness of screening. However, the upward trend for the age below 50 needs a detailed study of etiological (dietary, environmental, behavioral, hereditary) factors. Effective early diagnostics requires considering the phenotypic characteristics and hereditary history associated with a high risk of CRC onset.


2021 ◽  
Author(s):  
Jehison-Alirio Herrera-Pulido ◽  
Orlando Ricaurte Guerrero ◽  
Jinneth Acosta Forero ◽  
Gustavo Hernández Suárez ◽  
Pablo Moreno-Acosta ◽  
...  

2021 ◽  
Vol 60 (2) ◽  
pp. 9-21
Author(s):  
G. A. Afonin ◽  
N. A. Baltayev ◽  
D. R. Kaidarova ◽  
P. B. Kalmenova

Relevance: In the Republic of Kazakhstan, colorectal cancer (CRC) ranks third in the structure of oncological pathology. In 2008-2019, the CRC incidence in the Republic was growing each year. There is an upward trend in CRC incidence among young people. Cohort studies show that, in young patients, CRC is characterized by distal localization of the tumor process, “late” stages of the disease, an aggressive course, and low tumor differentiation. The known association of phenotypic signs with clinical characteristics of the disease, such as the response to therapy and survival rates, urges addressing this problem. The phenotypic and molecular genetic aspects of CRC in young people have not been systematically studied in Kazakhstan. The purpose of the study was to compare the phenotypic features of hereditary and sporadic colorectal cancer in young patients and patients over 65 years. Results: The study involved 185 patients aged 17 to 50 years (Group 1) and 112 patients aged 65 to 85 (Group 2). In Group 1, a locally advanced process (stage III) was 14.8% more often than in Group 2; stage IV was 1.23 times more common in men; and multiple primary tumors were 3.1% more often, with a prevailing metachronous course. In Groups 1 & 2, most tumors were localized in the rectum; 84.8% and 78.6% of tumors, respectively, occurred in the left half of the colon. The frequency of right-sided tumors increased with age modified by gender (in Group 2). Hereditary burdened anamnesis was detected in 14.6% patients before 50 (6.57% more than in Group 2); family history of CRC – in 4.8% patients. The latter is consistent with published data. The studied syndromic variants met the diagnostic criteria for familial adenomatous polyposis, Lynch syndrome, Peutz-Jeghers syndrome, and familial type X colorectal cancer. Conclusion: The increase in CRC incidence at the age of 50-70 years is explained by the effectiveness of screening. However, the upward trend for the age below 50 needs a detailed study of etiological (dietary, environmental, behavioral, hereditary) factors. Effective early diagnostics requires considering the phenotypic characteristics and hereditary history associated with a high risk of CRC onset


Author(s):  
Naohiro Tomita ◽  
Hideyuki Ishida ◽  
Kohji Tanakaya ◽  
Tatsuro Yamaguchi ◽  
Kensuke Kumamoto ◽  
...  

AbstractHereditary colorectal cancer (HCRC) accounts for < 5% of all colorectal cancer cases. Some of the unique characteristics commonly encountered in HCRC cases include early age of onset, synchronous/metachronous cancer occurrence, and multiple cancers in other organs. These characteristics necessitate different management approaches, including diagnosis, treatment or surveillance, from sporadic colorectal cancer management. There are two representative HCRC, named familial adenomatous polyposis and Lynch syndrome. Other than these two HCRC syndromes, related disorders have also been reported. Several guidelines for hereditary disorders have already been published worldwide. In Japan, the first guideline for HCRC was prepared by the Japanese Society for Cancer of the Colon and Rectum (JSCCR), published in 2012 and revised in 2016. This revised version of the guideline was immediately translated into English and published in 2017. Since then, several new findings and novel disease concepts related to HCRC have been discovered. The currently diagnosed HCRC rate in daily clinical practice is relatively low; however, this is predicted to increase in the era of cancer genomic medicine, with the advancement of cancer multi-gene panel testing or whole genome testing, among others. Under these circumstances, the JSCCR guidelines 2020 for HCRC were prepared by consensus among members of the JSCCR HCRC Guideline Committee, based on a careful review of the evidence retrieved from literature searches, and considering the medical health insurance system and actual clinical practice settings in Japan. Herein, we present the English version of the JSCCR guidelines 2020 for HCRC.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Naoya Ozawa ◽  
Takehiko Yokobori ◽  
Katsuya Osone ◽  
Chika Katayama ◽  
Kunihiko Suga ◽  
...  

AbstractUlcerative colitis (UC) is a DNA damage-associated chronic inflammatory disease; the DNA double-strand break (DSB) repair pathway participates in UC-associated dysplasia/colitic cancer carcinogenesis. The DSB/interferon regulatory factor-1 (IRF-1) pathway can induce PD-L1 expression transcriptionally. However, the association of PD-L1/DSB/IRF-1 with sporadic colorectal cancer (SCRC), and UC-associated dysplasia/colitic cancer, remains elusive. Therefore, we investigated the significance of the PD-L1/DSB repair pathway using samples from 17 SCRC and 12 UC patients with rare UC-associated dysplasia/colitic cancer cases by immunohistochemical analysis. We compared PD-L1 expression between patients with SCRC and UC-associated dysplasia/colitic cancer and determined the association between PD-L1 and the CD8+ T-cell/DSB/IRF-1 axis in UC-associated dysplasia/colitic cancer. PD-L1 expression in UC and UC-associated dysplasia/colitic cancer was higher than in normal mucosa or SCRC, and in CD8-positive T lymphocytes in UC-associated dysplasia/colitic cancer than in SCRC. Moreover, PD-L1 upregulation was associated with γH2AX (DSB marker) and IRF-1 upregulation in UC-associated dysplasia/colitic cancer. IRF-1 upregulation was associated with γH2AX upregulation in UC-associated dysplasia/colitic cancer but not in SCRC. Multicolour immunofluorescence staining validated γH2AX/IRF-1/PD-L1 co-expression in colitic cancer tissue sections. Thus, immune cell-induced inflammation might activate the DSB/IRF-1 axis, potentially serving as the primary regulatory mechanism of PD-L1 expression in UC-associated carcinogenesis.


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