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For: Sweetser S, Jones A, Smyrk TC, Sinicrope FA. Sessile Serrated Polyps are Precursors of Colon Carcinomas With Deficient DNA Mismatch Repair. Clin Gastroenterol Hepatol 2016;14:1056-9. [PMID: 26898652 DOI: 10.1016/j.cgh.2016.01.021] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/10/2015] [Revised: 01/22/2016] [Accepted: 01/24/2016] [Indexed: 02/07/2023]

For:	Sweetser S, Jones A, Smyrk TC, Sinicrope FA. Sessile Serrated Polyps are Precursors of Colon Carcinomas With Deficient DNA Mismatch Repair. Clin Gastroenterol Hepatol 2016;14:1056-9. [PMID: 26898652 DOI: 10.1016/j.cgh.2016.01.021] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/10/2015] [Revised: 01/22/2016] [Accepted: 01/24/2016] [Indexed: 02/07/2023]

Number

Cited by Other Article(s)

Kim BS, Cho M, Chung GE, Lee J, Kang HY, Yoon D, Cho WS, Lee JC, Bae JH, Kong HJ, Kim S. Density clustering-based automatic anatomical section recognition in colonoscopy video using deep learning. Sci Rep 2024;14:872. [PMID: 38195632 PMCID: PMC10776865 DOI: 10.1038/s41598-023-51056-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/06/2023] [Accepted: 12/29/2023] [Indexed: 01/11/2024] Open

Affiliation(s)

Byeong Soo Kim Interdisciplinary Program in Bioengineering, Graduate School, Seoul National University, Seoul, 08826, Korea
Minwoo Cho Innovative Medical Technology Research Institute, Seoul National University Hospital, Seoul, 03080, Korea Department of Transdisciplinary Medicine, Seoul National University Hospital, Seoul, 03080, Korea Department of Medicine, Seoul National University College of Medicine, Seoul, 03080, Korea
Goh Eun Chung Department of Internal Medicine and Healthcare Research Institute, Healthcare System Gangnam Center, Seoul National University Hospital, Seoul, 06236, Korea
Jooyoung Lee Department of Internal Medicine and Healthcare Research Institute, Healthcare System Gangnam Center, Seoul National University Hospital, Seoul, 06236, Korea
Hae Yeon Kang Department of Internal Medicine and Healthcare Research Institute, Healthcare System Gangnam Center, Seoul National University Hospital, Seoul, 06236, Korea
Dan Yoon Interdisciplinary Program in Bioengineering, Graduate School, Seoul National University, Seoul, 08826, Korea
Woo Sang Cho Interdisciplinary Program in Bioengineering, Graduate School, Seoul National University, Seoul, 08826, Korea
Jung Chan Lee Department of Biomedical Engineering, Seoul National University College of Medicine, Seoul, 03080, Korea Institute of Bioengineering, Seoul National University, Seoul, 08826, Republic of Korea Institute of Medical and Biological Engineering, Medical Research Center, Seoul National University, Seoul, 03080, Korea
Jung Ho Bae Department of Internal Medicine and Healthcare Research Institute, Healthcare System Gangnam Center, Seoul National University Hospital, Seoul, 06236, Korea.
Hyoun-Joong Kong Innovative Medical Technology Research Institute, Seoul National University Hospital, Seoul, 03080, Korea. Department of Transdisciplinary Medicine, Seoul National University Hospital, Seoul, 03080, Korea. Department of Medicine, Seoul National University College of Medicine, Seoul, 03080, Korea. Medical Big Data Research Center, Seoul National University College of Medicine, Seoul, 03087, Korea.
Sungwan Kim Department of Biomedical Engineering, Seoul National University College of Medicine, Seoul, 03080, Korea. Institute of Bioengineering, Seoul National University, Seoul, 08826, Republic of Korea. Artificial Intelligence Institute, Seoul National University, Research Park Building 942, 2 Fl., Seoul, 08826, Korea.

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Iwatate M, Hirata D, Francisco CPD, Co JT, Byeon J, Joshi N, Banerjee R, Quach DT, Aye TT, Chiu H, Lau LHS, Ng SC, Ang TL, Khomvilai S, Li X, Ho S, Sano W, Hattori S, Fujita M, Murakami Y, Shimatani M, Kodama Y, Sano Y, The CATCH project team. Efficacy of international web-based educational intervention in the detection of high-risk flat and depressed colorectal lesions higher (CATCH project) with a video: Randomized trial. Dig Endosc 2022;34:1166-1175. [PMID: 35122323 PMCID: PMC9540870 DOI: 10.1111/den.14244] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/29/2021] [Revised: 01/14/2022] [Accepted: 01/23/2022] [Indexed: 02/08/2023]

Affiliation(s)

Mineo Iwatate Gastrointestinal Center and Institute of Minimally‐invasive Endoscopic Care (iMEC)Sano HospitalHyogoJapan
Daizen Hirata Gastrointestinal Center and Institute of Minimally‐invasive Endoscopic Care (iMEC)Sano HospitalHyogoJapan Department of Gastroenterology and HepatologyKindai UniversityOsakaJapan
Carlos Paolo D. Francisco Institute of Digestive and Liver DiseasesSt. Luke’s Medical CenterTaguig CityPhilippines
Jonard Tan Co Institute of Digestive and Liver DiseasesSt. Luke’s Medical CenterTaguig CityPhilippines
Jeong‐Sik Byeon Department of GastroenterologyAsan Medical CenterUniversity of Ulsan College of MedicineSeoulKorea
Neeraj Joshi Gastro Enterology UnitNepal Cancer Hospital and Research CentreLalitpurNepal
Rupa Banerjee Medical GastroenterologyAsian Institute of GastroenterologyNew DelhiIndia
Duc Trong Quach University of Medicine and Pharmacy at Ho Chi Minh CityHo Chi MinhVietnam
Than Than Aye University of Medicine 2YangonMyanmar
Han‐Mo Chiu Department of Internal MedicineNational Taiwan University HospitalTaipeiTaiwan
Louis H. S. Lau Department of Medicine and TherapeuticsFaculty of MedicineInstitute of Digestive DiseaseThe Chinese University of Hong KongHong KongChina
Siew C. Ng Department of Medicine and TherapeuticsFaculty of MedicineInstitute of Digestive DiseaseThe Chinese University of Hong KongHong KongChina
Tiing Leong Ang Department of Gastroenterology and HepatologyChangi General HospitalSingHealthSingapore
Supakij Khomvilai Surgical EndoscopyColorectal DivisionDepartment of SurgeryFaculty of MedicineChulalongkorn UniversityBangkokThailand
Xiao‐Bo Li Division of Gastroenterology and HepatologyKey Laboratory of Gastroenterology and HepatologyMinistry of Health, Renji HospitalSchool of MedicineShanghai Institute of Digestive DiseaseShanghai Jiao Tong UniversityShanghaiChina
Shiaw‐Hooi Ho Department of MedicineFaculty of MedicineUniversity of MalayaKuala LumpurMalaysia
Wataru Sano Gastrointestinal Center and Institute of Minimally‐invasive Endoscopic Care (iMEC)Sano HospitalHyogoJapan
Santa Hattori Gastrointestinal Center and Institute of Minimally‐invasive Endoscopic Care (iMEC)Sano HospitalHyogoJapan
Mikio Fujita Gastrointestinal Center and Institute of Minimally‐invasive Endoscopic Care (iMEC)Sano HospitalHyogoJapan
Yoshitaka Murakami Department of Medical StatisticsToho UniversityTokyoJapan
Masaaki Shimatani The Third Department of Internal MedicineDivision of Gastroenterology and HepatologyKansai Medical University Medical CenterOsakaJapan
Yuzo Kodama Division of GastroenterologyDepartment of Internal MedicineKobe University Graduate School of MedicineHyogoJapan
Yasushi Sano Gastrointestinal Center and Institute of Minimally‐invasive Endoscopic Care (iMEC)Sano HospitalHyogoJapan Kansai Medical UniversityOsakaJapan
The CATCH project team

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Chu JE, Hamm J, Gentile L, Telford JJ, Schaeffer DF. Serrated Lesion Detection in a Population-based Colon Screening Program. J Clin Gastroenterol 2022;56:243-248. [PMID: 33780220 DOI: 10.1097/mcg.0000000000001519] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/04/2020] [Accepted: 01/28/2021] [Indexed: 12/10/2022]

Shaukat A, Colucci D, Erisson L, Phillips S, Ng J, Iglesias JE, Saltzman JR, Somers S, Brugge W. Improvement in adenoma detection using a novel artificial intelligence-aided polyp detection device. Endosc Int Open 2021;9:E263-E270. [PMID: 33553591 PMCID: PMC7857961 DOI: 10.1055/a-1321-1317] [Citation(s) in RCA: 18] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/04/2020] [Accepted: 10/20/2020] [Indexed: 12/11/2022] Open

Abstract

Background and study aims Detecting colorectal neoplasia is the goal of high-quality screening and surveillance colonoscopy, as reflected by high adenoma detection rate (ADR) and adenomas per colonoscopy (APC). The aim of our study was to evaluate the performance of a novel artificial intelligence (AI)-aided polyp detection device, Skout, with the primary endpoints of ADR and APC in routine colonoscopy. Patients and methods We compared ADR and APC in a cohort of outpatients undergoing routine high-resolution colonoscopy with and without the use of a real-time, AI-aided polyp detection device. Patients undergoing colonoscopy with Skout were enrolled in a single-arm, unblinded, prospective trial and the results were compared with a historical cohort. All resected polyps were examined histologically. Results Eighty-three patients undergoing screening and surveillance colonoscopy at an outpatient endoscopy center were enrolled and outcomes compared with 283 historical control patients. Overall, ADR with and without Skout was 54.2 % and 40.6 % respectively ( P = 0.028) and 53.6 % and 30.8 %, respectively, in screening exams ( P = 0.024). Overall, APC rate with and without Skout was 1.46 and 1.01, respectively, ( P = 0.104) and 1.18 and 0.50, respectively, in screening exams ( P = 0.002). Overall, true histology rate (THR) with and without Skout was 73.8 % and 78.4 %, respectively, ( P = 0.463) and 75.0 % and 71.0 %, respectively, in screening exams ( P = 0.731). Conclusion We have demonstrated that our novel AI-aided polyp detection device increased the ADR in a cohort of patients undergoing screening and surveillance colonoscopy without a significant concomitant increase in hyperplastic polyp resection. AI-aided colonoscopy has the potential for improving the outcomes of patients undergoing colonoscopy.

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Meester RGS, van Herk MMAGC, Lansdorp-Vogelaar I, Ladabaum U. Prevalence and Clinical Features of Sessile Serrated Polyps: A Systematic Review. Gastroenterology 2020;159:105-118.e25. [PMID: 32199884 PMCID: PMC8653879 DOI: 10.1053/j.gastro.2020.03.025] [Citation(s) in RCA: 56] [Impact Index Per Article: 11.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/02/2019] [Revised: 02/24/2020] [Accepted: 03/09/2020] [Indexed: 12/14/2022]

Abstract

BACKGROUND & AIMS

Sessile serrated polyps (SSPs) could account for a substantial proportion of colorectal cancers. We aimed to increase clarity on SSP prevalence and clinical features.

METHODS

We performed a systematic review of MEDLINE, Web of Science, Embase, and Cochrane databases for original studies published in English since 2000. We included studies of different populations (United States general or similar), interventions (colonoscopy, autopsy), comparisons (world regions, alternative polyp definitions, adenoma), outcomes (prevalence, clinical features), and study designs (cross-sectional). Random-effects regression was used for meta-analysis where possible.

RESULTS

We identified 74 relevant colonoscopy studies. SSP prevalence varied by world region, from 2.6% in Asia (95% confidence interval [CI], 0-5.9) to 10.5% in Australia (95% CI, 2.8-18.2). Prevalence values did not differ significantly between the United States and Europe (P = .51); the pooled prevalence was 4.6% (95% CI, 3.4-5.8), and SSPs accounted for 9.4% of polyps with malignant potential (95% CI, 6.6-12.3). The mean prevalence was higher when assessed through high-performance examinations (9.1%; 95% CI, 4.0-14.2; P = .04) and with an alternative definition of clinically relevant serrated polyps (12.3%; 95% CI, 9.3-15.4; P < .001). Increases in prevalence with age were not statistically significant, and prevalence did not differ significantly by sex. Compared with adenomas, a higher proportion of SSPs were solitary (69.0%; 95% CI, 45.9-92.1; P = .08), with diameters of 10 mm or more (19.3%; 95% CI, 12.4-26.2; P = .13) and were proximal (71.5%; 95% CI, 63.5-79.5; P = .008). The mean ages for detection of SSP without dysplasia, with any or low-grade dysplasia, and with high-grade dysplasia were 60.8 years, 65.6 years, and 70.2 years, respectively. The range for proportions of SSPs with dysplasia was 3.7%-42.9% across studies, possibly reflecting different study populations.

CONCLUSIONS

In a systematic review, we found that SSPs are relatively uncommon compared with adenoma. More research is needed on appropriate diagnostic criteria, variations in detection, and long-term risk.

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Song M, Emilsson L, Bozorg SR, Nguyen LH, Joshi AD, Staller K, Nayor J, Chan AT, Ludvigsson JF. Risk of colorectal cancer incidence and mortality after polypectomy: a Swedish record-linkage study. Lancet Gastroenterol Hepatol 2020;5:537-547. [PMID: 32192628 PMCID: PMC7234902 DOI: 10.1016/s2468-1253(20)30009-1] [Citation(s) in RCA: 72] [Impact Index Per Article: 14.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/14/2019] [Revised: 01/12/2020] [Accepted: 01/13/2020] [Indexed: 12/14/2022]

Abstract

BACKGROUND

Long-term colorectal cancer incidence and mortality after colorectal polyp removal remains unclear. We aimed to assess colorectal cancer incidence and mortality in individuals with removal of different histological subtypes of polyps relative to the general population.

METHODS

We did a matched cohort study through prospective record linkage in Sweden in patients aged at least 18 years with a first diagnosis of colorectal polyps in the nationwide gastrointestinal ESPRESSO histopathology cohort (1993-2016). For each polyp case, we identified up to five matched reference individuals from the Total Population Register on the basis of birth year, age, sex, calendar year of biopsy, and county of residence. We excluded patients and reference individuals with a diagnosis of colorectal cancer either before or within the first 6 months after diagnosis of the index polyp. Polyps were classified by morphology codes into hyperplastic polyps, sessile serrated polyps, tubular adenomas, tubulovillous adenomas, and villous adenomas. Colorectal cancer cases were identified from the Swedish Cancer Registry, and cause-of-death data were retrieved from the Cause of Death Register. We collected information about the use of endoscopic examination before and after the index biopsy from the Swedish National Patient Registry, and counted the number of endoscopies done before and after the index biopsies. We calculated cumulative risk of colorectal cancer incidence and mortality at 3, 5, 10, and 15 years, and computed hazard ratios (HRs) and 95% CIs for colorectal cancer incidence and mortality using a stratified Cox proportional hazards model within each of the matched pairs.

FINDINGS

178 377 patients with colorectal polyps and 864 831 matched reference individuals from the general population were included in our study. The mean age of patients at polyp diagnosis was 58·6 (SD 13·9) years for hyperplastic polyps, 59·7 (14·2) years for sessile serrated polyps, 63·9 (12·9) years for tubular adenomas, 67·1 (12·1) years for tubulovillous adenomas, and 68·9 (11·8) years for villous adenomas. During a median of 6·6 years (IQR 3·0-11·6) of follow-up, we documented 4278 incident colorectal cancers and 1269 colorectal cancer-related deaths in patients with a polyp, and 14 350 incident colorectal cancers and 5242 colorectal cancer deaths in general reference individuals. The 10-year cumulative incidence of colorectal cancer was 1·6% (95% CI 1·5-1·7) for hyperplastic polyps, 2·5% (1·9-3·3) for sessile serrated polyps, 2·7% (2·5-2·9) for tubular adenomas, 5·1% (4·8-5·4) for tubulovillous adenomas, and 8·6% (7·4-10·1) for villous adenomas compared with 2·1% (2·0-2·1) in reference individuals. Compared with reference individuals, patients with any polyps had an increased risk of colorectal cancer, with multivariable HR of 1·11 (95% CI 1·02-1·22) for hyperplastic polyps, 1·77 (1·34-2·34) for sessile serrated polyps, 1·41 (1·30-1·52) for tubular adenomas, 2·56 (2·36-2·78) for tubulovillous adenomas, and 3·82 (3·07-4·76) for villous adenomas (p<0·05 for all polyp subtypes). There was a higher proportion of incident proximal colon cancer in patients with serrated (hyperplastic and sessile) polyps (52-57%) than in those with conventional (tubular, tubulovillous, and villous) adenomas (30-46%). For colorectal cancer mortality, a positive association was found for sessile serrated polyps (HR 1·74, 95% CI 1·08-2·79), tubulovillous adenomas (1·95, 1·69-2·24), and villous adenomas (3·45, 2·40-4·95), but not for hyperplastic polyps (0·90, 0·76-1·06) or tubular adenomas (0·97, 0·84-1·12).

INTERPRETATION

In a largely screening-naive population, compared with individuals from the general population, patients with any polyps had a higher colorectal cancer incidence, and those with sessile serrated polyps, tubulovillous adenomas, and villous adenomas had a higher colorectal cancer mortality.

FUNDING

US National Institutes of Health, American Cancer Society, American Gastroenterological Association, Union for International Cancer Control.

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Affiliation(s)

Mingyang Song Department of Epidemiology and Department of Nutrition, Harvard T H Chan School of Public Health, Boston, MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
Louise Emilsson Institute of Health and Society, University of Oslo, Oslo, Norway; Vårdcentralen Årjäng and Centre for Clinical Research, County Council of Värmland, Värmland, Sweden; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
Soran R Bozorg Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
Long H Nguyen Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
Amit D Joshi Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
Kyle Staller Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA
Jennifer Nayor Division of Gastroenterology, Brigham and Women's Hospital, Boston, MA, USA
Andrew T Chan Department of Epidemiology and Department of Nutrition, Harvard T H Chan School of Public Health, Boston, MA, USA; Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA; Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA, USA
Jonas F Ludvigsson Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Orebro University Hospital, Orebro, Sweden; Division of Digestive and Liver Disease, Department of Medicine, Columbia University Medical Center, New York, NY, USA; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK.

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Fujiwara-Tani R, Fujii K, Mori S, Kishi S, Sasaki T, Ohmori H, Nakashima C, Kawahara I, Nishiguchi Y, Mori T, Sho M, Kondoh M, Luo Y, Kuniyasu H. Role of Clostridium perfringens Enterotoxin on YAP Activation in Colonic Sessile Serrated Adenoma/ Polyps with Dysplasia. Int J Mol Sci 2020;21:ijms21113840. [PMID: 32481659 PMCID: PMC7313056 DOI: 10.3390/ijms21113840] [Citation(s) in RCA: 20] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/23/2020] [Revised: 05/26/2020] [Accepted: 05/26/2020] [Indexed: 12/11/2022] Open

Abstract

Sessile serrated adenoma/polyp with dysplasia (SSA/P-D) is an SSA/P with cellular dysplasia and has a higher risk of progressing to colon carcinogenesis. Previously, we reported that tight junction impairment by Clostridiumperfringens enterotoxin (CPE) leads to activation of the transcriptional co-activator yes-associated protein (YAP) in oral squamous cell carcinoma. Here, we investigated whether CPE activates YAP to promote the malignant progression of SSA/P. E-cadherin expression was lower in the 12 cases with SSA/P-D examined than that in normal mucosa, SSA/P, or tubular adenoma (TA). Furthermore, intracellular translocation of claudin-4 (CLDN4) and nuclear translocation of YAP were observed. The CPE gene was detected in DNA extracted from SSA/P-D lesions, but not in SSA/P or TA. Treatment of the rat intestinal epithelial cell line IEC6 with low-dose CPE resulted in intracellular translocation of CLDN4 to the cytoplasmic membrane. Cytoplasmic CLDN4 showed co-precipitation with transcriptional co-activator with PDZ-binding motif, zonula occludens (ZO)-1, large tumor suppressor, and mammalian Ste20-like. Additionally, YAP co-precipitated with ZO-2 under CPE treatment led to decreased YAP phosphorylation and nuclear translocation. YAP activation promoted increase in nuclear TEA domain family member level, expression of cyclin D1, snail, vimentin, CD44, NS and decrease in E-cadherin levels, thereby inducing stemness and epithelial-mesenchymal-transition (EMT). The Hippo complex with the incorporation of CLDN4 increased stability. Upon low-dose CPE treatment, HT29 cells with BRAF^V600E gene mutation showed increased growth, enhanced invasive potential, stemness, and induced EMT phenotype, whereas HCT116 cells, which carry KRAS^G13D gene mutation, did not show such changes. In an examination of 10 colorectal cancers, an increase in EMT and stemness was observed in CPE (+) and BRAF mutation (+) cases. These findings suggest that C.perfringens might enhance the malignant transformation of SSA/P-D via YAP activation. Our findings further highlight the importance of controlling intestinal flora using probiotics or antibiotics.

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Affiliation(s)

Rina Fujiwara-Tani Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Kiyomu Fujii Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Shiori Mori Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Shingo Kishi Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Takamitsu Sasaki Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Hitoshi Ohmori Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Chie Nakashima Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Isao Kawahara Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Yukiko Nishiguchi Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Takuya Mori Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.)
Masayuki Sho Department of Surgery, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8522, Japan;
Masuo Kondoh Drug Innovation Center, Graduate School of Pharmaceutical Sciences, Osaka University, 6-1 Yamadaoka, Suita, Osaka 565-0871, Japan;
Yi Luo Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong 226001, Jiangsu Province, China Correspondence: (Y.L.); (H.K.); Tel.: +86-0513-8505-1805 (Y.L.); +81-744-22-3051 (H.K.); Fax: +81-744-25-7308 (H.K.)
Hiroki Kuniyasu Department of Molecular Pathology, Nara Medical University, 840 Shijo-cho, Kashihara, Nara 634-8521, Japan; (R.F.-T.); (K.F.); (S.M.); (S.K.); (T.S.); (H.O.); (C.N.); (I.K.); (Y.N.); (T.M.) Correspondence: (Y.L.); (H.K.); Tel.: +86-0513-8505-1805 (Y.L.); +81-744-22-3051 (H.K.); Fax: +81-744-25-7308 (H.K.)

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Wang SM, Jiang B, Deng Y, Huang SL, Fang MZ, Wang Y. Clinical significance of MLH1/MSH2 for stage II/III sporadic colorectal cancer. World J Gastrointest Oncol 2019;11:1065-1080. [PMID: 31798786 PMCID: PMC6883179 DOI: 10.4251/wjgo.v11.i11.1065] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/28/2019] [Revised: 08/10/2019] [Accepted: 09/10/2019] [Indexed: 02/05/2023] Open

Abstract

BACKGROUND

The development of colorectal cancer (CRC) is a complicated multistep process that involves an accumulation of mutations in tumor suppressor genes and oncogenes. In the process of DNA replication, base mismatch often occurs due to various factors leading to abnormal expression of mismatch repair genes (MMR), among which MLH1 and MSH2 are the most important. Recently, numerous studies indicated that MLH1/MSH2 phenotype is associated with CRC. We wanted to elucidate the role of MLH1/MSH2 in the prediction and prognosis of CRC through long-term clinical observation.

AIM

To evaluate the prognostic and predictive significance of MLH1/MSH2 in patients with stage II-III CRC using immunohistochemical analysis and GeneScan.

METHODS

Specimens from 681 patients with CRC (395 stage II and 286 stage III, 387 males and 294 females) who underwent curative surgical resection from 2013 to 2016 were tested. Immunohistochemistry was used to analyze MMR status and the microsatellite status of 133 patients was determined by GeneScan analysis.

RESULTS

Five hundred and fifty (80.76%) patients were MLH1/MSH2 positive and 131 (19.24%) were negative by immunohistochemistry. MLH1/MSH2-positive tumors were significantly more frequent in the colon than in the rectum, and had poor differentiation and less mucin production (P < 0.05). Patients of different groups did not differ in terms of age, gender, tumor size, tumor stage, lymphocytic infiltration, or circumscribed margin. MLH1/MSH2-negative patients had a more favorable OS than MLH1/MSH2-positive patients (P < 0.001). Univariate and multivariate analyses demonstrated MLH1/MSH2 expression as an independent prognostic and predictive factor for stage II/III CRC. MLH1/MSH2 expression was a strong prognostic factor in all patients [P < 0.001, hazard ratio (HR) = 4.064, 95%CI: 2.241–7.369]. Adjuvant chemotherapy had a greater correlation with survival advantage in MLH1/MSH2-negative patients with stage III disease (P < 0.001, HR = 7.660, 95%CI: 2.974–15.883). However, patients with stage II disease or MLH1/MSH2-positive patients with stage III disease did not benefit from adjuvant chemotherapy. GeneScan analysis demonstrated that among 133 patients, 105 (78.95%) were microsatellite stable, and 28 (21.05%) had microsatellite instability (MSI), including 18 (13.53%) with high MSI and 10 (7.52%) with low MSI. This is consistent with the immunohistochemical results.

CONCLUSION

MLH1/MSH2 phenotype constitutes a pathologically and clinically distinct subtype of sporadic CRC. MLH1/MSH2 is an independent prognostic and predictive factor for outcome of stage II-III CRC.

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Thomas R, Trapani D, Goodyer-Sait L, Tomkova M, Fernandez-Rozadilla C, Sahnane N, Woolley C, Davis H, Chegwidden L, Kriaucionis S, Maughan T, Leedham S, Palles C, Furlan D, Tomlinson I, Lewis A. The polymorphic variant rs1800734 influences methylation acquisition and allele-specific TFAP4 binding in the MLH1 promoter leading to differential mRNA expression. Sci Rep 2019;9:13463. [PMID: 31530880 PMCID: PMC6748923 DOI: 10.1038/s41598-019-49952-x] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/09/2018] [Accepted: 08/29/2019] [Indexed: 12/14/2022] Open

Affiliation(s)

Rachael Thomas Cancer Gene Regulation Group, Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK
Davide Trapani Anatomic Pathology Unit, Department of Medicine and Surgery and Research Center of Hereditary and Familial Tumors, University of Insubria, Varese, 21100, Italy
Lily Goodyer-Sait Institute of Structural and Molecular Biology, Department of, Biological Sciences, Birkbeck, London, UK
Marketa Tomkova Ludwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building, Roosevelt Drive, Oxford, OX3 7DQ, UK
Ceres Fernandez-Rozadilla Fundación Pública Galega de Medicina Xenómica, Grupo de Medicina Xenómica, IDIS, Santiago de Compostela, Spain
Nora Sahnane Anatomic Pathology Unit, Department of Medicine and Surgery and Research Center of Hereditary and Familial Tumors, University of Insubria, Varese, 21100, Italy
Connor Woolley Cancer Genetics and Evolution Laboratory, Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
Hayley Davis Intestinal Stem Cell Biology Group, Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford, OX3 7BN, UK
Laura Chegwidden Gastrointestinal Cancer Genetics Laboratory, Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
Skirmantas Kriaucionis Ludwig Institute for Cancer Research Ltd, University of Oxford, Nuffield Department of Clinical Medicine, Old Road Campus Research Building, Roosevelt Drive, Oxford, OX3 7DQ, UK
Timothy Maughan Oxford Institute of Radiation Oncology, University of Oxford, Old Road Campus Research Building, Roosevelt Drive, Oxford, OX3 7DQ, UK
Simon Leedham Intestinal Stem Cell Biology Group, Wellcome Trust Centre for Human Genetics, Oxford University, Roosevelt Drive, Oxford, OX3 7BN, UK
Claire Palles Gastrointestinal Cancer Genetics Laboratory, Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
Daniela Furlan Anatomic Pathology Unit, Department of Medicine and Surgery and Research Center of Hereditary and Familial Tumors, University of Insubria, Varese, 21100, Italy
Ian Tomlinson Cancer Genetics and Evolution Laboratory, Institute of Cancer and Genomic Sciences, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK
Annabelle Lewis Cancer Gene Regulation Group, Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK. Division of Biosciences, Department of Life Sciences, Brunel University London, Old Road Campus Research Building, Roosevelt Drive, Uxbridge, UB8 3PN, UK.

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Yozu M, Kem M, Cenaj O, Mino-Kenudson M, Odze RD, Misdraji J. Loss of expression of MLH1 in non-dysplastic crypts is a harbinger of neoplastic progression in sessile serrated adenomas/polyps. Histopathology 2019;75:376-384. [PMID: 30974487 DOI: 10.1111/his.13874] [Citation(s) in RCA: 7] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/05/2019] [Accepted: 04/08/2019] [Indexed: 01/26/2023]

Nouraie M, Ashktorab H, Atefi N, Azam S, Tarjoman T, Lee E, Shokrani B, Afsari A, Soleimani A, Laiyemo AO, Singh S, Brim H. Can the rate and location of sessile serrated polyps be part of colorectal Cancer disparity in African Americans? BMC Gastroenterol 2019;19:77. [PMID: 31126232 PMCID: PMC6534887 DOI: 10.1186/s12876-019-0996-y] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/24/2018] [Accepted: 05/16/2019] [Indexed: 12/17/2022] Open

Abstract

BACKGROUND

Up to 30% of colorectal cancers develop through the serrated pathway. African Americans (AAs) suffer a disproportionate burden of colorectal cancer. The aim of this study was to evaluate clinicopathological features of AA patients diagnosed with sessile serrated polyps (SSPs).

METHODS

We conducted a retrospective study of all colonoscopies (n = 12,085) performed at Howard University Hospital, from January 1st, 2010 to December 31st, 2015, of which 83% were in AA patients, (n = 10,027). Among AAs, pathology reports confirmed 4070 patients with polyps including 252 with SSPs. Demographic and clinical variables (i.e. sex, age, BMI, anatomic location, clinical symptoms, polyp size, and clinical indications were collected at colonoscopy.

RESULTS

In the AA population, the median age was 56 with interquartile range (IQR) of 51 to 62 years, 54% were female, and 48% had a BMI > 30. The most common reason for colonoscopy was screening (53%), whereas the prevalent reasons for diagnostic colonoscopies were changes in bowel habits (18%) and gastrointestinal bleeding (17%). The total number of SSPs among the 252 AA (diagnosed with SSPs) was 338. Of these, 9% (n = 29/338) had some degree of cytological dysplasia, primarily in the ascending colon (n = 6/42, 14%), Transverse colon (n = 2/16, 13%) and rectosigmoid (n = 19/233, 8%). About 24% of patients had more than 2 polyps. Most patients (76%) had distal SSPs (rectal and rectosigmoid), in comparison to 14% of proximal polyps and 10% of bilateral locations. Median SSA/P size for all locations was 0.6 cm.

CONCLUSION

The prevalence of SSPs accounts for 6% of all polyps in AA patients and was diagnosed in 2.5% of all colonoscopies (n = 252/10,027), which is higher than Caucasians in the US. SSPs were predominantly located in the left side, as compared to published literature showing the predominance in the right side of the colon. Screening of CRC will have the chance to detect high risk SSA/P in this population.

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Leung JW, Yen AW, Jia H, Opada C, Melnik A, Atkins J, Feller C, Wilson MD, Leung FW. A prospective RCT comparing combined chromoendoscopy with water exchange (CWE) vs water exchange (WE) vs air insufflation (AI) in adenoma detection in screening colonoscopy. United European Gastroenterol J 2019;7:477-487. [PMID: 31065365 DOI: 10.1177/2050640619832196] [Citation(s) in RCA: 11] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/16/2018] [Accepted: 01/22/2019] [Indexed: 12/15/2022] Open

Hale VL, Jeraldo P, Chen J, Mundy M, Yao J, Priya S, Keeney G, Lyke K, Ridlon J, White BA, French AJ, Thibodeau SN, Diener C, Resendis-Antonio O, Gransee J, Dutta T, Petterson XM, Sung J, Blekhman R, Boardman L, Larson D, Nelson H, Chia N. Distinct microbes, metabolites, and ecologies define the microbiome in deficient and proficient mismatch repair colorectal cancers. Genome Med 2018;10:78. [PMID: 30376889 PMCID: PMC6208080 DOI: 10.1186/s13073-018-0586-6] [Citation(s) in RCA: 100] [Impact Index Per Article: 14.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/13/2018] [Accepted: 10/08/2018] [Indexed: 01/14/2023] Open

Abstract

BACKGROUND

Links between colorectal cancer (CRC) and the gut microbiome have been established, but the specific microbial species and their role in carcinogenesis remain an active area of inquiry. Our understanding would be enhanced by better accounting for tumor subtype, microbial community interactions, metabolism, and ecology.

METHODS

We collected paired colon tumor and normal-adjacent tissue and mucosa samples from 83 individuals who underwent partial or total colectomies for CRC. Mismatch repair (MMR) status was determined in each tumor sample and classified as either deficient MMR (dMMR) or proficient MMR (pMMR) tumor subtypes. Samples underwent 16S rRNA gene sequencing and a subset of samples from 50 individuals were submitted for targeted metabolomic analysis to quantify amino acids and short-chain fatty acids. A PERMANOVA was used to identify the biological variables that explained variance within the microbial communities. dMMR and pMMR microbial communities were then analyzed separately using a generalized linear mixed effects model that accounted for MMR status, sample location, intra-subject variability, and read depth. Genome-scale metabolic models were then used to generate microbial interaction networks for dMMR and pMMR microbial communities. We assessed global network properties as well as the metabolic influence of each microbe within the dMMR and pMMR networks.

RESULTS

We demonstrate distinct roles for microbes in dMMR and pMMR CRC. Bacteroides fragilis and sulfidogenic Fusobacterium nucleatum were significantly enriched in dMMR CRC, but not pMMR CRC. These findings were further supported by metabolic modeling and metabolomics indicating suppression of B. fragilis in pMMR CRC and increased production of amino acid proxies for hydrogen sulfide in dMMR CRC.

CONCLUSIONS

Integrating tumor biology and microbial ecology highlighted distinct microbial, metabolic, and ecological properties unique to dMMR and pMMR CRC. This approach could critically improve our ability to define, predict, prevent, and treat colorectal cancers.

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Affiliation(s)

Vanessa L Hale Department of Veterinary Preventive Medicine, The Ohio State University College of Veterinary Medicine, Columbus, OH, USA Microbiome Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA Division of Surgical Research, Department of Surgery, Mayo Clinic, Rochester, MN, USA
Patricio Jeraldo Microbiome Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA Division of Surgical Research, Department of Surgery, Mayo Clinic, Rochester, MN, USA
Jun Chen Microbiome Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA
Michael Mundy Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA
Janet Yao Microbiome Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA
Sambhawa Priya Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN, USA
Gary Keeney Division of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA
Kelly Lyke Division of Surgical Research, Department of Surgery, Mayo Clinic, Rochester, MN, USA
Jason Ridlon Carl R. Woese Institute for Genomic Biology, Department of Animal Sciences, Division of Nutritional Sciences, University of Illinois, Urbana-Champaign, IL, USA
Bryan A White Carl R. Woese Institute for Genomic Biology, Department of Animal Sciences, Division of Nutritional Sciences, University of Illinois, Urbana-Champaign, IL, USA
Amy J French Division of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA
Stephen N Thibodeau Division of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN, USA
Christian Diener Human Systems Biology Laboratory, National Institute of Genomic Medicine, Mexico City, Mexico
Osbaldo Resendis-Antonio Human Systems Biology Laboratory, National Institute of Genomic Medicine, Mexico City, Mexico Coordinación de la Investigación Científica, Red de Apoyo a la Investigación, UNAM, Mexico City, Mexico
Jaime Gransee Mayo Clinic Metabolomics Core Laboratory, Mayo Clinic, Rochester, MN, USA
Tumpa Dutta Mayo Clinic Metabolomics Core Laboratory, Mayo Clinic, Rochester, MN, USA
Xuan-Mai Petterson Mayo Clinic Metabolomics Core Laboratory, Mayo Clinic, Rochester, MN, USA
Jaeyun Sung Microbiome Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA Division of Surgical Research, Department of Surgery, Mayo Clinic, Rochester, MN, USA
Ran Blekhman Department of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN, USA
Lisa Boardman Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA
David Larson Division of Colon and Rectal Surgery, Department of Surgery, Mayo Clinic, Rochester, MN, USA
Heidi Nelson Microbiome Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA Division of Colon and Rectal Surgery, Department of Surgery, Mayo Clinic, Rochester, MN, USA
Nicholas Chia Microbiome Program, Center for Individualized Medicine, Mayo Clinic, Rochester, MN, USA. Division of Surgical Research, Department of Surgery, Mayo Clinic, Rochester, MN, USA.

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Lin SH, Raju GS, Huff C, Ye Y, Gu J, Chen JS, Hildebrandt MAT, Liang H, Menter DG, Morris J, Hawk E, Stroehlein JR, Futreal A, Kopetz S, Mishra L, Wu X. The somatic mutation landscape of premalignant colorectal adenoma. Gut 2018;67:1299-1305. [PMID: 28607096 PMCID: PMC6031265 DOI: 10.1136/gutjnl-2016-313573] [Citation(s) in RCA: 46] [Impact Index Per Article: 6.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/15/2016] [Revised: 05/02/2017] [Accepted: 05/04/2017] [Indexed: 02/06/2023]

Affiliation(s)

Shu-Hong Lin Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA,The University of Texas Graduate School of Biomedical Sciences at Houston and MD Anderson Cancer Center, Houston, Texas, USA
Gottumukkala S Raju Department of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Chad Huff Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Yuanqing Ye Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Jian Gu Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Jiun-Sheng Chen Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA,The University of Texas Graduate School of Biomedical Sciences at Houston and MD Anderson Cancer Center, Houston, Texas, USA
Michelle A T Hildebrandt Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Han Liang Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
David G Menter Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Jeffery Morris Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Ernest Hawk Division of Cancer Prevention and Population Science, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
John R Stroehlein Department of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Andrew Futreal Department of Genomic Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Scott Kopetz Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Lopa Mishra Department of Gastroenterology, Hepatology and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA
Xifeng Wu Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA

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Dwyer JP, Tan JYC, Urquhart P, Secomb R, Bunn C, Reynolds J, La Nauze R, Kemp W, Roberts S, Brown G. A prospective comparison of cold snare polypectomy using traditional or dedicated cold snares for the resection of small sessile colorectal polyps. Endosc Int Open 2017;5:E1062-E1068. [PMID: 29250580 PMCID: PMC5659868 DOI: 10.1055/s-0043-113564] [Citation(s) in RCA: 21] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/02/2016] [Accepted: 05/22/2017] [Indexed: 02/07/2023] Open

Abstract

BACKGROUND AND STUDY AIMS

The evidence for efficacy and safety of cold snare polypectomy is limited. The aim of this study was to assess the completeness of resection and safety of cold snare polypectomy, using either traditional or dedicated cold snares.

PATIENTS AND METHODS

This was a prospective, non-randomized study performed at a single tertiary hospital. Adult patients with at least one colorectal polyp (size ≤ 10 mm) removed by cold snare were included. In the first phase, all patients had polyps removed by traditional snare without diathermy. In the second phase, all patients had polyps removed by dedicated cold snare. Complete endoscopic resection was determined from histological examination of quadrantic polypectomy margin biopsies. Immediate or delayed bleeding within 2 weeks was recorded.

RESULTS

In total, 181 patients with 299 eligible polyps (n = 93 (173 polyps) traditional snare group, n = 88 (126 polyps) dedicated cold snare group) were included. Patient demographics and procedure indications were similar between groups. Mean polyp size was 6 mm in both groups ( P = 0.25). Complete polyp resection was 165 /173 (95.4 %; 95 %CI 90.5 - 97.6 %) in the traditional snare group and 124/126 (98.4 %; 95 %CI 93.7 - 99.6 %) in the dedicated cold snare group ( P = 0.16). Serrated polyps, compared with adenomatous polyps, had a higher rate of incomplete resection (7 % vs. 2 %, P = 0.03). There was no statistically significant difference in the rate of immediate bleeding (3 % vs. 1 %, P = 0.41) and there were no delayed hemorrhages or perforations.

CONCLUSIONS

Cold snare polypectomy is effective and safe for the complete endoscopic resection of small (≤ 10 mm) colorectal polyps with either traditional or dedicated cold snares.

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Clinicopathologic parameters associated with postoperative complications and risk factors for tumor recurrence and mortality after tumor resection of patients with colorectal cancer. Clin Transl Oncol 2017;20:176-192. [PMID: 28710725 DOI: 10.1007/s12094-017-1708-0] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/18/2017] [Accepted: 06/20/2017] [Indexed: 01/05/2023]

Abstract

OBJECTIVE

To delineate the association of postoperative complications with clinicopathologic factors and to identify risk factors for tumor recurrence and mortality after tumor resection in patients with colorectal cancer (CRC).

METHODS

The clinical data of 1144 patients with CRC who underwent surgical intervention between 2003 and 2013 were retrieved. Correlations of postoperative complications with clinicopathologic factors were examined using univariate analysis. Risk factors for tumor recurrence and mortality of the patients after tumor resection were identified using multivariate Cox proportional hazards models. Time to relapse and overall survival were analyzed using log-rank test of Kaplan-Meier analysis.

RESULTS

Blood carcinoembryonic antigen (CEA) significantly correlated with early symptoms, preoperative manifestations, and tumor pathology. Low differentiation grade of tumor increased the risk of recurrence after surgery in all patients with CRC. In the same cohort of patients, elevated blood CEA, low differentiation grade of tumor, laparotomy, smoking history, and TNM stage IV and III increased the mortality risk after tumor resection. In patients with advanced colon cancer, risk for postoperative mortality was increased by blood CEA, advanced tumor stage, and low tumor differentiation grade; while in those with advanced rectal cancer, blood CEA, pathologic type other than mucinous/adenocarcinoma, and laparotomy were identified as significant risk factors. In both groups of patients, postoperative chemotherapy significantly reduced the risk of mortality.

CONCLUSIONS

The present work has identified clinical factors increasing the risk of recurrence as well as mortality after surgery in more than 1,000 patients with CRC. Postoperative chemotherapy is associated with a significant reduction in the risk of mortality. All of these findings should provide insights into the better management of critically ill patients with CRC.

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Anderson JC, Robertson DJ. Serrated Polyp Detection by the Fecal Immunochemical Test: An Imperfect FIT. Clin Gastroenterol Hepatol 2017;15:880-882. [PMID: 27847280 DOI: 10.1016/j.cgh.2016.11.014] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/01/2016] [Revised: 11/07/2016] [Accepted: 11/08/2016] [Indexed: 02/07/2023]

Rashtak S, Rego R, Sweetser SR, Sinicrope FA. Sessile Serrated Polyps and Colon Cancer Prevention. Cancer Prev Res (Phila) 2017;10:270-278. [PMID: 28325827 DOI: 10.1158/1940-6207.capr-16-0264] [Citation(s) in RCA: 25] [Impact Index Per Article: 3.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/14/2016] [Revised: 11/21/2016] [Accepted: 03/15/2017] [Indexed: 11/16/2022]