Incidences of colorectal adenomas and cancers under colonoscopy surveillance suggest an accelerated “Big Bang” pathway to CRC in three of the four Lynch syndromes
Background Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid prog...
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| Published in | Hereditary cancer in clinical practice Vol. 22; no. 1; pp. 6 - 12 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
13.05.2024
BioMed Central Ltd BMC |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1897-4287 1731-2302 1897-4287 |
| DOI | 10.1186/s13053-024-00279-3 |
Cover
| Abstract | Background
Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair (
path_MMR
) genes.
Materials and methods
We examined the CRC and colorectal adenoma incidences in 3,574
path_MLH1, path_MSH2, path_MSH6
and
path_PMS2
carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms.
Results
Most of the
path_MMR
carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in
path_PMS2
carriers.
Conclusions
Colonoscopy prevented CRC in
path_PMS2
carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports. |
|---|---|
| AbstractList | BackgroundColorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair (path_MMR) genes.Materials and methodsWe examined the CRC and colorectal adenoma incidences in 3,574 path_MLH1, path_MSH2, path_MSH6 and path_PMS2 carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms.ResultsMost of the path_MMR carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in path_PMS2 carriers.ConclusionsColonoscopy prevented CRC in path_PMS2 carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports. Background Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair ( path_MMR ) genes. Materials and methods We examined the CRC and colorectal adenoma incidences in 3,574 path_MLH1, path_MSH2, path_MSH6 and path_PMS2 carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms. Results Most of the path_MMR carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in path_PMS2 carriers. Conclusions Colonoscopy prevented CRC in path_PMS2 carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports. Abstract Background Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair (path_MMR) genes. Materials and methods We examined the CRC and colorectal adenoma incidences in 3,574 path_MLH1, path_MSH2, path_MSH6 and path_PMS2 carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms. Results Most of the path_MMR carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in path_PMS2 carriers. Conclusions Colonoscopy prevented CRC in path_PMS2 carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports. Background Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair (path_MMR) genes. Materials and methods We examined the CRC and colorectal adenoma incidences in 3,574 path_MLH1, path_MSH2, path_MSH6 and path_PMS2 carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms. Results Most of the path_MMR carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in path_PMS2 carriers. Conclusions Colonoscopy prevented CRC in path_PMS2 carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports. Keywords: MSI, MLH1, MSH2, MSH6, PMS2, dMMR, Lynch syndromes, Colorectal, cancer, Adenoma, Colonoscopy, Sojourn time Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair (path_MMR) genes. We examined the CRC and colorectal adenoma incidences in 3,574 path_MLH1, path_MSH2, path_MSH6 and path_PMS2 carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms. Most of the path_MMR carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in path_PMS2 carriers. Colonoscopy prevented CRC in path_PMS2 carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports. Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair (path_MMR) genes. We examined the CRC and colorectal adenoma incidences in 3,574 path_MLH1, path_MSH2, path_MSH6 and path_PMS2 carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms. Most of the path_MMR carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in path_PMS2 carriers. Colonoscopy prevented CRC in path_PMS2 carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports. Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair (path_MMR) genes.BACKGROUNDColorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with deficient mismatch repair have an increased probability of acquiring additional cancer driver mutation(s) resulting in more rapid progression to malignancy. If this model was accurate, the success of colonoscopy in preventing CRC would be a function of the intervals between colonoscopies and mean sojourn time of detectable adenomas. Contrary to expectations, colonoscopy did not decrease incidence of CRC in the Lynch syndromes and shorter colonoscopy intervals have not been effective in reducing CRC incidence. The prospective Lynch Syndrome Database (PLSD) was designed to examine these issues in carriers of pathogenic variants of the mis-match repair (path_MMR) genes.We examined the CRC and colorectal adenoma incidences in 3,574 path_MLH1, path_MSH2, path_MSH6 and path_PMS2 carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms.MATERIALS AND METHODSWe examined the CRC and colorectal adenoma incidences in 3,574 path_MLH1, path_MSH2, path_MSH6 and path_PMS2 carriers subjected to regular colonoscopy with polypectomy, and considered the results based on sojourn times and stochastic probability paradigms.Most of the path_MMR carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in path_PMS2 carriers.RESULTSMost of the path_MMR carriers in each genetic group had no adenomas. There was no association between incidences of CRC and the presence of adenomas. There was no CRC observed in path_PMS2 carriers.Colonoscopy prevented CRC in path_PMS2 carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports.CONCLUSIONSColonoscopy prevented CRC in path_PMS2 carriers but not in the others. Our findings are consistent with colonoscopy surveillance blocking the adenoma-carcinoma pathway by removing identified adenomas which might otherwise become CRCs. However, in the other carriers most CRCs likely arised from dMMR cells in the crypts that have an increased mutation rate with increased stochastic chaotic probabilities for mutations. Therefore, this mechanism, that may be associated with no or only a short sojourn time of MSI tumours as adenomas, could explain the findings in our previous and current reports. |
| ArticleNumber | 6 |
| Audience | Academic |
| Author | Laish, Ido Ahadova, Aysel Hovig, Eivind Seppälä, Toni Therkildsen, Christina Winship, Ingrid da Silva, Leandro Apolinário Heuveline, Vincent Sampson, Julian R. Sunde, Lone Katz, Lior Cavestro, Giulia Martina Bernstein, Inge Half, Elizabeth Monahan, Kevin Burn, John Capella, Gabriel Lindblom, Annika Horisberger, Karoline Klarskov, Louise L Møller, Pål Haupt, Saskia Möslein, Gabriela Lautrup, Charlotte Macrae, Finlay Kloor, Matthias Evans, D. Gareth Dominguez-Valentin, Mev Vainer, Elez |
| Author_xml | – sequence: 1 givenname: Pål surname: Møller fullname: Møller, Pål email: moller.pal@gmail.com organization: Department of Tumour Biology, Institute of Cancer Research, The Norwegian Radium Hospital – sequence: 2 givenname: Saskia surname: Haupt fullname: Haupt, Saskia organization: Engineering Mathematics and Computing Lab (EMCL), Interdisciplinary Center for Scientific Computing (IWR), Heidelberg University, Data Mining and Uncertainty Quantification (DMQ), Heidelberg Institute for Theoretical Studies (HITS) – sequence: 3 givenname: Aysel surname: Ahadova fullname: Ahadova, Aysel organization: Department of Applied Tumour Biology, Institute of Pathology, Heidelberg University Hospital, Clinical Cooperation Unit Applied Tumour Biology, German Cancer Research Centre (DKFZ) – sequence: 4 givenname: Matthias surname: Kloor fullname: Kloor, Matthias organization: Department of Applied Tumour Biology, Institute of Pathology, Heidelberg University Hospital, Clinical Cooperation Unit Applied Tumour Biology, German Cancer Research Centre (DKFZ) – sequence: 5 givenname: Julian R. surname: Sampson fullname: Sampson, Julian R. organization: Institute of Medical Genetics, Division of Cancer and Genetics, Cardiff University School of Medicine – sequence: 6 givenname: Lone surname: Sunde fullname: Sunde, Lone organization: Department of Clinical Genetics, Aalborg University Hospital, Department of Biomedicine, Aarhus University, Clinical Cancer Research Center, Aalborg University Hospital – sequence: 7 givenname: Toni surname: Seppälä fullname: Seppälä, Toni organization: Faculty of Medicine and Health Technology, Tays Cancer Center, Tampere University, Tampere University Hospital, Department of Gastrointestinal Surgery, Helsinki University Central Hospital, University of Helsinki, Applied Tumour Genomics, Research Program Unit, University of Helsinki – sequence: 8 givenname: John surname: Burn fullname: Burn, John organization: Faculty of Medical Sciences, Newcastle University – sequence: 9 givenname: Inge surname: Bernstein fullname: Bernstein, Inge organization: Dept. of Quality and Coherence, Aalborg University Hospital, Department of Clinical Medicine, Aalborg University Hospital, Aalborg University – sequence: 10 givenname: Gabriel surname: Capella fullname: Capella, Gabriel organization: Hereditary Cancer Program, Institut Català d’Oncologia-IDIBELL, L; Hospitalet de Llobregat – sequence: 11 givenname: D. Gareth surname: Evans fullname: Evans, D. Gareth organization: Manchester Centre for Genomic Medicine, Division of Evolution, Infection and Genomic Sciences, University of Manchester, Manchester University NHS Foundation Trust – sequence: 12 givenname: Annika surname: Lindblom fullname: Lindblom, Annika organization: Department of Molecular Medicine and Surgery, Karolinska Institutet, Dept Clinical Genetics, Karolinska University Hospital – sequence: 13 givenname: Ingrid surname: Winship fullname: Winship, Ingrid organization: Genomic Medicine, The Royal Melbourne Hospital, Department of Medicine, University of Melbourne – sequence: 14 givenname: Finlay surname: Macrae fullname: Macrae, Finlay organization: Department of Medicine, University of Melbourne – sequence: 15 givenname: Lior surname: Katz fullname: Katz, Lior organization: Department of Gastroenterology, Medical Center, Faculty of Medicine, Hebrew University of Jerusalem – sequence: 16 givenname: Ido surname: Laish fullname: Laish, Ido organization: Gastroenerolgy institute, Sheba medical center and Faculty of medicine Tel Aviv university – sequence: 17 givenname: Elez surname: Vainer fullname: Vainer, Elez organization: Department of Gastroenterology, Medical Center, Faculty of Medicine, Hebrew University of Jerusalem – sequence: 18 givenname: Kevin surname: Monahan fullname: Monahan, Kevin organization: Lynch Syndrome & Family Cancer Clinic, Centre for Familial Intestinal Caner, St Mark’s Hospital – sequence: 19 givenname: Elizabeth surname: Half fullname: Half, Elizabeth organization: Gastrointestinal Cancer Prevention Unit, Gastroenterology Department, Rambam Health Care Campus – sequence: 20 givenname: Karoline surname: Horisberger fullname: Horisberger, Karoline organization: Department of Surgery, Universitätsmedizin Mainz – sequence: 21 givenname: Leandro Apolinário surname: da Silva fullname: da Silva, Leandro Apolinário organization: Hospital Universitário Oswaldo Cruz, Universidade de Pernambuco, Recife, Brazil & SEQUIPE – sequence: 22 givenname: Vincent surname: Heuveline fullname: Heuveline, Vincent organization: Engineering Mathematics and Computing Lab (EMCL), Interdisciplinary Center for Scientific Computing (IWR), Heidelberg University, Data Mining and Uncertainty Quantification (DMQ), Heidelberg Institute for Theoretical Studies (HITS) – sequence: 23 givenname: Christina surname: Therkildsen fullname: Therkildsen, Christina organization: Gastro Unit, The Danish HNPCC Register, Copenhagen University Hospital – Amager and Hvidovre – sequence: 24 givenname: Charlotte surname: Lautrup fullname: Lautrup, Charlotte organization: Department of Clinical Genetics, Aarhus University Hospital – sequence: 25 givenname: Louise L surname: Klarskov fullname: Klarskov, Louise L organization: Dept of Pathology, Copenhagen University Hospital - Herlev and Gentofte, Dept of Clinical Medicine, University of Copenhagen – sequence: 26 givenname: Giulia Martina surname: Cavestro fullname: Cavestro, Giulia Martina organization: Gastroenterology and Gastrointestinal Endoscopy Unit, Division of Experimental Oncology, IRCCS San Raffaele Scientific Institute, Vita-Salute San Raffaele University – sequence: 27 givenname: Gabriela surname: Möslein fullname: Möslein, Gabriela organization: Surgical Center for Hereditary Tumors, University Düsseldorf – sequence: 28 givenname: Eivind surname: Hovig fullname: Hovig, Eivind organization: Department of Tumour Biology, Institute of Cancer Research, The Norwegian Radium Hospital, Centre for bioinformatics, Department of Informatics, University of Oslo – sequence: 29 givenname: Mev surname: Dominguez-Valentin fullname: Dominguez-Valentin, Mev organization: Department of Tumour Biology, Institute of Cancer Research, The Norwegian Radium Hospital |
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| CitedBy_id | crossref_primary_10_1186_s13053_025_00305_y crossref_primary_10_1007_s10689_024_00423_x crossref_primary_10_1111_cge_14670 crossref_primary_10_3390_cancers16234021 |
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| Keywords | dMMR MSI Colorectal Colonoscopy Sojourn time cancer Adenoma Lynch syndromes MSH6 MSH2 PMS2 MLH1 |
| Language | English |
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| PublicationTitle | Hereditary cancer in clinical practice |
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| Snippet | Background
Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model... Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas with... Background Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model... BackgroundColorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this model adenomas... Abstract Background Colorectal cancers (CRCs) in the Lynch syndromes have been assumed to emerge through an accelerated adenoma-carcinoma pathway. In this... |
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| SubjectTerms | Adenoma Age Analysis Biomedical and Life Sciences Biomedicine Cancer Cancer Research Carcinoma Colon Colonoscopy Colorectal cancer dMMR Genetic disorders Human Genetics Immune system Malignancy Medical prognosis Mismatch repair MLH1 MLH1 protein MSH2 MSH2 protein MSH6 MSH6 protein MSI Mutation Mutation rates Oncology PMS2 Polyps Prevention Regression analysis Surveillance Tumors |
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| Title | Incidences of colorectal adenomas and cancers under colonoscopy surveillance suggest an accelerated “Big Bang” pathway to CRC in three of the four Lynch syndromes |
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