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5. Supplementary Data from Lynch Syndrome–Associated Breast Cancers: Clinicopathologic Characteristics of a Case Series from the Colon Cancer Family Registry

Author

Walsh, Michael D., primary, Buchanan, Daniel D., primary, Cummings, Margaret C., primary, Pearson, Sally-Ann, primary, Arnold, Sven T., primary, Clendenning, Mark, primary, Walters, Rhiannon, primary, McKeone, Diane M., primary, Spurdle, Amanda B., primary, Hopper, John L., primary, Jenkins, Mark A., primary, Phillips, Kerry D., primary, Suthers, Graeme K., primary, George, Jill, primary, Goldblatt, Jack, primary, Muir, Amanda, primary, Tucker, Kathy, primary, Pelzer, Elise, primary, Gattas, Michael R., primary, Woodall, Sonja, primary, Parry, Susan, primary, Macrae, Finlay A., primary, Haile, Robert W., primary, Baron, John A., primary, Potter, John D., primary, Le Marchand, Loic, primary, Bapat, Bharati, primary, Thibodeau, Stephen N., primary, Lindor, Noralane M., primary, McGuckin, Michael A., primary, and Young, Joanne P., primary

Published
2023
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6. Data from Lynch Syndrome–Associated Breast Cancers: Clinicopathologic Characteristics of a Case Series from the Colon Cancer Family Registry

Author

Walsh, Michael D., primary, Buchanan, Daniel D., primary, Cummings, Margaret C., primary, Pearson, Sally-Ann, primary, Arnold, Sven T., primary, Clendenning, Mark, primary, Walters, Rhiannon, primary, McKeone, Diane M., primary, Spurdle, Amanda B., primary, Hopper, John L., primary, Jenkins, Mark A., primary, Phillips, Kerry D., primary, Suthers, Graeme K., primary, George, Jill, primary, Goldblatt, Jack, primary, Muir, Amanda, primary, Tucker, Kathy, primary, Pelzer, Elise, primary, Gattas, Michael R., primary, Woodall, Sonja, primary, Parry, Susan, primary, Macrae, Finlay A., primary, Haile, Robert W., primary, Baron, John A., primary, Potter, John D., primary, Le Marchand, Loic, primary, Bapat, Bharati, primary, Thibodeau, Stephen N., primary, Lindor, Noralane M., primary, McGuckin, Michael A., primary, and Young, Joanne P., primary

Published
2023
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10. Aspirin Synergizes with Regorafenib to Reduce Growth of Colorectal Cancer

Author

Su, Chang, primary, Fennell, Lochlan J, additional, Bond, Catherine E, additional, Kane, Alexandra M, additional, Kerr, Genevieve, additional, Jardé, Thierry, additional, Micati, Diana, additional, Engel, Rebekah M, additional, Chan, Wing Hei, additional, Hlavca, Sara, additional, Archer, Stuart, additional, McMurrick, Paul J, additional, Hammerlindl, Heinz, additional, Lim, Fayth, additional, Salik, Basit, additional, McKeone, Diane M, additional, Hartel, Gunter, additional, Borowsky, Jennifer, additional, Ladwa, Rahul, additional, Leggett, Barbara A, additional, Schaider, Helmut, additional, Abud, Helen E, additional, Boyle, Glen M, additional, Burge, Matthew E, additional, and Whitehall, Vicki LJ, additional

Published
2022
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11. Oncogenic BRAF mutation induces DNA methylation changes in a murine model for human serrated colorectal neoplasia

Author

Bond, Catherine E., primary, Liu, Cheng, additional, Kawamata, Futoshi, additional, McKeone, Diane M., additional, Fernando, Winnie, additional, Jamieson, Saara, additional, Pearson, Sally-Ann, additional, Kane, Alexandra, additional, Woods, Susan L., additional, Lannagan, Tamsin R. M., additional, Somashekar, Roshini, additional, Lee, Young, additional, Dumenil, Troy, additional, Hartel, Gunter, additional, Spring, Kevin J., additional, Borowsky, Jennifer, additional, Fennell, Lochlan, additional, Bettington, Mark, additional, Lee, Jason, additional, Worthley, Daniel L., additional, Leggett, Barbara A., additional, and Whitehall, Vicki L. J., additional

Published
2018
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14. Oncogenic <italic>BRAF</italic> mutation induces DNA methylation changes in a murine model for human serrated colorectal neoplasia.

Author

Bond, Catherine E., Liu, Cheng, Kawamata, Futoshi, McKeone, Diane M., Fernando, Winnie, Jamieson, Saara, Pearson, Sally-Ann, Kane, Alexandra, Woods, Susan L., Lannagan, Tamsin R. M., Somashekar, Roshini, Lee, Young, Dumenil, Troy, Hartel, Gunter, Spring, Kevin J., Borowsky, Jennifer, Fennell, Lochlan, Bettington, Mark, Lee, Jason, and Worthley, Daniel L.

Abstract

Colorectal cancer is a major cause of cancer death and approximately 20% arises within serrated polyps, which are under-recognized and poorly understood. Human serrated colorectal polyps frequently exhibit both oncogenic BRAF mutation and widespread DNA methylation changes, which are important in silencing genes restraining neoplastic progression. Here, we investigated whether in vivo induction of mutant Braf is sufficient to result in coordinated promoter methylation changes for multiple cancer-related genes. The BrafV637E mutation was induced in murine intestine on an FVB;C57BL/6J background and assessed for morphological and DNA methylation changes at multiple time points from 10 days to 14 months. Extensive intestinal hyperplasia developed by 10 days post-induction of the mutation. By 8 months, most mice had murine serrated adenomas with dysplasia and invasive cancer developed in 40% of mice by 14 months. From 5 months onwards, Braf mutant mice showed extensive, gene-specific increases in DNA methylation even in hyperplastic mucosa without lesions. This demonstrates that persistent oncogenic Braf signaling is sufficient to induce widespread DNA methylation changes. This occurs over an extended period of time, mimicking the long latency followed by rapid progression of human serrated neoplasia. This study establishes for the first time that DNA methylation arises slowly in direct response to prolonged oncogenic Braf signaling in serrated polyps; this finding has implications both for chemoprevention and for understanding the origin of DNA hypermethylation in cancer generally. [ABSTRACT FROM AUTHOR]

Published
2018
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15. RNF43 is mutated less frequently in Lynch Syndrome compared with sporadic microsatellite unstable colorectal cancers.

Author

Fennell, Lochlan J., Clendenning, Mark, McKeone, Diane M., Jamieson, Saara H., Balachandran, Samanthy, Borowsky, Jennifer, Liu, John, Kawamata, Futoshi, Bond, Catherine E., Rosty, Christophe, Burge, Matthew E., Buchanan, Daniel D., Leggett, Barbara A., and Whitehall, Vicki L. J.

Abstract

The WNT signaling pathway is commonly altered during colorectal cancer development. The E3 ubiquitin ligase, RNF43, negatively regulates the WNT signal through increased ubiquitination and subsequent degradation of the Frizzled receptor. RNF43 has recently been reported to harbor frequent truncating frameshift mutations in sporadic microsatellite unstable (MSI) colorectal cancers. This study assesses the relative frequency of RNF43 mutations in hereditary colorectal cancers arising in the setting of Lynch syndrome. The entire coding region of RNF43 was Sanger sequenced in 24 colorectal cancers from 23 patients who either (i) carried a germline mutation in one of the DNA mismatch repair genes ( MLH1, MSH6, MSH2, PMS2), or (ii) showed immunohistochemical loss of expression of one or more of the DNA mismatch repair proteins, was BRAF wild type at V600E, were under 60 years of age at diagnosis, and demonstrated no promoter region methylation for MLH1 in tumor DNA. A validation cohort of 44 colorectal cancers from mismatch repair germline mutation carriers from the Australasian Colorectal Cancer Family Registry (ACCFR) were sequenced for the most common truncating mutation hotspots (X117 and X659). RNF43 mutations were found in 9 of 24 (37.5%) Lynch syndrome colorectal cancers. The majority of mutations were frameshift deletions in the G659 G7 repeat tract (29%); 2 cancers (2/24, 8%) from the one patient harbored frameshift mutations at codon R117 (C6 repeat tract) within exon 3. In the ACCFR validation cohort, RNF43 hotspot mutations were identified in 19/44 (43.2%) of samples, which was not significantly different to the initial series. The proportion of mutant RNF43 in Lynch syndrome related colorectal cancers is significantly lower than the previously reported mutation rate found in sporadic MSI colorectal cancers. These findings identify further genetic differences between sporadic and hereditary colorectal cancers. This may be because Lynch Syndrome cancers commonly arise in colorectal adenomas already bearing the APC mutation, whereas sporadic microsatellite unstable colorectal cancers arise from serrated polyps typically lacking APC mutation, decreasing the selection pressure on other WNT signaling related loci in Lynch syndrome. [ABSTRACT FROM AUTHOR]

Published
2018
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16. GNAS mutations are present in colorectal traditional serrated adenomas, serrated tubulovillous adenomas and serrated adenocarcinomas with adverse prognostic features.

Author

Liu, Cheng, McKeone, Diane M, Walker, Neal I, Bettington, Mark L, Leggett, Barbara A, and Whitehall, Vicki L J

Subjects
*COLON cancer prognosis, *GENE expression, *ADENOMA, *GENETIC mutation, *TUMORS
Abstract

Aims Activating mutations in GNAS are important in the development of a range of neoplasms, including a small proportion of conventional adenomas and colorectal carcinomas ( CRCs). However, their contribution to serrated pathway neoplasia is unclear, as mutations have only been examined in small series of sessile serrated adenomas ( SSAs) and traditional serrated adenomas ( TSAs), and not in serrated tubulovillous adenomas ( sTVAs). The aim of this study was to investigate the frequency and significance of GNAS mutations in colorectal adenomas and CRCs. Methods and results Using a large, well-characterized series, we identified GNAS mutations in 9.2% (18 of 196) of TSAs, 7.1% (four of 56) of sTVAs and 2.0% (nine of 459) of CRCs. Mutations were absent in SSAs (none of 43), tubular adenomas (none of 50) and conventional tubulovillous adenomas (none of 50). A BRAF or KRAS mutation was seen in 77.4% of GNAS mutant lesions, suggesting a synergistic effect with the mitogen-activated protein kinase pathway. In CRCs, GNAS mutations were associated with mucinous differentiation and serrated morphological features. Conclusions GNAS mutations contribute significantly to the development of a subset of serrated adenomas and CRCs. [ABSTRACT FROM AUTHOR]

Published
2017
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19. Cancer Risks for Relatives of Patients With Serrated Polyposis

Author

Win, Aung Ko, primary, Walters, Rhiannon J, additional, Buchanan, Daniel D, additional, Jenkins, Mark A, additional, Sweet, Kevin, additional, Frankel, Wendy L, additional, de la Chapelle, Albert, additional, McKeone, Diane M, additional, Walsh, Michael D, additional, Clendenning, Mark, additional, Pearson, Sally-Ann, additional, Pavluk, Erika, additional, Nagler, Belinda, additional, Hopper, John L, additional, Gattas, Michael R, additional, Goldblatt, Jack, additional, George, Jill, additional, Suthers, Graeme K, additional, Phillips, Kerry D, additional, Woodall, Sonja, additional, Arnold, Julie, additional, Tucker, Kathy, additional, Field, Michael, additional, Greening, Sian, additional, Gallinger, Steve, additional, Aronson, Melyssa, additional, Perrier, Renee, additional, Woods, Michael O, additional, Green, Jane S, additional, Walker, Neal, additional, Rosty, Christophe, additional, Parry, Susan, additional, and Young, Joanne P, additional

Published
2012
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20. Oncogenic BRAFmutation induces DNA methylation changes in a murine model for human serrated colorectal neoplasia

Author

Bond, Catherine E., Liu, Cheng, Kawamata, Futoshi, McKeone, Diane M., Fernando, Winnie, Jamieson, Saara, Pearson, Sally-Ann, Kane, Alexandra, Woods, Susan L., Lannagan, Tamsin R. M., Somashekar, Roshini, Lee, Young, Dumenil, Troy, Hartel, Gunter, Spring, Kevin J., Borowsky, Jennifer, Fennell, Lochlan, Bettington, Mark, Lee, Jason, Worthley, Daniel L., Leggett, Barbara A., and Whitehall, Vicki L. J.

Abstract

ABSTRACTColorectal cancer is a major cause of cancer death and approximately 20% arises within serrated polyps, which are under-recognized and poorly understood. Human serrated colorectal polyps frequently exhibit both oncogenic BRAFmutation and widespread DNA methylation changes, which are important in silencing genes restraining neoplastic progression. Here, we investigated whether in vivoinduction of mutant Brafis sufficient to result in coordinated promoter methylation changes for multiple cancer-related genes. The BrafV637Emutation was induced in murine intestine on an FVB;C57BL/6J background and assessed for morphological and DNA methylation changes at multiple time points from 10 days to 14 months. Extensive intestinal hyperplasia developed by 10 days post-induction of the mutation. By 8 months, most mice had murine serrated adenomas with dysplasia and invasive cancer developed in 40% of mice by 14 months. From 5 months onwards, Brafmutant mice showed extensive, gene-specific increases in DNA methylation even in hyperplastic mucosa without lesions. This demonstrates that persistent oncogenic Brafsignaling is sufficient to induce widespread DNA methylation changes. This occurs over an extended period of time, mimicking the long latency followed by rapid progression of human serrated neoplasia. This study establishes for the first time that DNA methylation arises slowly in direct response to prolonged oncogenic Brafsignaling in serrated polyps; this finding has implications both for chemoprevention and for understanding the origin of DNA hypermethylation in cancer generally.

Published
2018
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21. Hyperplastic Polyposis and the smoking paradox in females

Author

Buchanan, Daniel D, primary, Jenkins, Mark A, additional, Win, Aung K, additional, Walsh, Michael D, additional, McKeone, Diane M, additional, Macrae, Finlay, additional, Rosty, Christophe, additional, Walker, Neal I, additional, Parry, Susan, additional, and Young, Joanne P, additional

Published
2011
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22. Risk Factors for Colorectal Cancer in Patients with Multiple Serrated Polyps: A Cross-Sectional Case Series from Genetics Clinics

Author

Buchanan, Daniel D., primary, Sweet, Kevin, additional, Drini, Musa, additional, Jenkins, Mark A., additional, Win, Aung Ko, additional, English, Dallas R., additional, Walsh, Michael D., additional, Clendenning, Mark, additional, McKeone, Diane M., additional, Walters, Rhiannon J., additional, Roberts, Aedan, additional, Pearson, Sally-Ann, additional, Pavluk, Erika, additional, Hopper, John L., additional, Gattas, Michael R., additional, Goldblatt, Jack, additional, George, Jill, additional, Suthers, Graeme K., additional, Phillips, Kerry D., additional, Woodall, Sonja, additional, Arnold, Julie, additional, Tucker, Kathy, additional, Muir, Amanda, additional, Field, Michael, additional, Greening, Sian, additional, Gallinger, Steven, additional, Perrier, Renee, additional, Baron, John A., additional, Potter, John D., additional, Haile, Robert, additional, Frankel, Wendy, additional, de la Chapelle, Albert, additional, Macrae, Finlay, additional, Rosty, Christophe, additional, Walker, Neal I., additional, Parry, Susan, additional, and Young, Joanne P., additional

Published
2010
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24. S1677 Over-Expression of the Chromosome 11 Mucins is Associated With CIMP and BRAF Mutation in Colorectal Cancer

Author

Walsh, Michael D., primary, Buchanan, Daniel D., additional, Pearson, Sally-Ann, additional, Walters, Rhiannon J., additional, McKeone, Diane M., additional, Clendenning, Mark, additional, Hopper, John, additional, Jenkins, Mark A., additional, Giles, Graham G., additional, English, Dallas, additional, Rosty, Christophe, additional, McGuckin, Michael A., additional, and Young, Joanne P., additional

Published
2010
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25. Lynch Syndrome–Associated Breast Cancers: Clinicopathologic Characteristics of a Case Series from the Colon Cancer Family Registry

Author

Walsh, Michael D., primary, Buchanan, Daniel D., additional, Cummings, Margaret C., additional, Pearson, Sally-Ann, additional, Arnold, Sven T., additional, Clendenning, Mark, additional, Walters, Rhiannon, additional, McKeone, Diane M., additional, Spurdle, Amanda B., additional, Hopper, John L., additional, Jenkins, Mark A., additional, Phillips, Kerry D., additional, Suthers, Graeme K., additional, George, Jill, additional, Goldblatt, Jack, additional, Muir, Amanda, additional, Tucker, Kathy, additional, Pelzer, Elise, additional, Gattas, Michael R., additional, Woodall, Sonja, additional, Parry, Susan, additional, Macrae, Finlay A., additional, Haile, Robert W., additional, Baron, John A., additional, Potter, John D., additional, Le Marchand, Loic, additional, Bapat, Bharati, additional, Thibodeau, Stephen N., additional, Lindor, Noralane M., additional, McGuckin, Michael A., additional, and Young, Joanne P., additional

Published
2010
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