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1. A collaborative resource platform for non-human primate neuroimaging

Author

Messinger, A., Sirmpilatze, N., Heuer, K., Loh, K.K., Mars, R.B., Sein, J., Xu, T., Glen, D., Jung, B., Seidlitz, J., Taylor, P., Toro, R., Garza-Villarreal, E.A., Sponheim, C., Wang, X., Benn, R.A., Cagna, B., Dadarwal, R., Evrard, H.C., Garcia-Saldivar, P., Giavasis, S., Hartig, R., Lepage, C., Liu, C., Majka, P., Merchant, H., Milham, M.P., Rosa, M.G.P., Tasserie, J., Uhrig, L., Margulies, D.S., Klink, P.C., Messinger, A., Sirmpilatze, N., Heuer, K., Loh, K.K., Mars, R.B., Sein, J., Xu, T., Glen, D., Jung, B., Seidlitz, J., Taylor, P., Toro, R., Garza-Villarreal, E.A., Sponheim, C., Wang, X., Benn, R.A., Cagna, B., Dadarwal, R., Evrard, H.C., Garcia-Saldivar, P., Giavasis, S., Hartig, R., Lepage, C., Liu, C., Majka, P., Merchant, H., Milham, M.P., Rosa, M.G.P., Tasserie, J., Uhrig, L., Margulies, D.S., and Klink, P.C.

Abstract

Contains fulltext : 226482.pdf (publisher's version ) (Open Access), Neuroimaging non-human primates (NHPs) is a growing, yet highly specialized field of neuroscience. Resources that were primarily developed for human neuroimaging often need to be significantly adapted for use with NHPs or other animals, which has led to an abundance of custom, in-house solutions. In recent years, the global NHP neuroimaging community has made significant efforts to transform the field towards more open and collaborative practices. Here we present the PRIMatE Resource Exchange (PRIME-RE), a new collaborative online platform for NHP neuroimaging. PRIME-RE is a dynamic community-driven hub for the exchange of practical knowledge, specialized analytical tools, and open data repositories, specifically related to NHP neuroimaging. PRIME-RE caters to both researchers and developers who are either new to the field, looking to stay abreast of the latest developments, or seeking to collaboratively advance the field.

Published
2021

2. Refined cut-off for TP53 immunohistochemistry improves prediction of TP53 mutation status in ovarian mucinous tumors: implications for outcome analyses.

Author

Friedlander M., Russell P., Links M., Grygiel J., Hill J., Byth K., Jaworski R., Harnett P., Wain G., Ward B., Papadimos D., Crandon A., Cummings M., Horwood K., Obermair A., Perrin L., Wyld D., Nicklin J., Davy M., Oehler M.K., Hall C., Dodd T., Healy T., Pittman K., Henderson D., Miller J., Pierdes J., Blomfield P., Challis D., McIntosh R., Parker A., Brown B., Rome R., Allen D., Grant P., Hyde S., Laurie R., Robbie M., Healy D., Jobling T., Manolitsas T., McNealage J., Rogers P., Susil B., Sumithran E., Simpson I., Phillips K., Rischin D., Fox S., Johnson D., Lade S., Loughrey M., O'Callaghan N., Murray W., Waring P., Billson V., Pyman J., Neesham D., Quinn M., Underhill C., Bell R., Ng L.F., Blum R., Ganju V., Hammond I., Leung Y., McCartney A., Buck M., Haviv I., Purdie D., Whiteman D., Zeps N., Kaufmann S., Meagher N.S., Ramus S.J., Campbell I., Cheasley D., Wakefield M.J., Ryland G.L., Allan P.E., Alsop K., Ananda S., Anglesio M.S., Au-Yeung G., Bohm M., Bowtell D.D.L., Brand A., Chenevix-Trench G., Christie M., Chiew Y.-E., Churchman M., DeFazio A., Dudley R., Fairweather N., Fereday S., Fox S.B., Gilks C.B., Gourley C., Hacker N.F., Hadley A.M., Hendley J., Ho G.-Y., Huntsman D.G., Hunter S.M., Jobling T.W., Kalli K.R., Kaufmann S.H., Kennedy C.J., Kobel M., Le Page C., McNally O.M., McAlpine J.N., Mileshkin L., Jan Pyman, Rahimi K., Samimi G., Sharma R., Stephens A.N., Traficante N., Antill Y.C., Scott C.L., Campbell I.G., Gorringe K.L., Kang E.Y., LePage C., da Cunha Torres M., Rowley S., Salazar C., Xing Z., Allan P., Mes-Masson A.-M., Provencher D.M., Kelemen L.E., Fasching P.A., Doherty J.A., Goodman M.T., Goode E.L., Deen S., Pharoah P.D.P., Brenton J.D., Sieh W., Mateoiu C., Sundfeldt K., Cook L.S., Le N.D., Bowtell D., Green A., Webb P., Gertig D., Moore S., Hung J., Harrap K., Sadkowsky T., Pandeya N., Malt M., Mellon A., Robertson R., Bergh T.V., Jones M., Mackenzie P., Maidens J., Nattress K., Chiew Y.E., Stenlake A., Sullivan H., Alexander B., Ashover P., Brown S., Corrish T., Green L., Jackman L., Ferguson K., Martin K., Martyn A., Ranieri B., White J., Jayde V., Mamers P., Bowes L., Galletta L., Giles D., Schmidt T., Shirley H., Ball C., Young C., Viduka S., Tran H., Bilic S., Glavinas L., Brooks J., Stuart-Harris R., Kirsten F., Rutovitz J., Clingan P., Glasgow A., Proietto A., Braye S., Otton G., Shannon J., Bonaventura T., Stewart J., Begbie S., Bell D., Baron-Hay S., Ferrier A., Gard G., Nevell D., Pavlakis N., Valmadre S., Young B., Camaris C., Crouch R., Edwards L., Hacker N., Marsden D., Robertson G., Beale P., Beith J., Carter J., Dalrymple C., Houghton R., Friedlander M., Russell P., Links M., Grygiel J., Hill J., Byth K., Jaworski R., Harnett P., Wain G., Ward B., Papadimos D., Crandon A., Cummings M., Horwood K., Obermair A., Perrin L., Wyld D., Nicklin J., Davy M., Oehler M.K., Hall C., Dodd T., Healy T., Pittman K., Henderson D., Miller J., Pierdes J., Blomfield P., Challis D., McIntosh R., Parker A., Brown B., Rome R., Allen D., Grant P., Hyde S., Laurie R., Robbie M., Healy D., Jobling T., Manolitsas T., McNealage J., Rogers P., Susil B., Sumithran E., Simpson I., Phillips K., Rischin D., Fox S., Johnson D., Lade S., Loughrey M., O'Callaghan N., Murray W., Waring P., Billson V., Pyman J., Neesham D., Quinn M., Underhill C., Bell R., Ng L.F., Blum R., Ganju V., Hammond I., Leung Y., McCartney A., Buck M., Haviv I., Purdie D., Whiteman D., Zeps N., Kaufmann S., Meagher N.S., Ramus S.J., Campbell I., Cheasley D., Wakefield M.J., Ryland G.L., Allan P.E., Alsop K., Ananda S., Anglesio M.S., Au-Yeung G., Bohm M., Bowtell D.D.L., Brand A., Chenevix-Trench G., Christie M., Chiew Y.-E., Churchman M., DeFazio A., Dudley R., Fairweather N., Fereday S., Fox S.B., Gilks C.B., Gourley C., Hacker N.F., Hadley A.M., Hendley J., Ho G.-Y., Huntsman D.G., Hunter S.M., Jobling T.W., Kalli K.R., Kaufmann S.H., Kennedy C.J., Kobel M., Le Page C., McNally O.M., McAlpine J.N., Mileshkin L., Jan Pyman, Rahimi K., Samimi G., Sharma R., Stephens A.N., Traficante N., Antill Y.C., Scott C.L., Campbell I.G., Gorringe K.L., Kang E.Y., LePage C., da Cunha Torres M., Rowley S., Salazar C., Xing Z., Allan P., Mes-Masson A.-M., Provencher D.M., Kelemen L.E., Fasching P.A., Doherty J.A., Goodman M.T., Goode E.L., Deen S., Pharoah P.D.P., Brenton J.D., Sieh W., Mateoiu C., Sundfeldt K., Cook L.S., Le N.D., Bowtell D., Green A., Webb P., Gertig D., Moore S., Hung J., Harrap K., Sadkowsky T., Pandeya N., Malt M., Mellon A., Robertson R., Bergh T.V., Jones M., Mackenzie P., Maidens J., Nattress K., Chiew Y.E., Stenlake A., Sullivan H., Alexander B., Ashover P., Brown S., Corrish T., Green L., Jackman L., Ferguson K., Martin K., Martyn A., Ranieri B., White J., Jayde V., Mamers P., Bowes L., Galletta L., Giles D., Schmidt T., Shirley H., Ball C., Young C., Viduka S., Tran H., Bilic S., Glavinas L., Brooks J., Stuart-Harris R., Kirsten F., Rutovitz J., Clingan P., Glasgow A., Proietto A., Braye S., Otton G., Shannon J., Bonaventura T., Stewart J., Begbie S., Bell D., Baron-Hay S., Ferrier A., Gard G., Nevell D., Pavlakis N., Valmadre S., Young B., Camaris C., Crouch R., Edwards L., Hacker N., Marsden D., Robertson G., Beale P., Beith J., Carter J., Dalrymple C., and Houghton R.

Abstract

TP53 mutations are implicated in the progression of mucinous borderline tumors (MBOT) to mucinous ovarian carcinomas (MOC). Optimized immunohistochemistry (IHC) for TP53 has been established as a proxy for the TP53 mutation status in other ovarian tumor types. We aimed to confirm the ability of TP53 IHC to predict TP53 mutation status in ovarian mucinous tumors and to evaluate the association of TP53 mutation status with survival among patients with MBOT and MOC. Tumor tissue from an initial cohort of 113 women with MBOT/MOC was stained with optimized IHC for TP53 using tissue microarrays (75.2%) or full sections (24.8%) and interpreted using established criteria as normal or abnormal (overexpression, complete absence, or cytoplasmic). Cases were considered concordant if abnormal IHC staining predicted deleterious TP53 mutations. Discordant tissue microarray cases were re-evaluated on full sections and interpretational criteria were refined. The initial cohort was expanded to a total of 165 MBOT and 424 MOC for the examination of the association of survival with TP53 mutation status, assessed either by TP53 IHC and/or sequencing. Initially, 82/113 (72.6%) cases were concordant using the established criteria. Refined criteria for overexpression to account for intratumoral heterogeneity and terminal differentiation improved concordance to 93.8% (106/113). In the expanded cohort, 19.4% (32/165) of MBOT showed evidence for TP53 mutation and this was associated with a higher risk of recurrence, disease-specific death, and all-cause mortality (overall survival: HR = 4.6, 95% CI 1.5-14.3, p = 0.0087). Within MOC, 61.1% (259/424) harbored a TP53 mutation, but this was not associated with survival (overall survival, p = 0.77). TP53 IHC is an accurate proxy for TP53 mutation status with refined interpretation criteria accounting for intratumoral heterogeneity and terminal differentiation in ovarian mucinous tumors. TP53 mutation status is an important biomarker to identify MB

Published
2021

3. Refined cut-off for TP53 immunohistochemistry improves prediction of TP53 mutation status in ovarian mucinous tumors: implications for outcome analyses.

Author

Friedlander M., Russell P., Links M., Grygiel J., Hill J., Byth K., Jaworski R., Harnett P., Wain G., Ward B., Papadimos D., Crandon A., Cummings M., Horwood K., Obermair A., Perrin L., Wyld D., Nicklin J., Davy M., Oehler M.K., Hall C., Dodd T., Healy T., Pittman K., Henderson D., Miller J., Pierdes J., Blomfield P., Challis D., McIntosh R., Parker A., Brown B., Rome R., Allen D., Grant P., Hyde S., Laurie R., Robbie M., Healy D., Jobling T., Manolitsas T., McNealage J., Rogers P., Susil B., Sumithran E., Simpson I., Phillips K., Rischin D., Fox S., Johnson D., Lade S., Loughrey M., O'Callaghan N., Murray W., Waring P., Billson V., Pyman J., Neesham D., Quinn M., Underhill C., Bell R., Ng L.F., Blum R., Ganju V., Hammond I., Leung Y., McCartney A., Buck M., Haviv I., Purdie D., Whiteman D., Zeps N., Kaufmann S., Meagher N.S., Ramus S.J., Campbell I., Cheasley D., Wakefield M.J., Ryland G.L., Allan P.E., Alsop K., Ananda S., Anglesio M.S., Au-Yeung G., Bohm M., Bowtell D.D.L., Brand A., Chenevix-Trench G., Christie M., Chiew Y.-E., Churchman M., DeFazio A., Dudley R., Fairweather N., Fereday S., Fox S.B., Gilks C.B., Gourley C., Hacker N.F., Hadley A.M., Hendley J., Ho G.-Y., Huntsman D.G., Hunter S.M., Jobling T.W., Kalli K.R., Kaufmann S.H., Kennedy C.J., Kobel M., Le Page C., McNally O.M., McAlpine J.N., Mileshkin L., Jan Pyman, Rahimi K., Samimi G., Sharma R., Stephens A.N., Traficante N., Antill Y.C., Scott C.L., Campbell I.G., Gorringe K.L., Kang E.Y., LePage C., da Cunha Torres M., Rowley S., Salazar C., Xing Z., Allan P., Mes-Masson A.-M., Provencher D.M., Kelemen L.E., Fasching P.A., Doherty J.A., Goodman M.T., Goode E.L., Deen S., Pharoah P.D.P., Brenton J.D., Sieh W., Mateoiu C., Sundfeldt K., Cook L.S., Le N.D., Bowtell D., Green A., Webb P., Gertig D., Moore S., Hung J., Harrap K., Sadkowsky T., Pandeya N., Malt M., Mellon A., Robertson R., Bergh T.V., Jones M., Mackenzie P., Maidens J., Nattress K., Chiew Y.E., Stenlake A., Sullivan H., Alexander B., Ashover P., Brown S., Corrish T., Green L., Jackman L., Ferguson K., Martin K., Martyn A., Ranieri B., White J., Jayde V., Mamers P., Bowes L., Galletta L., Giles D., Schmidt T., Shirley H., Ball C., Young C., Viduka S., Tran H., Bilic S., Glavinas L., Brooks J., Stuart-Harris R., Kirsten F., Rutovitz J., Clingan P., Glasgow A., Proietto A., Braye S., Otton G., Shannon J., Bonaventura T., Stewart J., Begbie S., Bell D., Baron-Hay S., Ferrier A., Gard G., Nevell D., Pavlakis N., Valmadre S., Young B., Camaris C., Crouch R., Edwards L., Hacker N., Marsden D., Robertson G., Beale P., Beith J., Carter J., Dalrymple C., Houghton R., Friedlander M., Russell P., Links M., Grygiel J., Hill J., Byth K., Jaworski R., Harnett P., Wain G., Ward B., Papadimos D., Crandon A., Cummings M., Horwood K., Obermair A., Perrin L., Wyld D., Nicklin J., Davy M., Oehler M.K., Hall C., Dodd T., Healy T., Pittman K., Henderson D., Miller J., Pierdes J., Blomfield P., Challis D., McIntosh R., Parker A., Brown B., Rome R., Allen D., Grant P., Hyde S., Laurie R., Robbie M., Healy D., Jobling T., Manolitsas T., McNealage J., Rogers P., Susil B., Sumithran E., Simpson I., Phillips K., Rischin D., Fox S., Johnson D., Lade S., Loughrey M., O'Callaghan N., Murray W., Waring P., Billson V., Pyman J., Neesham D., Quinn M., Underhill C., Bell R., Ng L.F., Blum R., Ganju V., Hammond I., Leung Y., McCartney A., Buck M., Haviv I., Purdie D., Whiteman D., Zeps N., Kaufmann S., Meagher N.S., Ramus S.J., Campbell I., Cheasley D., Wakefield M.J., Ryland G.L., Allan P.E., Alsop K., Ananda S., Anglesio M.S., Au-Yeung G., Bohm M., Bowtell D.D.L., Brand A., Chenevix-Trench G., Christie M., Chiew Y.-E., Churchman M., DeFazio A., Dudley R., Fairweather N., Fereday S., Fox S.B., Gilks C.B., Gourley C., Hacker N.F., Hadley A.M., Hendley J., Ho G.-Y., Huntsman D.G., Hunter S.M., Jobling T.W., Kalli K.R., Kaufmann S.H., Kennedy C.J., Kobel M., Le Page C., McNally O.M., McAlpine J.N., Mileshkin L., Jan Pyman, Rahimi K., Samimi G., Sharma R., Stephens A.N., Traficante N., Antill Y.C., Scott C.L., Campbell I.G., Gorringe K.L., Kang E.Y., LePage C., da Cunha Torres M., Rowley S., Salazar C., Xing Z., Allan P., Mes-Masson A.-M., Provencher D.M., Kelemen L.E., Fasching P.A., Doherty J.A., Goodman M.T., Goode E.L., Deen S., Pharoah P.D.P., Brenton J.D., Sieh W., Mateoiu C., Sundfeldt K., Cook L.S., Le N.D., Bowtell D., Green A., Webb P., Gertig D., Moore S., Hung J., Harrap K., Sadkowsky T., Pandeya N., Malt M., Mellon A., Robertson R., Bergh T.V., Jones M., Mackenzie P., Maidens J., Nattress K., Chiew Y.E., Stenlake A., Sullivan H., Alexander B., Ashover P., Brown S., Corrish T., Green L., Jackman L., Ferguson K., Martin K., Martyn A., Ranieri B., White J., Jayde V., Mamers P., Bowes L., Galletta L., Giles D., Schmidt T., Shirley H., Ball C., Young C., Viduka S., Tran H., Bilic S., Glavinas L., Brooks J., Stuart-Harris R., Kirsten F., Rutovitz J., Clingan P., Glasgow A., Proietto A., Braye S., Otton G., Shannon J., Bonaventura T., Stewart J., Begbie S., Bell D., Baron-Hay S., Ferrier A., Gard G., Nevell D., Pavlakis N., Valmadre S., Young B., Camaris C., Crouch R., Edwards L., Hacker N., Marsden D., Robertson G., Beale P., Beith J., Carter J., Dalrymple C., and Houghton R.

Abstract

TP53 mutations are implicated in the progression of mucinous borderline tumors (MBOT) to mucinous ovarian carcinomas (MOC). Optimized immunohistochemistry (IHC) for TP53 has been established as a proxy for the TP53 mutation status in other ovarian tumor types. We aimed to confirm the ability of TP53 IHC to predict TP53 mutation status in ovarian mucinous tumors and to evaluate the association of TP53 mutation status with survival among patients with MBOT and MOC. Tumor tissue from an initial cohort of 113 women with MBOT/MOC was stained with optimized IHC for TP53 using tissue microarrays (75.2%) or full sections (24.8%) and interpreted using established criteria as normal or abnormal (overexpression, complete absence, or cytoplasmic). Cases were considered concordant if abnormal IHC staining predicted deleterious TP53 mutations. Discordant tissue microarray cases were re-evaluated on full sections and interpretational criteria were refined. The initial cohort was expanded to a total of 165 MBOT and 424 MOC for the examination of the association of survival with TP53 mutation status, assessed either by TP53 IHC and/or sequencing. Initially, 82/113 (72.6%) cases were concordant using the established criteria. Refined criteria for overexpression to account for intratumoral heterogeneity and terminal differentiation improved concordance to 93.8% (106/113). In the expanded cohort, 19.4% (32/165) of MBOT showed evidence for TP53 mutation and this was associated with a higher risk of recurrence, disease-specific death, and all-cause mortality (overall survival: HR = 4.6, 95% CI 1.5-14.3, p = 0.0087). Within MOC, 61.1% (259/424) harbored a TP53 mutation, but this was not associated with survival (overall survival, p = 0.77). TP53 IHC is an accurate proxy for TP53 mutation status with refined interpretation criteria accounting for intratumoral heterogeneity and terminal differentiation in ovarian mucinous tumors. TP53 mutation status is an important biomarker to identify MB

Published
2021

4. A collaborative resource platform for non-human primate neuroimaging

Author

Messinger, A., Sirmpilatze, N., Heuer, K., Loh, K.K., Mars, R.B., Sein, J., Xu, T., Glen, D., Jung, B., Seidlitz, J., Taylor, P., Toro, R., Garza-Villarreal, E.A., Sponheim, C., Wang, X., Benn, R.A., Cagna, B., Dadarwal, R., Evrard, H.C., Garcia-Saldivar, P., Giavasis, S., Hartig, R., Lepage, C., Liu, C., Majka, P., Merchant, H., Milham, M.P., Rosa, M.G.P., Tasserie, J., Uhrig, L., Margulies, D.S., Klink, P.C., Messinger, A., Sirmpilatze, N., Heuer, K., Loh, K.K., Mars, R.B., Sein, J., Xu, T., Glen, D., Jung, B., Seidlitz, J., Taylor, P., Toro, R., Garza-Villarreal, E.A., Sponheim, C., Wang, X., Benn, R.A., Cagna, B., Dadarwal, R., Evrard, H.C., Garcia-Saldivar, P., Giavasis, S., Hartig, R., Lepage, C., Liu, C., Majka, P., Merchant, H., Milham, M.P., Rosa, M.G.P., Tasserie, J., Uhrig, L., Margulies, D.S., and Klink, P.C.

Abstract

Contains fulltext : 226482.pdf (publisher's version ) (Open Access), Neuroimaging non-human primates (NHPs) is a growing, yet highly specialized field of neuroscience. Resources that were primarily developed for human neuroimaging often need to be significantly adapted for use with NHPs or other animals, which has led to an abundance of custom, in-house solutions. In recent years, the global NHP neuroimaging community has made significant efforts to transform the field towards more open and collaborative practices. Here we present the PRIMatE Resource Exchange (PRIME-RE), a new collaborative online platform for NHP neuroimaging. PRIME-RE is a dynamic community-driven hub for the exchange of practical knowledge, specialized analytical tools, and open data repositories, specifically related to NHP neuroimaging. PRIME-RE caters to both researchers and developers who are either new to the field, looking to stay abreast of the latest developments, or seeking to collaboratively advance the field.

Published
2021

5. Amyloid and tau pathology associations with personality traits, neuropsychiatric symptoms, and cognitive lifestyle in the preclinical phases of sporadic and autosomal dominant Alzheimer’s disease

Author

Pichet Binette, A., Vachon-Presseau, É., Morris, J., Bateman, R., Benzinger, T., Collins, D.L., Poirier, J., Breitner, J.C.S., Villeneuve, S., Allegri, R., Amtashar, F., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, Jill, Buckles, V., Chea, S., Chhatwal, J., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D‘Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., DiBari, S.H., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Levin, J., Marcus, D., Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J.H., Salloway, S., Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Tam, A., Labonté, A., Faubert, A-M, Mathieu, A., Madjar, C., Carrier, C.E., Dansereau, C., Kazazian, C., Lepage, C., Picard, C., Maillet, D., Michaud, D., Couture, D., Dea, D., Cuello, C., Barkun, A., Evans, A., Courcot, B., Tardif, C., Debacker, C., Jack, C.R., Fontaine, D., Knopman, D.S., Maultaup, G., Near, J., Leoutsakos, J-M, Maltais, J-R, Brandt, J., Pruessner, J., Morris, J.C., Cheewakriengkrai, L., Münter, L-M, Collins, L., Chakravarty, M., Sager, M.A., Dauar-Tedeschi, M., Eisenberg, M., Rajah, N., Aisen, P., Toussaint, J., Rosa-Neto, P., Bellec, P., Kostopoulos, P., Etienne, P., Tariot, P.N., Orban, P., Sperling, R.A., Hoge, R., Thomas, R.G., Gauthier, S., Craft, S., Montine, T.J., Nair, V., Bohbot, V., Venugopalan, V., Fonov, V., Ituria-Medina, Y., Khachaturian, Z.S., Teigner, E., Anthal, E., Yu, E., Ferdinand, F., Pogossova, G., Mayrand, G., Duclair, G., Gagné, G., Newbold-Fox, H., Leppert, I., Vallée, I., Vogel, J.W., Tremblay-Mercier, J., Frenette, J., Frappier, J., Kat, J., Miron, J., Wan, K., Mahar, L., Carmo, L., Théroux, L., Dadar, M., Dufour, M., Lafaille-Magnan, M-E, Appleby, M., Savard, M., Tuwaig, M., Petkova, M., Rioux, P., Meyer, P-F, El-Khoury, R., Gordon, R., Giles, R., Das, S., Wang, S., Tabrizi, S., Mathotaarachchi, S., Dubuc, S., Lee, T., Beaudry, T., Gervais, V., Pagé, V., Gonneaud, J., Ayranci, G., Pascoal, T.A., Desautels, R., Benbouhoud, F., Saint-Fort, E.F., Verfaillie, S.C.J., Farzin, S., Salaciak, A., Tullo, S., Vachon-Presseau, E., Daoust, L-A, Köbe, T., Spreng, N., McSweeney, M., Nilsson, N., Pishnamazi, M., Bedetti, C., Pichet Binette, A., Vachon-Presseau, É., Morris, J., Bateman, R., Benzinger, T., Collins, D.L., Poirier, J., Breitner, J.C.S., Villeneuve, S., Allegri, R., Amtashar, F., Berman, S., Bodge, C., Brandon, S., Brooks, W., Buck, Jill, Buckles, V., Chea, S., Chhatwal, J., Chrem, P., Chui, H., Cinco, J., Clifford, J., Cruchaga, C., D‘Mello, M., Donahue, T., Douglas, J., Edigo, N., Erekin-Taner, N., Fagan, A., Farlow, M., Farrar, A., Feldman, H., Flynn, G., Fox, N., Franklin, E., Fujii, H., Gant, C., Gardener, S., Ghetti, B., Goate, A., Goldman, J., Gordon, B., Graff-Radford, N., Gray, J., Gurney, J., Hassenstab, J., Hirohara, M., Holtzman, D., Hornbeck, R., DiBari, S.H., Ikeuchi, T., Ikonomovic, S., Jerome, G., Jucker, M., Karch, C., Kasuga, K., Kawarabayashi, T., Klunk, W., Koeppe, R., Kuder-Buletta, E., Laske, C., Lee, J-H, Levin, J., Marcus, D., Martins, R., Mason, N.S., Masters, C., Maue-Dreyfus, D., McDade, E., Montoya, L., Mori, H., Nagamatsu, A., Neimeyer, K., Noble, J., Norton, J., Perrin, R., Raichle, M., Ringman, J., Roh, J.H., Salloway, S., Schofield, P., Shimada, H., Shiroto, T., Shoji, M., Sigurdson, W., Sohrabi, H., Sparks, P., Suzuki, K., Swisher, L., Taddei, K., Wang, J., Wang, P., Weiner, M., Wolfsberger, M., Xiong, C., Xu, X., Tam, A., Labonté, A., Faubert, A-M, Mathieu, A., Madjar, C., Carrier, C.E., Dansereau, C., Kazazian, C., Lepage, C., Picard, C., Maillet, D., Michaud, D., Couture, D., Dea, D., Cuello, C., Barkun, A., Evans, A., Courcot, B., Tardif, C., Debacker, C., Jack, C.R., Fontaine, D., Knopman, D.S., Maultaup, G., Near, J., Leoutsakos, J-M, Maltais, J-R, Brandt, J., Pruessner, J., Morris, J.C., Cheewakriengkrai, L., Münter, L-M, Collins, L., Chakravarty, M., Sager, M.A., Dauar-Tedeschi, M., Eisenberg, M., Rajah, N., Aisen, P., Toussaint, J., Rosa-Neto, P., Bellec, P., Kostopoulos, P., Etienne, P., Tariot, P.N., Orban, P., Sperling, R.A., Hoge, R., Thomas, R.G., Gauthier, S., Craft, S., Montine, T.J., Nair, V., Bohbot, V., Venugopalan, V., Fonov, V., Ituria-Medina, Y., Khachaturian, Z.S., Teigner, E., Anthal, E., Yu, E., Ferdinand, F., Pogossova, G., Mayrand, G., Duclair, G., Gagné, G., Newbold-Fox, H., Leppert, I., Vallée, I., Vogel, J.W., Tremblay-Mercier, J., Frenette, J., Frappier, J., Kat, J., Miron, J., Wan, K., Mahar, L., Carmo, L., Théroux, L., Dadar, M., Dufour, M., Lafaille-Magnan, M-E, Appleby, M., Savard, M., Tuwaig, M., Petkova, M., Rioux, P., Meyer, P-F, El-Khoury, R., Gordon, R., Giles, R., Das, S., Wang, S., Tabrizi, S., Mathotaarachchi, S., Dubuc, S., Lee, T., Beaudry, T., Gervais, V., Pagé, V., Gonneaud, J., Ayranci, G., Pascoal, T.A., Desautels, R., Benbouhoud, F., Saint-Fort, E.F., Verfaillie, S.C.J., Farzin, S., Salaciak, A., Tullo, S., Vachon-Presseau, E., Daoust, L-A, Köbe, T., Spreng, N., McSweeney, M., Nilsson, N., Pishnamazi, M., and Bedetti, C.

Abstract

Background Major prevention trials for Alzheimer’s disease (AD) are now focusing on multidomain lifestyle interventions. However, the exact combination of behavioral factors related to AD pathology remains unclear. In 2 cohorts of cognitively unimpaired individuals at risk of AD, we examined which combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle (years of education or lifetime cognitive activity) related to the pathological hallmarks of AD, amyloid-β, and tau deposits. Methods A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. Separately, we studied 117 mutation carriers from the DIAN (Dominant Inherited Alzheimer Network) study group cohort with amyloid positron emission tomography and behavioral data. Using partial least squares analysis, we identified latent variables relating amyloid or tau pathology with combinations of personality traits, neuropsychiatric symptoms, and cognitive lifestyle. Results In PREVENT-AD, lower neuroticism, neuropsychiatric burden, and higher education were associated with less amyloid deposition (p = .014). Lower neuroticism and neuropsychiatric features, along with higher measures of openness and extraversion, were related to less tau deposition (p = .006). In DIAN, lower neuropsychiatric burden and higher education were also associated with less amyloid (p = .005). The combination of these factors accounted for up to 14% of AD pathology. Conclusions In the preclinical phase of both sporadic and autosomal dominant AD, multiple behavioral features were associated with AD pathology. These results may suggest potential pathways by which multidomain interventions might help delay AD onset or progression.

Published
2020

6. Oxaliplatin, fluorouracil, and leucovorin with or without cetuximab in patients with resected stage III colon cancer (PETACC-8): an open-label, randomised phase 3 trial

Author

Taieb, J, Tabernero, J, Mini, E, Subtil, F, Folprecht, G, Van Laethem, J, Thaler, J, Bridgewater, J, Petersen, L, Blons, H, Collette, L, Van Cutsem, E, Rougier, P, Salazar, R, Bedenne, L, Emile, J, Laurent-Puig, P, Lepage, C, Bidoli, P, Taieb J, Tabernero J, Mini E, Subtil F, Folprecht G, Van Laethem JL, Thaler J, Bridgewater J, Petersen LN, Blons H, Collette L, Van Cutsem E, Rougier P, Salazar R, Bedenne L, Emile JF, Laurent-Puig P, Lepage C, Bidoli P, Taieb, J, Tabernero, J, Mini, E, Subtil, F, Folprecht, G, Van Laethem, J, Thaler, J, Bridgewater, J, Petersen, L, Blons, H, Collette, L, Van Cutsem, E, Rougier, P, Salazar, R, Bedenne, L, Emile, J, Laurent-Puig, P, Lepage, C, Bidoli, P, Taieb J, Tabernero J, Mini E, Subtil F, Folprecht G, Van Laethem JL, Thaler J, Bridgewater J, Petersen LN, Blons H, Collette L, Van Cutsem E, Rougier P, Salazar R, Bedenne L, Emile JF, Laurent-Puig P, Lepage C, and Bidoli P

Abstract

Background: Since the 1990s, fluorouracil-based adjuvant chemotherapy has significantly reduced the risk of tumour recurrence in patients with stage III colon cancer. We aimed to assess whether the addition of cetuximab to standard adjuvant oxaliplatin, fluorouracil, and leucovorin chemotherapy (FOLFOX4) in patients with stage III colon cancer improved disease-free survival (DFS). Methods: For this open-label, randomised phase 3 study done in nine European countries, we enrolled patients through an interactive voice response system to the central randomisation centre, with a central stratified permuted block randomisation procedure. We randomly assigned patieNts with resected (R0) stage III disease (1:1) to receive 12 cycles of FOLFOX4 twice a week with or without cetuximab. Patients were stratified by N-status (N1 vs N2), T-status (T1-3 vs T4), and obstruction or perforation status (no obstruction and no perforation vs obstruction or perforation or both). A protocol amendment (applied in June, 2008, after 2096 patients had been randomly assigned to treatment-restricted enrolment to patients with tumours wild-type at codons 12 and 13 in exon 2 of the KRAS gene (KRAS exon 2 wild-type). The primary endpoint was DFS. Analysis was intention to treat in all patients with KRAS exon 2 wild-type tumours. The study is registered at EudraCT, number 2005-003463-23. Findings: Between Dec 22, 2005, and Nov 5, 2009, 2559 patients from 340 sites in Europe were randomly assigned. Of these patients, 1602 had KRAS exon 2 wild-type tumours (intention-to-treat population), 791 in the FOLFOX4 plus cetuximab group and 811 in the FOLFOX4 group. Median follow-up was 3·3 years (IQR 3·2-3·4). In the experimental and control groups, DFS was similar in the intention-to-treat population (hazard ratio [HR] 1·05; 95% CI 0·85-1·29; p=0·66), and in patients with KRAS exon 2/. BRAF wild-type (n=984, HR 0·99; 95% CI 0·76-1·28) or KRAS exon 2-mutated tumours (n=742, HR 1·06; 95% CI 0·82-1·37). We note

Published
2014

7. Prognostic value of KRAS mutations in stage III colon cancer: post hoc analysis of the PETACC8 phase III trial dataset

Author

Blons, H, Emile, J, Le Malicot, K, Julié, C, Zaanan, A, Tabernero, J, Mini, E, Folprecht, G, Van Laethem, J, Thaler, J, Bridgewater, J, Nørgård-Petersen, L, Van Cutsem, E, Lepage, C, Zawadi, M, Salazar, R, Laurent-Puig, P, Taieb, J, Bidoli, P, Blons H, Emile JF, Le Malicot K, Julié C, Zaanan A, Tabernero J, Mini E, Folprecht G, Van Laethem JL, Thaler J, Bridgewater J, Nørgård-Petersen L, Van Cutsem E, Lepage C, Zawadi MA, Salazar R, Laurent-Puig P, Taieb J, Bidoli P, Blons, H, Emile, J, Le Malicot, K, Julié, C, Zaanan, A, Tabernero, J, Mini, E, Folprecht, G, Van Laethem, J, Thaler, J, Bridgewater, J, Nørgård-Petersen, L, Van Cutsem, E, Lepage, C, Zawadi, M, Salazar, R, Laurent-Puig, P, Taieb, J, Bidoli, P, Blons H, Emile JF, Le Malicot K, Julié C, Zaanan A, Tabernero J, Mini E, Folprecht G, Van Laethem JL, Thaler J, Bridgewater J, Nørgård-Petersen L, Van Cutsem E, Lepage C, Zawadi MA, Salazar R, Laurent-Puig P, Taieb J, and Bidoli P

Abstract

Background: The prognostic value of KRAS mutations in colon adenocarcinoma is controversial. We examined this question as an ancillary study of the PETACC8 phase III trial. Patients and methods: We analyzed the pronostic impact of KRAS exon 2 mutations in stage III colon cancer patients (n = 1657) receiving adjuvant FOLFOX ± cetuximab therapy included in the PETACC8 trial. Patients with BRAF-mutated cancers were excluded and, as no difference was found for time to recurrence (TTR) and disease-free survival (DFS) between treatment arms, both were pooled for analysis. Associations with TTR and DFS were analyzed using a Cox proportional hazards model. Results: KRAS mutations were found in 638 of 1657 tumors and linked to shorter TTR (P < 0.001). However, when specific mutations were compared with wild-type, codon 12 mutations [hazard ratio (HR) 1.67, 95% confidence interval (CI) 1.35-2.04; P < 0.001] but not codon 13 (HR 1.23, 95% CI 0.85-1.79; P = 0.26) were significantly associated with shorter TTR, independently of other covariates. The interaction test showed that, regarding tumor location (distal versus proximal), KRAS genotype affects differently on recurrence (P = 0.02) and DFS (P = 0.042). Subgroup analysis showed that KRAS only affected TTR and DFS in distal tumors (n = 1043; 692 wild type; 351 mutated), with an increased risk of relapse (HR 1.96, 95% CI 1.51-2.56; P < 0.0001) for KRAS codon 12 mutations and a borderline significance for codon 13 mutations (HR 1.59, 95% CI 1.00-2.56; P = 0.051). Conclusion: KRAS exon 2 mutations are independent predictors of shorter TTR in patients with resected stage III distal colon cancers receiving adjuvant therapy. Future clinical trials in the adjuvant setting should consider both the tumor location and KRAS mutations as important stratification factors

Published
2014

8. Poorly differentiated gastro-entero-pancreatic neuroendocrine carcinomas: Are they really heterogeneous? Insights from the FFCD-GTE national cohort.

Author

UCL - SSS/IREC/GAEN - Pôle d'Hépato-gastro-entérologie, UCL - (SLuc) Service de gastro-entérologie, Walter, T, Tougeron, D, Baudin, E, Le Malicot, K, Lecomte, T, Malka, D, Hentic, O, Manfredi, S, Bonnet, I, Guimbaud, R, Coriat, R, Lepère, C, Desauw, C, Thirot-Bidault, A, Dahan, L, Roquin, G, Aparicio, T, Legoux, J-L, Lombard-Bohas, C, Scoazec, J-Y, Lepage, C, Cadiot, G, CEPD investigators, Borbath, Ivan, UCL - SSS/IREC/GAEN - Pôle d'Hépato-gastro-entérologie, UCL - (SLuc) Service de gastro-entérologie, Walter, T, Tougeron, D, Baudin, E, Le Malicot, K, Lecomte, T, Malka, D, Hentic, O, Manfredi, S, Bonnet, I, Guimbaud, R, Coriat, R, Lepère, C, Desauw, C, Thirot-Bidault, A, Dahan, L, Roquin, G, Aparicio, T, Legoux, J-L, Lombard-Bohas, C, Scoazec, J-Y, Lepage, C, Cadiot, G, CEPD investigators, and Borbath, Ivan

Abstract

BACKGROUND: Diagnosis and management of poorly differentiated gastro-entero-pancreatic (GEP) neuroendocrine carcinomas (NECs) remain challenging. Recent studies suggest prognostic heterogeneity. We designed within the French Group of Endocrine Tumours a prospective cohort to gain insight in the prognostic stratification and treatment of GEP-NEC. PATIENTS AND METHODS: All patients with a diagnosis of GEP-NEC between 1st January 2010 and 31st December 2013 could be included in this national cohort. Adenoneuroendocrine tumours were excluded. RESULTS: 253 patients from 49 centres were included. Median age was 66 years. Main primary locations were pancreas (21%), colorectal (27%), oesophagus-stomach (18%); primary location was unknown in 20%. Tumours were metastatic at diagnosis in 78% of cases. Performance status (PS) at diagnosis was 0-1 in 79% of patients. Among the 147 (58%) cases reviewed by an expert pathological network, 39% were classified as small cell NEC and 61% as large cell NEC. Median Ki67 index was 75% (range, 20-100). Median overall survival was 15.6 (13.6-17.0) months. Significant adverse prognostic factors in univariate analysis were PS > 1 (hazard ratio [HR] = 2.5), metastatic disease (HR = 1.6), NSE>2 upper limit of normal [ULN]; HR = 3.2), CgA>2 ULN (HR = 1.7) and lactate dehydrogenase >2 ULN (HR = 2.1). After first-line palliative chemotherapy (CT1) with platinum-etoposide (n = 152), objective response, progression-free survival and overall survival were 50%, 6.2 and 11.6 months; they were 24%, 2.9 and 5.9, respectively, after post-CT1 FOLFIRI regimen (n = 72). CONCLUSIONS: We report a large prospective series of GEP-NEC which show the predominance of large cell type and advanced stage at diagnosis. Prognosis was found more homogeneous than previously reported, mainly impacted by PS and tumour burden.

Published
2017

9. Prospective validation of a lymphocyte infiltration prognostic test in stage III colon cancer patients treated with adjuvant FOLFOX

Author

Emile, J, Julie, C, Le Malicot, K, Lepage, C, Tabernero, J, Mini, E, Folprecht, G, Van Laethem, J, Dimet, S, Boulagnon-Rombi, C, Allard, M, Penault-Llorca, F, Bennouna, J, Laurent-Puig, P, Taieb, J, Bidoli, P, Emile, JF, Van Laethem, JL, Allard, MA, Emile, J, Julie, C, Le Malicot, K, Lepage, C, Tabernero, J, Mini, E, Folprecht, G, Van Laethem, J, Dimet, S, Boulagnon-Rombi, C, Allard, M, Penault-Llorca, F, Bennouna, J, Laurent-Puig, P, Taieb, J, Bidoli, P, Emile, JF, Van Laethem, JL, and Allard, MA

Abstract

Background The prognostic value of lymphocyte infiltration (LI) of colorectal carcinoma (CC) has been demonstrated by several groups. However, no validated test is currently available for clinical practice. We previously described an automated and reproducible method for testing LI and aimed to validate it for clinical use. Patients and methods According to National Institutes of Health criteria, we designed a prospective validation of this biomarker in patients included in the PETACC8 phase III study. Primary objective was to compare percentage of patients alive and without recurrence at 2 years in patients with high versus low LI (#NCT02364024). Associations of LI with patient recurrence and survival were analysed, and multivariable models were adjusted for treatment and relevant factors. Automated testing of LI was performed on virtual slides without access to clinical data. Results Among the 1220 CC patients enrolled, LI was high, low and not evaluable in 241 (19.8%), 790 (64.8%) and 189 (15.5%), respectively. Primary objective was met with a 2-year recurrence rate of 14.4% versus 21.1% in patients with high and low LI, respectively (p = 0.02). Patients with high LI also had better disease free survival (DFS) and overall survival (OS). Tumour stage, grade, RAS status and BRAF status were with LI the only prognostic markers in multivariable analysis for OS. Subgroup analyses revealed that high LI had better DFS and OS in mismatch repair (MMR) proficient patients, and in patients without RAS mutation, but not in MMR deficient and RAS mutated patients. Conclusion Although this is the first validation with high level of evidence (IIB) of the prognostic value of a LI test in colon cancers, it still needs to be confirmed in independent series of colon cancer patients. © 2017 Elsevier Ltd

Published
2017

10. Prognostic value of KRAS mutations in stage III colon cancer: post hoc analysis of the PETACC8 phase III trial dataset.

Author

Blons, Helene, Emile, Jean-François, Le Malicot, K, Julié, C., Zaanan, A, Tabernero, Josep, Mini, E, Folprecht, Gunnar, Van Laethem, Jean-Luc, Thaler, J., Bridgewater, J, Petersen, Lars, Van Cutsem, Eric, Lepage, C, Zawadi, M A, Salazar, R, Laurent-Puig, Pierre, Taieb, J, Blons, Helene, Emile, Jean-François, Le Malicot, K, Julié, C., Zaanan, A, Tabernero, Josep, Mini, E, Folprecht, Gunnar, Van Laethem, Jean-Luc, Thaler, J., Bridgewater, J, Petersen, Lars, Van Cutsem, Eric, Lepage, C, Zawadi, M A, Salazar, R, Laurent-Puig, Pierre, and Taieb, J

Abstract

The prognostic value of KRAS mutations in colon adenocarcinoma is controversial. We examined this question as an ancillary study of the PETACC8 phase III trial., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2014

11. Prognostic value of KRAS mutations in stage III colon cancer: post hoc analysis of the PETACC8 phase III trial dataset.

Author

Blons, Helene, Emile, Jean-François, Le Malicot, K, Julié, C., Zaanan, A, Tabernero, Josep, Mini, E, Folprecht, Gunnar, Van Laethem, Jean-Luc, Thaler, J., Bridgewater, J, Petersen, Lars, Van Cutsem, Eric, Lepage, C, Zawadi, M A, Salazar, R, Laurent-Puig, Pierre, Taieb, J, Blons, Helene, Emile, Jean-François, Le Malicot, K, Julié, C., Zaanan, A, Tabernero, Josep, Mini, E, Folprecht, Gunnar, Van Laethem, Jean-Luc, Thaler, J., Bridgewater, J, Petersen, Lars, Van Cutsem, Eric, Lepage, C, Zawadi, M A, Salazar, R, Laurent-Puig, Pierre, and Taieb, J

Abstract

The prognostic value of KRAS mutations in colon adenocarcinoma is controversial. We examined this question as an ancillary study of the PETACC8 phase III trial., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2014

12. Patients with colorectal tumors with microsatellite instability and large deletions in HSP110 T17 have improved response to 5-fluorouracil-based chemotherapy

Author

Collura, A., Lagrange, A., Svrcek, M., Marisa, L., Buhard, O., Guilloux, A., Wanherdrick, K., Dorard, C., Taieb, A., Saget, A., Loh, M., Soong, R., Zeps, Nikolajs, Platell, C., Mews, A., Iacopetta, B., De Thonel, A., Seigneuric, R., Marcion, G., Chapusot, C., Lepage, C., Bouvier, A., Gaub, M., Milano, G., Selves, J., Senet, P., Delarue, P., Arzouk, H., Lacoste, C., Coquelle, A., Bengrine-Lefèvre, L., Tournigand, C., Lefèvre, J., Parc, Y., Biard, D., Fléjou, J., Garrido, C., Duval, A., Collura, A., Lagrange, A., Svrcek, M., Marisa, L., Buhard, O., Guilloux, A., Wanherdrick, K., Dorard, C., Taieb, A., Saget, A., Loh, M., Soong, R., Zeps, Nikolajs, Platell, C., Mews, A., Iacopetta, B., De Thonel, A., Seigneuric, R., Marcion, G., Chapusot, C., Lepage, C., Bouvier, A., Gaub, M., Milano, G., Selves, J., Senet, P., Delarue, P., Arzouk, H., Lacoste, C., Coquelle, A., Bengrine-Lefèvre, L., Tournigand, C., Lefèvre, J., Parc, Y., Biard, D., Fléjou, J., Garrido, C., and Duval, A.

Abstract

Background & Aims: Patients with colorectal tumors with microsatellite instability (MSI) have better prognoses than patients with tumors without MSI, but have a poor response to 5-fluorouracil–based chemotherapy. A dominant-negative form of heat shock protein (HSP)110 (HSP110DE9) expressed by cancer cells with MSI, via exon skipping caused by somatic deletions in the T17 intron repeat, sensitizes the cells to 5-fluorouracil and oxaliplatin. We investigated whether HSP110 T17 could be used to identify patients with colorectal cancer who would benefit from adjuvant chemotherapy with 5-fluorouracil and oxaliplatin. Methods: We characterized the interaction between HSP110 and HSP110DE9 using surface plasmon resonance. By using polymerase chain reaction and fragment analysis, we examined how the size of somatic allelic deletions in HSP110 T17 affected the HSP110 protein expressed by tumor cells. We screened 329 consecutive patients with stage II–III colorectal tumors with MSI who underwent surgical resection at tertiary medical centers for HSP110 T17.Results: HSP110 and HSP110DE9 interacted in a 1:1 ratio. Tumor cells with large deletions in T17 had increased ratios of HSP110DE9:HSP110, owing to the loss of expression of full-length HSP110. Deletions in HSP110 T17 were mostly biallelic in primary tumor samples with MSI. Patients with stage II–III cancer who received chemotherapy and had large HSP110 T17 deletions (≥5 bp; 18 of 77 patients, 23.4%) had longer times of relapse-free survival than patients with small or no deletions (≤4 bp; 59 of 77 patients, 76.6%) in multivariate analysis (hazard ratio, 0.16; 95% confidence interval, 0.012–0.8; P = .03). We found a significant interaction between chemotherapy and T17 deletion (P = .009). Conclusions: About 25% of patients with stages II–III colorectal tumors with MSI have an excellent response to chemotherapy, due to large, biallelic deletions in the T17 intron repeat of HSP110 in tumor DNA.

Published
2014

13. Brain Plasticity and Intellectual Ability Are Influenced by Shared Genes

Author

Brans, R.G.H., Kahn, R.S., Schnack, H.G., van Baal, G.C.M., Posthuma, D., van Haren, N.E.M., Lepage, C., Lerch, J.P., Collins, D.L., Evans, A.C., Boomsma, D.I., Hulshoff Pol, H.E., Brans, R.G.H., Kahn, R.S., Schnack, H.G., van Baal, G.C.M., Posthuma, D., van Haren, N.E.M., Lepage, C., Lerch, J.P., Collins, D.L., Evans, A.C., Boomsma, D.I., and Hulshoff Pol, H.E.

Abstract

Although the adult brain is considered to be fully developed and stable until senescence when its size steadily decreases, such stability seems at odds with continued human (intellectual) development throughout life. Moreover, although variation in human brain size is highly heritable, we do not know the extent to which genes contribute to individual differences in brain plasticity. In this longitudinal magnetic resonance imaging study in twins, we report considerable thinning of the frontal cortex and thickening of the medial temporal cortex with increasing age and find this change to be heritable and partly related to cognitive ability. Specifically, adults with higher intelligence show attenuated cortical thinning and more pronounced cortical thickening over time than do subjects with average or below average IQ. Genes influencing variability in both intelligence and brain plasticity partly drive these associations. Thus, not only does the brain continue to change well into adulthood, these changes are functionally relevant because they are related to intelligence. Copyright©2010 the authors.

Published
2010
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14. Brain Plasticity and Intellectual Ability Are Influenced by Shared Genes

Author

Brans, R.G.H., Kahn, R.S., Schnack, H.G., van Baal, G.C.M., Posthuma, D., van Haren, N.E.M., Lepage, C., Lerch, J.P., Collins, D.L., Evans, A.C., Boomsma, D.I., Hulshoff Pol, H.E., Brans, R.G.H., Kahn, R.S., Schnack, H.G., van Baal, G.C.M., Posthuma, D., van Haren, N.E.M., Lepage, C., Lerch, J.P., Collins, D.L., Evans, A.C., Boomsma, D.I., and Hulshoff Pol, H.E.

Abstract

Although the adult brain is considered to be fully developed and stable until senescence when its size steadily decreases, such stability seems at odds with continued human (intellectual) development throughout life. Moreover, although variation in human brain size is highly heritable, we do not know the extent to which genes contribute to individual differences in brain plasticity. In this longitudinal magnetic resonance imaging study in twins, we report considerable thinning of the frontal cortex and thickening of the medial temporal cortex with increasing age and find this change to be heritable and partly related to cognitive ability. Specifically, adults with higher intelligence show attenuated cortical thinning and more pronounced cortical thickening over time than do subjects with average or below average IQ. Genes influencing variability in both intelligence and brain plasticity partly drive these associations. Thus, not only does the brain continue to change well into adulthood, these changes are functionally relevant because they are related to intelligence. Copyright©2010 the authors.

Published
2010
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15. Companion Modelling approach: the AtollGame experience in Tarawa atoll (Republic of Kiribati)

Author

Dray, A, Perez, Pascal, LePage, C, D'Aquino, P, White, I, Dray, A, Perez, Pascal, LePage, C, D'Aquino, P, and White, I

Abstract

Low coral islands are heavily dependent on groundwater for freshwater supplies. The availability, quality, and management of groundwater are central to sustainable development and poverty alleviation in many developing small island nations. The declaration by the Government of Kiribati of water reserves on the atoll of Tarawa, over privately owned land, has lead to conflicts, illegal settlements and vandalism of public assets. Beside, the water consumption per capita tends to increase towards western-like standards, threatening the sustainability of the actual exploitation system. Finally, pollution generated by the 45 000 habitants of South Tarawa has already contaminated all the freshwater lenses, with the exception of the existing reserves so far.

Published
2005

16. Companion Modelling approach: the AtollGame experience in Tarawa atoll (Republic of Kiribati)

Author

Dray, A, Perez, Pascal, LePage, C, D'Aquino, P, White, I, Dray, A, Perez, Pascal, LePage, C, D'Aquino, P, and White, I

Abstract

Low coral islands are heavily dependent on groundwater for freshwater supplies. The availability, quality, and management of groundwater are central to sustainable development and poverty alleviation in many developing small island nations. The declaration by the Government of Kiribati of water reserves on the atoll of Tarawa, over privately owned land, has lead to conflicts, illegal settlements and vandalism of public assets. Beside, the water consumption per capita tends to increase towards western-like standards, threatening the sustainability of the actual exploitation system. Finally, pollution generated by the 45 000 habitants of South Tarawa has already contaminated all the freshwater lenses, with the exception of the existing reserves so far.

Published
2005

17. Companion Modelling approach: the AtollGame experience in Tarawa atoll (Republic of Kiribati)

Author

Dray, A, Perez, Pascal, LePage, C, D'Aquino, P, White, I, Dray, A, Perez, Pascal, LePage, C, D'Aquino, P, and White, I

Abstract

Low coral islands are heavily dependent on groundwater for freshwater supplies. The availability, quality, and management of groundwater are central to sustainable development and poverty alleviation in many developing small island nations. The declaration by the Government of Kiribati of water reserves on the atoll of Tarawa, over privately owned land, has lead to conflicts, illegal settlements and vandalism of public assets. Beside, the water consumption per capita tends to increase towards western-like standards, threatening the sustainability of the actual exploitation system. Finally, pollution generated by the 45 000 habitants of South Tarawa has already contaminated all the freshwater lenses, with the exception of the existing reserves so far.

Published
2005

18. Analysis of Chemical Warfare Agents by GC-MS: First Chemical Cluster CRTI Training Exercise

Author

DEFENCE RESEARCH AND DEVELOPMENT SUFFIELD (ALBERTA), D'Agostino, Paul A., Lepage, C. R., Hancock, J. R., Chenier, C. L., DEFENCE RESEARCH AND DEVELOPMENT SUFFIELD (ALBERTA), D'Agostino, Paul A., Lepage, C. R., Hancock, J. R., and Chenier, C. L.

Abstract

The Chemical Cluster, one of three clusters created by the Chemical, biological, radiological and nuclear Research and Technology Initiative (CRTI), was established to help Canada prepare for possible terrorist events. This working group, made up of representatives from Canadian government departments, has identified a number of chemicals of concern and assigned laboratories with appropriate expertise to provide the analytical support necessary to confirm these compounds in suspect samples. The Royal Canadian Mounted Police (RCMP), in its lead forensics role, will attempt to tentatively identify the chemical(s) of concern and pass on the samples to the responsible laboratory within the Chemical Cluster. Samples containing large amounts of relatively pure chemical warfare agents should trigger a response with one the chemical monitoring devices (e.g., Chemical Agent Monitor) used by the RCMP to triage samples. Defence R&D Canada - Suffield (DRDC Suffield) has been tasked to analyse samples suspected to contain chemical warfare agents for the Chemical Cluster and would receive this type of suspect sample. There remains a possibility that samples with a lower level of chemical warfare agent contamination might inadvertently find their way into a laboratory tasked with another type of analysis. To manage this possibility, the laboratories receiving these types of samples should have an analytical screening capability to allow for the tentative identification of chemical warfare agents in samples and sample extracts. This report summarizes the chemical warfare agent training course in sample preparation and analysis by gas chromatography-mass spectrometry (GC-MS) given by DRDC Suffield to other Chemical Cluster laboratories., and Summary in English and French.

Published
2003

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