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Rueda Daniel - One of the best experts on this subject based on the ideXlab platform.

  • Redefining synchronous colorectal cancers based on tumor clonality
    'Wiley', 2020
    Co-Authors: Perea José, García, Juan L., Corchete, Luis A., Lumbreras Eva, Arriba María, Rueda Daniel
    Abstract:

    To analyze the possible clonal origin of a part of Synchronous colorectal cancer (SCRC), we studied 104 paired‐SCRCs from 52 consecutive patients without hereditary forms of CRC. We used a Single‐Nucleotide Polymorphism array to characterize the genomic profiles, and subsequently used a Statistical Application to define them according to clonality within the same individual. We categorized the ensuing groups according to colonic location to identify differential phenotypes. The SCRC Monoclonal group (M) (19 cases) was divided into Monosegmental (MM) and Pancolonic (MP) groups. The SCRC Polyclonal group (P) (33 cases) was also divided into Monosegmental (PM) and Pancolonic (PP), the first exhibiting preference for left colon. The MM group showed a high rate of mucinous tumors, the lowest mean‐number of tumors and associated‐polyps, and the worst prognosis. The MP group included the largest mean‐number of associated‐polyps, best prognosis and familial cancer component. The PM group seemed to be a “frontier” group. Finally, the PP group also exhibited a mucin component, the highest mean‐number of tumors (4.6) compared with the mean‐number of polyps (7.7), poor prognosis and sporadic cases. Most relevant differential genomic regions within M groups were gains on 1q24 and 8q24, and deletions on 1p21 and 1p23 for MM, while within P were the gains on 7q36 and deletions on 1p36 for PM. The Statistical Application employed seems to define clonality more accurately in SCRC ‐more likely to be polyclonal in origin‐, and together with the tumor locations, helped us to configure a classification with prognostic and clinical value.This work was funded by Projects PI10/00683 and PI16/01650 to J.P, and PI16/01920 to R.G.S, from the Spanish Ministry of Health and Consumer Affairs and FEDER, by Project 2012–0036 from the Mutua Madrileña Foundation, and supported by the CA72851, CA181572, CA184792, CA187956 and CA202797 grants from the National Cancer Institute, National Institute of Health; RP140784 from the Cancer Prevention Research Institute of Texas; grants from the Sammons Cancer Center and Baylor Foundation, as well as funds from the Baylor Scott & White Research Institute, Dallas, TX, USA

  • Redefining synchronous colorectal cancers based on tumor clonality
    Wiley, 2019
    Co-Authors: Perea José, García, Juan L., Lumbreras Eva, Arriba María, Rueda Daniel, Corchete Luis, Tapial Sandra, Pérez Jessica, Vieiro Victoria, Rodríguez Yolanda
    Abstract:

    To analyze the possible clonal origin of a part of Synchronous colorectal cancer (SCRC), we studied 104 paired-SCRCs from 52 consecutive patients without hereditary forms of CRC. We used a Single-Nucleotide Polymorphism array to characterize the genomic profiles, and subsequently used a Statistical Application to define them according to clonality within the same individual. We categorized the ensuing groups according to colonic location to identify differential phenotypes. The SCRC Monoclonal group (M) (19 cases) was divided into Monosegmental (MM) and Pancolonic (MP) groups. The SCRC Polyclonal group (P) (33 cases) was also divided into Monosegmental (PM) and Pancolonic (PP), the first exhibiting preference for left colon. The MM group showed a high rate of mucinous tumors, the lowest mean-number of tumors and associated-polyps, and the worst prognosis. The MP group included the largest mean-number of associated-polyps, best prognosis and familial cancer component. The PM group seemed to be a "frontier" group. Finally, the PP group also exhibited a mucin component, the highest mean-number of tumors (4.6) compared with the mean-number of polyps (7.7), poor prognosis and sporadic cases. Most relevant differential genomic regions within M groups were gains on 1q24 and 8q24, and deletions on 1p21 and 1p23 for MM, while within P were the gains on 7q36 and deletions on 1p36 for PM. The Statistical Application employed seems to define clonality more accurately in SCRC -more likely to be polyclonal in origin-, and together with the tumor locations, helped us to configure a classification with prognostic and clinical value.This work was funded by Projects PI10/00683 and PI16/01650 to J.P, and PI16/01920 to R.G.S, from the Spanish Ministry of Health and Consumer Affairs and FEDER, by Project 2012–0036 from the Mutua Madrileña Foundation, and supported by the CA72851, CA181572, CA184792, CA187956 and CA202797 grants from the National Cancer Institute, National Institute of Health; RP140784 from the Cancer Prevention Research Institute of Texas; grants from the Sammons Cancer Center and Baylor Foundation, as well as funds from the Baylor Scott & White Research Institute, Dallas, TX, USA. We thank the Tumor Registry of the Pathology Department of the 12 de Octubre University Hospital for providing the paraffin‐embedded tissues, and Ron Hartong for his help with the English revision of this manuscript.N

Perea José - One of the best experts on this subject based on the ideXlab platform.

  • Redefining synchronous colorectal cancers based on tumor clonality
    'Wiley', 2020
    Co-Authors: Perea José, García, Juan L., Corchete, Luis A., Lumbreras Eva, Arriba María, Rueda Daniel
    Abstract:

    To analyze the possible clonal origin of a part of Synchronous colorectal cancer (SCRC), we studied 104 paired‐SCRCs from 52 consecutive patients without hereditary forms of CRC. We used a Single‐Nucleotide Polymorphism array to characterize the genomic profiles, and subsequently used a Statistical Application to define them according to clonality within the same individual. We categorized the ensuing groups according to colonic location to identify differential phenotypes. The SCRC Monoclonal group (M) (19 cases) was divided into Monosegmental (MM) and Pancolonic (MP) groups. The SCRC Polyclonal group (P) (33 cases) was also divided into Monosegmental (PM) and Pancolonic (PP), the first exhibiting preference for left colon. The MM group showed a high rate of mucinous tumors, the lowest mean‐number of tumors and associated‐polyps, and the worst prognosis. The MP group included the largest mean‐number of associated‐polyps, best prognosis and familial cancer component. The PM group seemed to be a “frontier” group. Finally, the PP group also exhibited a mucin component, the highest mean‐number of tumors (4.6) compared with the mean‐number of polyps (7.7), poor prognosis and sporadic cases. Most relevant differential genomic regions within M groups were gains on 1q24 and 8q24, and deletions on 1p21 and 1p23 for MM, while within P were the gains on 7q36 and deletions on 1p36 for PM. The Statistical Application employed seems to define clonality more accurately in SCRC ‐more likely to be polyclonal in origin‐, and together with the tumor locations, helped us to configure a classification with prognostic and clinical value.This work was funded by Projects PI10/00683 and PI16/01650 to J.P, and PI16/01920 to R.G.S, from the Spanish Ministry of Health and Consumer Affairs and FEDER, by Project 2012–0036 from the Mutua Madrileña Foundation, and supported by the CA72851, CA181572, CA184792, CA187956 and CA202797 grants from the National Cancer Institute, National Institute of Health; RP140784 from the Cancer Prevention Research Institute of Texas; grants from the Sammons Cancer Center and Baylor Foundation, as well as funds from the Baylor Scott & White Research Institute, Dallas, TX, USA

  • Redefining synchronous colorectal cancers based on tumor clonality
    Wiley, 2019
    Co-Authors: Perea José, García, Juan L., Lumbreras Eva, Arriba María, Rueda Daniel, Corchete Luis, Tapial Sandra, Pérez Jessica, Vieiro Victoria, Rodríguez Yolanda
    Abstract:

    To analyze the possible clonal origin of a part of Synchronous colorectal cancer (SCRC), we studied 104 paired-SCRCs from 52 consecutive patients without hereditary forms of CRC. We used a Single-Nucleotide Polymorphism array to characterize the genomic profiles, and subsequently used a Statistical Application to define them according to clonality within the same individual. We categorized the ensuing groups according to colonic location to identify differential phenotypes. The SCRC Monoclonal group (M) (19 cases) was divided into Monosegmental (MM) and Pancolonic (MP) groups. The SCRC Polyclonal group (P) (33 cases) was also divided into Monosegmental (PM) and Pancolonic (PP), the first exhibiting preference for left colon. The MM group showed a high rate of mucinous tumors, the lowest mean-number of tumors and associated-polyps, and the worst prognosis. The MP group included the largest mean-number of associated-polyps, best prognosis and familial cancer component. The PM group seemed to be a "frontier" group. Finally, the PP group also exhibited a mucin component, the highest mean-number of tumors (4.6) compared with the mean-number of polyps (7.7), poor prognosis and sporadic cases. Most relevant differential genomic regions within M groups were gains on 1q24 and 8q24, and deletions on 1p21 and 1p23 for MM, while within P were the gains on 7q36 and deletions on 1p36 for PM. The Statistical Application employed seems to define clonality more accurately in SCRC -more likely to be polyclonal in origin-, and together with the tumor locations, helped us to configure a classification with prognostic and clinical value.This work was funded by Projects PI10/00683 and PI16/01650 to J.P, and PI16/01920 to R.G.S, from the Spanish Ministry of Health and Consumer Affairs and FEDER, by Project 2012–0036 from the Mutua Madrileña Foundation, and supported by the CA72851, CA181572, CA184792, CA187956 and CA202797 grants from the National Cancer Institute, National Institute of Health; RP140784 from the Cancer Prevention Research Institute of Texas; grants from the Sammons Cancer Center and Baylor Foundation, as well as funds from the Baylor Scott & White Research Institute, Dallas, TX, USA. We thank the Tumor Registry of the Pathology Department of the 12 de Octubre University Hospital for providing the paraffin‐embedded tissues, and Ron Hartong for his help with the English revision of this manuscript.N

Rodríguez Yolanda - One of the best experts on this subject based on the ideXlab platform.

  • Redefining synchronous colorectal cancers based on tumor clonality
    Wiley, 2019
    Co-Authors: Perea José, García, Juan L., Lumbreras Eva, Arriba María, Rueda Daniel, Corchete Luis, Tapial Sandra, Pérez Jessica, Vieiro Victoria, Rodríguez Yolanda
    Abstract:

    To analyze the possible clonal origin of a part of Synchronous colorectal cancer (SCRC), we studied 104 paired-SCRCs from 52 consecutive patients without hereditary forms of CRC. We used a Single-Nucleotide Polymorphism array to characterize the genomic profiles, and subsequently used a Statistical Application to define them according to clonality within the same individual. We categorized the ensuing groups according to colonic location to identify differential phenotypes. The SCRC Monoclonal group (M) (19 cases) was divided into Monosegmental (MM) and Pancolonic (MP) groups. The SCRC Polyclonal group (P) (33 cases) was also divided into Monosegmental (PM) and Pancolonic (PP), the first exhibiting preference for left colon. The MM group showed a high rate of mucinous tumors, the lowest mean-number of tumors and associated-polyps, and the worst prognosis. The MP group included the largest mean-number of associated-polyps, best prognosis and familial cancer component. The PM group seemed to be a "frontier" group. Finally, the PP group also exhibited a mucin component, the highest mean-number of tumors (4.6) compared with the mean-number of polyps (7.7), poor prognosis and sporadic cases. Most relevant differential genomic regions within M groups were gains on 1q24 and 8q24, and deletions on 1p21 and 1p23 for MM, while within P were the gains on 7q36 and deletions on 1p36 for PM. The Statistical Application employed seems to define clonality more accurately in SCRC -more likely to be polyclonal in origin-, and together with the tumor locations, helped us to configure a classification with prognostic and clinical value.This work was funded by Projects PI10/00683 and PI16/01650 to J.P, and PI16/01920 to R.G.S, from the Spanish Ministry of Health and Consumer Affairs and FEDER, by Project 2012–0036 from the Mutua Madrileña Foundation, and supported by the CA72851, CA181572, CA184792, CA187956 and CA202797 grants from the National Cancer Institute, National Institute of Health; RP140784 from the Cancer Prevention Research Institute of Texas; grants from the Sammons Cancer Center and Baylor Foundation, as well as funds from the Baylor Scott & White Research Institute, Dallas, TX, USA. We thank the Tumor Registry of the Pathology Department of the 12 de Octubre University Hospital for providing the paraffin‐embedded tissues, and Ron Hartong for his help with the English revision of this manuscript.N

Marie Nicolas - One of the best experts on this subject based on the ideXlab platform.

García, Juan L. - One of the best experts on this subject based on the ideXlab platform.

  • Redefining synchronous colorectal cancers based on tumor clonality
    'Wiley', 2020
    Co-Authors: Perea José, García, Juan L., Corchete, Luis A., Lumbreras Eva, Arriba María, Rueda Daniel
    Abstract:

    To analyze the possible clonal origin of a part of Synchronous colorectal cancer (SCRC), we studied 104 paired‐SCRCs from 52 consecutive patients without hereditary forms of CRC. We used a Single‐Nucleotide Polymorphism array to characterize the genomic profiles, and subsequently used a Statistical Application to define them according to clonality within the same individual. We categorized the ensuing groups according to colonic location to identify differential phenotypes. The SCRC Monoclonal group (M) (19 cases) was divided into Monosegmental (MM) and Pancolonic (MP) groups. The SCRC Polyclonal group (P) (33 cases) was also divided into Monosegmental (PM) and Pancolonic (PP), the first exhibiting preference for left colon. The MM group showed a high rate of mucinous tumors, the lowest mean‐number of tumors and associated‐polyps, and the worst prognosis. The MP group included the largest mean‐number of associated‐polyps, best prognosis and familial cancer component. The PM group seemed to be a “frontier” group. Finally, the PP group also exhibited a mucin component, the highest mean‐number of tumors (4.6) compared with the mean‐number of polyps (7.7), poor prognosis and sporadic cases. Most relevant differential genomic regions within M groups were gains on 1q24 and 8q24, and deletions on 1p21 and 1p23 for MM, while within P were the gains on 7q36 and deletions on 1p36 for PM. The Statistical Application employed seems to define clonality more accurately in SCRC ‐more likely to be polyclonal in origin‐, and together with the tumor locations, helped us to configure a classification with prognostic and clinical value.This work was funded by Projects PI10/00683 and PI16/01650 to J.P, and PI16/01920 to R.G.S, from the Spanish Ministry of Health and Consumer Affairs and FEDER, by Project 2012–0036 from the Mutua Madrileña Foundation, and supported by the CA72851, CA181572, CA184792, CA187956 and CA202797 grants from the National Cancer Institute, National Institute of Health; RP140784 from the Cancer Prevention Research Institute of Texas; grants from the Sammons Cancer Center and Baylor Foundation, as well as funds from the Baylor Scott & White Research Institute, Dallas, TX, USA

  • Redefining synchronous colorectal cancers based on tumor clonality
    Wiley, 2019
    Co-Authors: Perea José, García, Juan L., Lumbreras Eva, Arriba María, Rueda Daniel, Corchete Luis, Tapial Sandra, Pérez Jessica, Vieiro Victoria, Rodríguez Yolanda
    Abstract:

    To analyze the possible clonal origin of a part of Synchronous colorectal cancer (SCRC), we studied 104 paired-SCRCs from 52 consecutive patients without hereditary forms of CRC. We used a Single-Nucleotide Polymorphism array to characterize the genomic profiles, and subsequently used a Statistical Application to define them according to clonality within the same individual. We categorized the ensuing groups according to colonic location to identify differential phenotypes. The SCRC Monoclonal group (M) (19 cases) was divided into Monosegmental (MM) and Pancolonic (MP) groups. The SCRC Polyclonal group (P) (33 cases) was also divided into Monosegmental (PM) and Pancolonic (PP), the first exhibiting preference for left colon. The MM group showed a high rate of mucinous tumors, the lowest mean-number of tumors and associated-polyps, and the worst prognosis. The MP group included the largest mean-number of associated-polyps, best prognosis and familial cancer component. The PM group seemed to be a "frontier" group. Finally, the PP group also exhibited a mucin component, the highest mean-number of tumors (4.6) compared with the mean-number of polyps (7.7), poor prognosis and sporadic cases. Most relevant differential genomic regions within M groups were gains on 1q24 and 8q24, and deletions on 1p21 and 1p23 for MM, while within P were the gains on 7q36 and deletions on 1p36 for PM. The Statistical Application employed seems to define clonality more accurately in SCRC -more likely to be polyclonal in origin-, and together with the tumor locations, helped us to configure a classification with prognostic and clinical value.This work was funded by Projects PI10/00683 and PI16/01650 to J.P, and PI16/01920 to R.G.S, from the Spanish Ministry of Health and Consumer Affairs and FEDER, by Project 2012–0036 from the Mutua Madrileña Foundation, and supported by the CA72851, CA181572, CA184792, CA187956 and CA202797 grants from the National Cancer Institute, National Institute of Health; RP140784 from the Cancer Prevention Research Institute of Texas; grants from the Sammons Cancer Center and Baylor Foundation, as well as funds from the Baylor Scott & White Research Institute, Dallas, TX, USA. We thank the Tumor Registry of the Pathology Department of the 12 de Octubre University Hospital for providing the paraffin‐embedded tissues, and Ron Hartong for his help with the English revision of this manuscript.N