TY - JOUR
T1 - Genetic evolution in the metastatic progression of human pancreatic cancer studied by CGH
AU - Armengol, Gemma
AU - Capellà, Gabriel
AU - Farré, Lourdes
AU - Peinado, Miguel Angel
AU - Miró, Rosa
AU - Caballín, Maria Rosa
PY - 2001/1/1
Y1 - 2001/1/1
N2 - Metastases are thought to be derived from emerging clones within primary tumors. Although the concept of the clonal evolution of cancer is well defined, the genetic grounds and significance of this process in human cancer progression are still poorly understood. To gain insight into the genetic basis and clonal evolution underlying the metastatic progression of human pancreatic cancer in vivo, we analyzed by comparative genomic hybridization (CGH) chromosomal imbalances in seven metastases originated in nude mice and their three corresponding orthotopically xenografted human pancreatic tumors. All metastases were found to be closely related to the corresponding orthotopic implant, adding many additional changes to the already altered copy number profile of the pancreatic tumors. Recurrent metastasis-specific alterations included gains at 16cen-q22 and 17q21-qter. CGH results from paired specimens strongly suggest that the majority of additional genetic alterations present in metastases are likely to be present in subclones in the primary tumor.
AB - Metastases are thought to be derived from emerging clones within primary tumors. Although the concept of the clonal evolution of cancer is well defined, the genetic grounds and significance of this process in human cancer progression are still poorly understood. To gain insight into the genetic basis and clonal evolution underlying the metastatic progression of human pancreatic cancer in vivo, we analyzed by comparative genomic hybridization (CGH) chromosomal imbalances in seven metastases originated in nude mice and their three corresponding orthotopically xenografted human pancreatic tumors. All metastases were found to be closely related to the corresponding orthotopic implant, adding many additional changes to the already altered copy number profile of the pancreatic tumors. Recurrent metastasis-specific alterations included gains at 16cen-q22 and 17q21-qter. CGH results from paired specimens strongly suggest that the majority of additional genetic alterations present in metastases are likely to be present in subclones in the primary tumor.
U2 - 10.1038/labinvest.3780383
DO - 10.1038/labinvest.3780383
M3 - Article
VL - 81
SP - 1703
EP - 1707
JO - Laboratory Investigation
JF - Laboratory Investigation
SN - 0023-6837
IS - 12
ER -
