Comparative genomic instabilities of thyroid and XXXX .

@entity3557 @entity5 @entity694 @entity14 @entity259 @entity1586
OBJECTIVES: To assess the forms and extent of genomic instability in @entity259 and @entity14 and to determine if such measurements could explain the generally excellent prognosis of @entity259 compared with @entity694 . DESIGN: Tumor genome analyses. Genomic instability was measured by the following 4 methods, listed in ascending order based on the size of events detected: inter-simple sequence repeat polymerase chain reaction (ISSR-PCR), fractional allelic loss (FAL) analysis, array-based comparative genomic hybridization (aCGH), and spectral karyotyping (SKY). RESULTS: The genomic instability index of 32 @entity259 , 59 @entity694 , and 11 @entity1586 was determined by ISSR-PCR; no difference was seen among the 3 groups by this method. Fractional allelic loss rates were comparable in @entity259 and @entity1586 and lower than FAL rates in @entity14 . Indolent @entity3557 were essentially diploid with no large-scale alterations in chromosome number or structure when evaluated by aCGH or SKY. In anaplastic @entity259 , aCGH revealed abundant chromosome alterations. @entity14 showed extensive copy number changes and chromosomal rearrangements when analyzed by aCGH and SKY. CONCLUSIONS: Genomic alterations in @entity3557 , such as in benign @entity1586 , are principally smaller events detected by ISSR-PCR. With the more aggressive @entity5 types (ie, anaplastic thyroid and @entity14 ), larger events detected by FAL analysis, aCGH, and SKY were revealed. We hypothesize that mutations caused by smaller genomic alterations enable thyroid cells to achieve a minimal malignant phenotype. Mutations for aggressive biological behavior appear with larger genomic events.
