Interphase cytogenetics on brain tumors

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    19-Nov-2016

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    59 IN S ITU HYBRID IZAT ION WITH A CHROMOSOME 1 SPECIF IC DNA PROBE ON INTERPHASE NUCLE I FROM PROSTATE CANCER CELLS . Josee J .K0nig, Sandra de Jong, Anne Hagemei jer*, Hans Romijn and Fritz H.SchrOder. Depts. of Uro logy and Genetics*, Erasmus Univers i ty Rotterdam, The Nether lands.

    With f low cytometry half of the prostate cancers show, apart from dip lo id cells, cons iderable populat ions of tetraplo id and/or aneuplo id cells. With co l lagenase t reatment -which is a widely used method to obtain cell suspensions from sol id tumors- near ly half of the nondip lo id cel ls is destroyed, as was shown by us earl ier. When the karyotype of these same tumors was invest igated, near ly all tumors were seemingly d ip lo id with occasional nonclonal aberrat ions. We used detect ion of numerical aberrat ions of chromosome 1 in interphase nuclei by in situ hybr id izat ion (ISH) with the SAT III probe PUC 1.77 for further invest igat ion of this problem. ISH was per formed on nuclei obtained before and after co l lagenase t reatment and after t issue culture and the results were compared. ISH and FCM results were congruent in showing a decl ine of nondip lo id cel ls after co l lagenase treatment. Two tumors showed high percentages of nondip lo id cel ls ( 23% and 59% ) in fresh preparat ions which had decl ined to 12% and 9% respect ive ly after t issue culture. Moreover, in both tumors all metaphases seemed normal diploid. We think this result is a clear indicat ion that se lect ion in favor of normal d ip lo id cel ls can occur in short term t issue culture of prostate epithel ium. More tumors need however be invest igated in this way to draw a def in i te conclusion. This study was supported by a grant of the Nether lands Cancer Foundation.

    60 COMBINED CYTOGENETIC AND IMMUNCYTOCHEMICAL STUDY ON PROSTATE CANCER

    B Wullich I, T Lindenmeir {, G. Seitz 2, Th. Zwergel 3, G Unteregger I qnst. f~r Humangenetik. Univ. des Saarlandes. D-6650 H0mburg Saar 2Inst . f i i r Pa tho log ie , Un iv . des Saar landes , D -6650 Homburg /Saar a l r ro log ische K l in ik , Un iv . des Saar landes , D -6650 Homburg /Saar

    Spec i f i c chromosomal changes have been d i scovered in severa l human sol id rumors and have been found to be use fu l too l s in the d iagnos is , p rognos is , and c lass i f i ca t ion of these d i seases . However , on ly few cytogenet ic data a re ava i lab le on pros ta t i c cancer , and spec i f i c chromosomal changes assoc ia ted w i th th i s k ind of tumor have yet been found . We s tar ted to per fo rm cytogenet ic ana lyses on cel l cu l tu res of p r imary pros ta t i c adenocarc inomas and metasta t i c les ions , lrp to no~, long- te rm cu l tu res were success fu l l y es tab l i shed from twe lve tumors by app ly ing enzymat ic d iges t ion or t i ssue exp lant of the resected tumor mater ia l . Cy logenet ic character i za t ion of h i ther to th ree tumors revea led loss of the Y chromosome as s ing le c lona l abnormal i ty in two tumors . One tumor showed normal karyotype . Conc lus ions about the s ign i f i cance of loss of the Y chromosome in deve lopment and/or p rogress ion of metas ta t i c cancer seem premature . Remarkab ly , the two tumors character i zed by loss of the Y chromosome were h i s topatho log ica l ly d iagnosed as moderate ly d i f fe rent ia ted and und i f fe rent ia ted adenocarc inomas . The one w i th normal karyotype was eva luated as moderate ly d i f fe rent ia ted . In o rder Io assess the e f fec ts of chromosomal changes on the pro l i fe ra t ion ac t iv i ty of p ros la t i c tumors , immunocytochemica l s tud ies on the tumor cel l cu l tu res have been per fo rmed by us ing the ant ibody K i -67 . All th ree tumors showed a pro l i fe ra t ion index in the range of 18 -25 %. Up to now, no cor re la t ion has been found beween K i -67 index and the express ion of EGF-R and fos. The combined approach of cy togenet ics , mo lecu la r genet ics and immunocytochemis t ry may he lp to de l ineate the pathogenet ic mechan isms in p ros ta t i c cancer .

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