Objective To further define the extent of chromosome 9p21 deletion in periampullary neoplasms.Methods The loss of heterozygosity at 5 microsatellite polymorphic markers on chromosome 9p21 was detected by polymerase ...Objective To further define the extent of chromosome 9p21 deletion in periampullary neoplasms.Methods The loss of heterozygosity at 5 microsatellite polymorphic markers on chromosome 9p21 was detected by polymerase chain reaction (PCR), polyacrylamide gel electrophoresis (PAGE) and silver staining in 35 specimens of periampullary neoplasms and their matching blood samples.Results Fifty percent (4/8) of pancreatic cancer cases showed the loss of heterozygosity at one or more microsatellite loci, with the more frequent sites of D9S974 (37.5%) and D9S942 (28.6%), and some showing consecutive allelic loss. Sixty-two point five percent (5/8) of ampullary carcinoma cases showed loss of heterozygosity at one or more of the loci, frequent site of loss being D9S942 (42.9%) and the next most frequent being IFNA (37.5%) and D9S171 (37.5%). Loss of one locus was observed in 14.2% (1/7) of insulinoma. Conclusion The minimal common region of chromosome deletion in periampullary neoplasms is defined between the D9S974 and D9S942 loci within a 15?kb interval in 9p21, suggesting the involvement of a novel tumor suppressor gene in their carcinogenesis.展开更多
Faithful transmission or restoration of epigenetic information such as repressive histone modifications through generations is crit- ical for the maintenance of cell identity. We report here that chromodomain Y-like p...Faithful transmission or restoration of epigenetic information such as repressive histone modifications through generations is crit- ical for the maintenance of cell identity. We report here that chromodomain Y-like protein （CDYL）, a chromodomain-containing transcription corepressor, is physically associated with chromatin assembly factor 1 （CAF-1） and the repiicative heUcase MCM complex. We showed that CDYL bridges CAF-1 and MCM, facilitating histone transfer and deposition during DNA replication. We demonstrated that CDYI. recruits histone-modifying enzymes G9a, SETDB1, and EZH2 to replication forks, leading to the addition of H3Kgme2/3 and H3K27me2/3 on newly deposited histone H3. Significantly, depletion of CDYL impedes early S phase progres- sion and sensitizes cells to DNA damage. Our data indicate that CDYL plays an important role in the transmission/restoration of repressive histone marks, thereby preserving the epigenetic landscape for the maintenance of cell identity.展开更多
文摘Objective To further define the extent of chromosome 9p21 deletion in periampullary neoplasms.Methods The loss of heterozygosity at 5 microsatellite polymorphic markers on chromosome 9p21 was detected by polymerase chain reaction (PCR), polyacrylamide gel electrophoresis (PAGE) and silver staining in 35 specimens of periampullary neoplasms and their matching blood samples.Results Fifty percent (4/8) of pancreatic cancer cases showed the loss of heterozygosity at one or more microsatellite loci, with the more frequent sites of D9S974 (37.5%) and D9S942 (28.6%), and some showing consecutive allelic loss. Sixty-two point five percent (5/8) of ampullary carcinoma cases showed loss of heterozygosity at one or more of the loci, frequent site of loss being D9S942 (42.9%) and the next most frequent being IFNA (37.5%) and D9S171 (37.5%). Loss of one locus was observed in 14.2% (1/7) of insulinoma. Conclusion The minimal common region of chromosome deletion in periampullary neoplasms is defined between the D9S974 and D9S942 loci within a 15?kb interval in 9p21, suggesting the involvement of a novel tumor suppressor gene in their carcinogenesis.
文摘Faithful transmission or restoration of epigenetic information such as repressive histone modifications through generations is crit- ical for the maintenance of cell identity. We report here that chromodomain Y-like protein （CDYL）, a chromodomain-containing transcription corepressor, is physically associated with chromatin assembly factor 1 （CAF-1） and the repiicative heUcase MCM complex. We showed that CDYL bridges CAF-1 and MCM, facilitating histone transfer and deposition during DNA replication. We demonstrated that CDYI. recruits histone-modifying enzymes G9a, SETDB1, and EZH2 to replication forks, leading to the addition of H3Kgme2/3 and H3K27me2/3 on newly deposited histone H3. Significantly, depletion of CDYL impedes early S phase progres- sion and sensitizes cells to DNA damage. Our data indicate that CDYL plays an important role in the transmission/restoration of repressive histone marks, thereby preserving the epigenetic landscape for the maintenance of cell identity.
