deletion review

Y chromosome instability in testicular cancer [An article from: Mutation Research-Reviews in Mutation Research]
$14.95
This digital document is a journal article from Mutation Research-Reviews in Mutation Research, published by Elsevier in 2006. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
Approximately 15-25% of male infertility cases carry extensive azoospermic factor (AZF) deletions. Moreover, about 80% of Finnish testicular germ cell tumors (TGCT) and about 23-25% of TGCTs from other geographic regions carry short and interstitial AZF deletions. In infertility cases the AZF deficiency occurs in the germ cells of the proband father giving rise to mosaic sperm populations comprising non-deleted and deleted sperms. Fertilization of an ovocyte by a Y deleted sperm will give rise to an AZF-deleted and infertile F1 male. In TGCTs the AZF deletions take place in the initial stages of embryogenesis producing individuals that are a mosaic of Y deleted and non-deleted cell lineages. Carcinoma in situ (CIS) is a premalignant lesion that some believe may develop in gonads of male embryos before the ninth week of age due to transformation of a totipotent primordial germ cell. If the transformed cell carries AZF deletions the resultant CIS will also have Y deletions. CIS will differentiate into seminoma or into embryonal carcinoma and non-seminomas in about 1x10^-^3 of the young adults carrying premalignant CIS outgrowths; if the CIS lesion has AZF deletions the derived forms of testicular cancer will also exhibit these deletions. AZF deletions play no role in the development of testicular cancers. On the other hand, they are a marker of Y chromosome instability and eventually of a more generalized pattern of genome instability associated with the appearance of TGCT. Genetic factors such as malfunction of metabolizing genes, DNA repairing genes, Y-linked or X-linked genes have been considered as possible causes of AZF deletions in testicular cancer. Yet, the exact identification of the genes involved remains elusive. AZF deletions have also been identified in non-Hodgkin lymphomas and in colorectal cancers, two forms of malignancy that have been found to be associated with TGCTs.

The index revision party [An article from: International Review of Financial Analysis]
$10.95
This digital document is a journal article from International Review of Financial Analysis, published by Elsevier in 2005. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Description:
This paper examines the annual revision of the AEX index in the Netherlands. This particular index is interesting because the revision rules enable investors to anticipate changes in both constituents and index weights long in advance. Our results suggest that attention and temporary price pressure play a role in the observed revision effect. A portfolio containing those stocks expected to benefit from the index revision is showing an outperformance of up to 7% in the weeks before the revision, while losers are unaffected. Around the revision day, we find indications of temporary price pressure for winners as well as losers.

Mechanisms of tandem repeat instability in bacteria [An articles review from: Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
$7.95
This digital document is a journal article from Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, published by Elsevier in 2006. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.

Abstract:
Hypermutable tandem repeat sequences (TRSs) are present in the genomes of both prokaryotic and eukaryotic organisms. Numerous studies have been conducted in several laboratories over the past decade to investigate the mechanisms responsible for expansions and contractions of microsatellites (a subset of TRSs with a repeat length of 1-6 nucleotides) in the model prokaryotic organism Escherichia coli. Both the frequency of tandem repeat instability (TRI), and the types of mutational events that arise, are markedly influenced by the DNA sequence of the repeat, the number of unit repeats, and the types of cellular pathways that process the TRS. DNA strand slippage is a general mechanism invoked to explain instability in TRSs. Misaligned DNA sequences are stabilized both by favorable base pairing of complementary sequences and by the propensity of TRSs to form relatively stable secondary structures. Several cellular processes, including replication, recombination and a variety of DNA repair pathways, have been shown to interact with such structures and influence TRI in bacteria. This paper provides an overview of our current understanding of mechanisms responsible for TRI in bacteria, with an emphasis on studies that have been carried out in E. coli. In addition, new experimental data are presented, suggesting that TLS polymerases (PolII, PolIV and PolV) do not contribute significantly to TRI in E. coli.