Squamous-cell carcinoma of the cervix and its precursor lesions are associated with human papillomavirus (HPV) infection. Epidemiological studies indicate that HPV infection in itself is not sufficient for cervical-cancer induction, suggesting that other factors contribute to carcinogenesis. We have investigated the potential role of host genetic background as one such factor. We screened a series of squamous-cell carcinomas of the cervix for HLA-class-II DQB1* alleles by the polymerase chain reaction and site-specific oligonucleotide probe hybridization and for HPV type from African-American women using a local, ethnically matched control panel. Statistically significant associations for increase in relative risk for cervical cancer were seen for DQB1*0303 and DQB1*0604. DQB1*0201 and the heterozygote DQB1*0301/*0501 showed a decrease in relative risk for cervical cancer. HPV typing revealed no association between virus type and DQB1 alleles. Our results confirm other studies showing an increase in relative risk for cervical cancer associated with HLA-DQ3 alleles in Caucasians.

A study of MCF-7 human breast cancer cells was undertaken to ascertain the degree of apoptosis induction by paclitaxel and if the induction of apoptosis could be enhanced by caffeine. Paclitaxel (0-20 ng/ml) caused concentration-dependent increases in morphologically identifiable apoptotic cells (up to 43% of cell population) and cells with DNA strand breaks (up to 38%), a commonly cited marker of apoptosis. Maximal DNA strand breakage occurred after 16 hr of exposure to paclitaxel and maximal apoptotic-appearing cells occurred after 24 hr. The remaining non-apoptotic paclitaxel-exposed cells were growth arrested in G2. A 4-hr exposure to caffeine concentration-dependently (0-20 mM) increased apoptosis to 88% of the cell population. Our results show induction of apoptosis in breast cancer cells by paclitaxel, and enhancement of this process by caffeine.

In der Domäne gefangen: Die Fähigkeit von polaren und unpolaren Domänen in ionischen Flüssigkeiten, Reaktionen durch Pseudoverkapselung von Reaktanten zu beeinflussen, wurde in nukleophilen Substitutionen mit einem kationischen Substrat und einer Reihe von Nukleophilen untersucht. Eine signifikante Reaktionsbeschleunigung wurde beobachtet, die mit der Konzentration der polaren Reagentien innerhalb der polaren Domänen der ionischen Flüssigkeiten korreliert ([CnMIM]=1‐Alkyl‐3‐methylimidazolium).

Genetic aberrations, such as loss of heterozygosity (LOH) and mutations leading to functional inactivation of the PTEN tumor suppressor gene, located on chromosome 10q23.3, have been shown to be associated with approximately one third of ovarian adenocarcinomas. In addition, microsatellite instability (MSI) leading to the functional inactivation of the PTEN gene has also been reported for ovarian adenocarcinomas with frequencies varying from 6 to 37%. However, the frequency of PTEN gene abnormalities has not been well studied or evaluated in lesions such as typical and atypical endometriosis. The aim of this study was to investigate a possible sequential progression from endometriosis through atypical endometriosis to ovarian carcinoma by assessing LOH at 10q23.3 and MSI in those entities. Genomic DNA was analyzed for LOH and MSI at 3 loci on chromosome 10, using polymerase chain reaction amplification. Significant differences in LOH were seen between endometriosis (4.3%) and ovarian carcinoma (23.5%) at D10S608. The differences at the other 2 loci were not significant. A high frequency of MSI was found in endometriosis (82.6%) and atypical endometriosis (75%); however, the differences were not significant. These results suggest that LOH at D105608 may possibly be an important molecular event in the progression of endometriosis to carcinoma. This study highlights that endometriosis and atypical endometriosis might act as precursor lesions that have the potential to progress into ovarian adenocarcinoma.