Subject(s)
Breast Neoplasms/pathology , Carcinoma, Ductal, Breast/pathology , Occupational Diseases/pathology , Occupational Health/statistics & numerical data , Adult , Breast , Breast Neoplasms/epidemiology , Breast Neoplasms/genetics , Carcinoma, Ductal, Breast/epidemiology , Carcinoma, Ductal, Breast/genetics , Case-Control Studies , Cluster Analysis , Female , Gene Expression Profiling , Gene Expression Regulation, Neoplastic , Humans , Immunohistochemistry , Middle Aged , Occupational Diseases/epidemiology , Occupational Diseases/genetics , Queensland/epidemiology , RNA, Neoplasm/genetics , RNA, Neoplasm/isolation & purification , Retrospective Studies , Risk FactorsABSTRACT
Previous reports from this laboratory demonstrated that persistent infections could be established in Jurkat cells with wild-type vaccinia virus (Jvac). The infected cells elicit increased expression of IL-2, IL-2Ralpha and IL-6 but not of IL-1beta nor of interferon-gamma. The persistently infected cells are also capable to transactivate the LTR gene of HIV-1 virus (HIV-1LTR). In addition, NFkappabeta and NFAT are found activated in Jvac. To find out whether the gene(s) responsible for establishment, maintenance and molecular characteristics of persistently infected cells are located in the terminal ends of the molecule, Jurkat cells were infected with a deletion mutant Vp811 that lacks 32.7 and 14.9 kb at the left and right terminal, respectively. The results indicate that the deletion mutant is capable of establishing persistent infections. The persistently infected cells show a similar pattern of expression to that observed in Jvac cells. It is concluded that the viral gene(s) involved in persistence and molecular cellular changes is (are) present in the mutant.
Subject(s)
Genes, Viral , T-Lymphocytes/virology , Vaccinia virus/genetics , Vaccinia virus/physiology , DNA, Viral , DNA-Binding Proteins/metabolism , Gene Expression , HIV Long Terminal Repeat , Humans , Interferon-gamma/genetics , Interleukin-1/genetics , Interleukin-2/genetics , Interleukin-2 Receptor alpha Subunit , Interleukin-6/genetics , Jurkat Cells , NF-kappa B/metabolism , NFATC Transcription Factors , Nuclear Proteins/metabolism , RNA, Messenger/analysis , Receptors, Interleukin/genetics , Sequence Deletion , Transcription Factors/metabolism , Transcriptional Activation , Virus LatencyABSTRACT
Gestational breast cancer (BC) is generally associated with rapid growth and increased mortality. Because the presence of MMTV-like sequences in BC has been associated with laminin receptor expression, a marker of poor prognosis, gestational BCs were analyzed for MMTV env gene-like sequences to explore whether MMTV-like sequences were also associated with its adverse outcome. Whereas 30-38% of sporadic BC have the sequences, in gestational BC the prevalence is 62%. We suggest that hormonal response elements present in the MMTV-like LTR may play a role in promoting cell growth, as they do in the mouse system.
