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Articles 1 - 11 of 11
Full-Text Articles in Life Sciences
Augmentation Of Ras-Induced Cell Transformation : A New Role For Mir-200a In Malignancy., Lindsey Erin Becker
Augmentation Of Ras-Induced Cell Transformation : A New Role For Mir-200a In Malignancy., Lindsey Erin Becker
Electronic Theses and Dissertations
Cancer is a multistep disease that begins with malignant cell transformation and frequently culminates in metastasis and death. MicroRNAs (miRNAs) are small regulatory 21-25-nt RNA molecules and are frequently deregulated in cancer. The majority of miRNAs are estimated to be co-expressed with neighboring miRNAs as clusters. Many miRNA clusters coordinately regulate multiple members of cellular signaling pathways or protein interaction networks. miR-200a is a member of the miR-200 family, which are known to be strong inhibitors of the epithelial to mesenchymal transition. As such, the tumor suppressive role of miR-200a in oncogenesis has been well studied; however, recent studies have …
Cd4 And Cd8 T Cells Directly Recognize Murine Gammaherpesvirus 68-Immortalized Cells And Prevent Tumor Outgrowth, Xiaozhan Liang, Rebecca L. Crepeau, Weijun Zhang, Samuel H. Speck, Edward J. Usherwood
Cd4 And Cd8 T Cells Directly Recognize Murine Gammaherpesvirus 68-Immortalized Cells And Prevent Tumor Outgrowth, Xiaozhan Liang, Rebecca L. Crepeau, Weijun Zhang, Samuel H. Speck, Edward J. Usherwood
Dartmouth Scholarship
There has been extensive research regarding T cell recognition of Epstein-Barr virus-transformed cells; however, less is known regarding the recognition of B cells immortalized by gamma-2 herpesviruses. Here we show that B cells immortalized by murine gammaherpesvirus 68 (MHV-68, γHV-68) can be controlled by either CD4 or CD8 T cells in vivo. We present evidence for the direct recognition of infected B cells by CD4 and CD8 T cells. These data will help in the development of immunotherapeutic approaches combating gamma-2 herpesvirus-related disease.
Orchestration Of The S-Phase And Dna Damage Checkpoint Pathways By Replication Forks From Early Origins, Julie M. Caldwell, Yinhuai Chen, Kaila L. Schollaert, James F. Theis, George F. Babcock, Carol S. Newlon, Yolanda Sanchez
Orchestration Of The S-Phase And Dna Damage Checkpoint Pathways By Replication Forks From Early Origins, Julie M. Caldwell, Yinhuai Chen, Kaila L. Schollaert, James F. Theis, George F. Babcock, Carol S. Newlon, Yolanda Sanchez
Dartmouth Scholarship
The S-phase checkpoint activated at replication forks coordinates DNA replication when forks stall because of DNA damage or low deoxyribonucleotide triphosphate pools. We explore the involvement of replication forks in coordinating the S-phase checkpoint using dun1Δ cells that have a defect in the number of stalled forks formed from early origins and are dependent on the DNA damage Chk1p pathway for survival when replication is stalled. We show that providing additional origins activated in early S phase and establishing a paused fork at a replication fork pause site restores S-phase checkpoint signaling to chk1Δ dun1Δ cells and relieves the reliance …
Examining The Link Between Chromosomal Instability And Aneuploidy In Human Cells, Sarah L. Thompson, Duane A. Compton
Examining The Link Between Chromosomal Instability And Aneuploidy In Human Cells, Sarah L. Thompson, Duane A. Compton
Dartmouth Scholarship
Solid tumors can be highly aneuploid and many display high rates of chromosome missegregation in a phenomenon called chromosomal instability (CIN). In principle, aneuploidy is the consequence of CIN, but the relationship between CIN and aneuploidy has not been clearly defined. In this study, we use live cell imaging and clonal cell analyses to evaluate the fidelity of chromosome segregation in chromosomally stable and unstable human cells. We show that improper microtubule–chromosome attachment (merotely) is a cause of chromosome missegregation in unstable cells and that increasing chromosome missegregation rates by elevating merotely during consecutive mitoses generates CIN in otherwise stable, …
Molecular Basis For Effects Of Carcinogenic Heavy Metals On Inducible Gene Expression, Joshua W. Hamilton, Ronald C. Kaltreider, Olga V. Bajenova, Michael A. Ihnat, Jennifer Mccaffrey, Bruce W. Turpie, Erin E. Rowell, Jannet Oh, Michael J. Nemeth, Carrie A. Pesce, Jean P. Lariviere
Molecular Basis For Effects Of Carcinogenic Heavy Metals On Inducible Gene Expression, Joshua W. Hamilton, Ronald C. Kaltreider, Olga V. Bajenova, Michael A. Ihnat, Jennifer Mccaffrey, Bruce W. Turpie, Erin E. Rowell, Jannet Oh, Michael J. Nemeth, Carrie A. Pesce, Jean P. Lariviere
Dartmouth Scholarship
Certain forms of the heavy metals arsenic and chromium are considered human carcinogens, although they are believed to act through very different mechanisms. Chromium(VI) is believed to act as a classic and mutagenic agent, and DNA/chromatin appears to be the principal target for its effects. In contrast, arsenic(III) is considered nongenotoxic, but is able to target specific cellular proteins, principally through sulfhydryl interactions. We had previously shown that various genotoxic chemical carcinogens, including chromium (VI), preferentially altered expression of several inducible genes but had little or no effect on constitutive gene expression. We were therefore interested in whether these carcinogenic …
Translational Regulation Of The C-Jun Proto-Oncogene, Anil Sehgal
Translational Regulation Of The C-Jun Proto-Oncogene, Anil Sehgal
Theses and Dissertations in Biomedical Sciences
The v-jun oncogene was originally isolated from the ASV17 virus in 1987. Ever since its isolation, extensive work has been done to understand the role of the v-jun oncogene in cell transformation. The c-Jun protein is a transcription factor which binds to the DNA target TGACTCA. The c-Jun protein binds to DNA in the form of dimers. It can form homodimers with itself and heterodimers with Jun family (JunB and JunD), Fos family (FosB, Fra1 and Fra2), or with CREB family members through the leucine zipper motif. Because the c-jun proto-oncogene plays an important role in cell transformation, extensive work …
Transformation Of A Continuous Rat Embryo Fibroblast Cell Line Requires Three Separate Domains Of Simian Virus 40 Large T Antigen., Jiyue Zhu, Philip W. Rice, Lisa Gorsch, Marina Abate, Charles N. Cole
Transformation Of A Continuous Rat Embryo Fibroblast Cell Line Requires Three Separate Domains Of Simian Virus 40 Large T Antigen., Jiyue Zhu, Philip W. Rice, Lisa Gorsch, Marina Abate, Charles N. Cole
Dartmouth Scholarship
Mouse C3H 10T1/2 cells and the established rat embryo fibroblast cell line REF-52 are two cell lines widely used in studies of viral transformation. Studies have shown that transformation of 10T1/2 cells requires only the amino-terminal 121 amino acids of simian virus 40 (SV40) large T antigen, while transformation of REF-52 cells requires considerably more of large T antigen, extending from near the N terminus to beyond residue 600. The ability of a large set of linker insertion, small deletion, and point mutants of SV40 T antigen to transform these two cell lines and to bind p105Rb was determined. Transformation …
The Ability Of Simian Virus 40 Large T Antigen To Immortalize Primary Mouse Embryo Fibroblasts Cosegregates With Its Ability To Bind To P53., Jiyue Y. Zhu, Marina Abate, Philip W. Rice, Charles N. Cole
The Ability Of Simian Virus 40 Large T Antigen To Immortalize Primary Mouse Embryo Fibroblasts Cosegregates With Its Ability To Bind To P53., Jiyue Y. Zhu, Marina Abate, Philip W. Rice, Charles N. Cole
Dartmouth Scholarship
The large T antigen encoded by simian virus 40 (SV40) plays essential roles in the infection of permissive cells, leading to production of progeny virions, and in the infection of nonpermissive cells, leading to malignant transformation. Primary mouse embryo fibroblasts (MEFs) are nonpermissive for SV40, and infection by wild-type SV40 leads to immortalization and transformation of a small percentage of infected cells. We examined the ability of an extensive set of mutants whose lesions affect SV40 large T antigen to immortalize MEFs. We found that immortalization activity was retained by all mutants whose lesions are located upstream of codon 346. …
Thermal Enhancement Of Cellular Radiation Damage: A Review Of Complementary And Synergistic Effects, G. Peter Raaphorst, J. G. Szekely
Thermal Enhancement Of Cellular Radiation Damage: A Review Of Complementary And Synergistic Effects, G. Peter Raaphorst, J. G. Szekely
Scanning Microscopy
Hyperthermia treatment can kill mammalian cells in a time and temperature dependent manner. Thermal sensitivity varies extensively among various cell lines in culture and cellular molecular and ultrastructural studies have not resolved which cellular mechanisms underlie thermal cell killing and radiosensitization. The response of cells to heat and radiation are complementary under certain conditions found in human tumors, such as hypoxia, low pH, low nutrient and the S-phase of the cell cycle. Thus, hyperthermia can be used as a complementary treatment modality in the radiotherapy of human cancer. Further studies show that heat treatment causes radiosensitization which is in part …
Absence Of A Structural Basis For Intracellular Recognition And Differential Localization Of Nuclear And Plasma Membrane-Associated Forms Of Simian Virus 40 Large Tumor Antigen., Donald L. Jarvis, Charles N. Cole, Janet S. Butel
Absence Of A Structural Basis For Intracellular Recognition And Differential Localization Of Nuclear And Plasma Membrane-Associated Forms Of Simian Virus 40 Large Tumor Antigen., Donald L. Jarvis, Charles N. Cole, Janet S. Butel
Dartmouth Scholarship
The simian virus 40 large tumor antigen (T-ag) is found in both the nuclei (nT-ag) and plasma membranes (mT-ag) of simian virus 40-infected or -transformed cells. It is not known how newly synthesized T-ag molecules are recognized, sorted, and transported to their ultimate subcellular destinations. One possibility is that these events depend upon structural differences between nT-ag and mT-ag. To test this possibility, we compared the structures of nT-ag and mT-ag from simian virus 40-infected cells. No differences between the two forms of T-ag were detected by migration in polyacrylamide gels, by Staphylococcus aureus V8 partial proteolytic mapping of methionine- …
The Effects Of Aging And Transformation On The Dna, Rna, Protein, And Hydroxyproline Content Of Fibroblasts (Wi 38) In Culture, James Michael Eichner
The Effects Of Aging And Transformation On The Dna, Rna, Protein, And Hydroxyproline Content Of Fibroblasts (Wi 38) In Culture, James Michael Eichner
University of the Pacific Theses and Dissertations
The study of the aging process is the investigation as to how the passage of time affects cells, organs, and organisms. Aging is a very complex and incompletely understood phenomenon. This is reflected by the number of theories attributing aging to a variety of causative factors such as: (1) the somatic mutations occurring spontaneously or produced by ionizing radiation, which are thought to have some effect on again but are not responsible for the normal process; (2) the alteration of macromolecules as the cells of an organism age forming neoantigens and functioning in the autoimmune reactions; the Cross-linkage theory which …