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Biomedical subjects

E L Jackson

Publications and source records attributed to E L Jackson.

6 recordsLinked to original sources
PubMed2005

Mouse models of human non-small-cell lung cancer: raising the bar.

Lung cancer is a devastating disease that presents a challenge to basic research to provide new steps toward therapeutic advances. The cell-type-specific responses to oncogenic mutations that initiate and regulate lung cancer remain poorly defined. A better understanding of the relevant signaling pathways and mechanisms that control therapeutic outcome could also provide new insight. Improved conditional mouse models are now available as tools to improve the understanding of the cellular and molecular origins of adenocarcinoma. These models have already proven their utility in proof-of-principle experiments with new technologies including genomics and imaging. Integrated thinking to apply technological advances while using the appropriate mouse model is likely to facilitate discoveries that will significantly improve lung cancer detection and intervention.

Animals↗
PubMed2001

Analysis of lung tumor initiation and progression using conditional expression of oncogenic K-ras.

Adenocarcinoma of the lung is the most common form of lung cancer, but the cell of origin and the stages of progression of this tumor type are not well understood. We have developed a new model of lung adenocarcinoma in mice harboring a conditionally activatable allele of oncogenic K-ras. Here we show that the use of a recombinant adenovirus expressing Cre recombinase (AdenoCre) to induce K-ras G12D expression in the lungs of mice allows control of the timing and multiplicity of tumor initiation. Through the ability to synchronize tumor initiation in these mice, we have been able to characterize the stages of tumor progression. Of particular significance, this system has led to the identification of a new cell type contributing to the development of pulmonary adenocarcinoma.

Adenocarcinoma↗
PubMed1999

Organization and dynamics of the Mu transpososome: recombination by communication between two active sites.

Movement of transposable genetic elements requires the cleavage of each end of the element genome and the subsequent joining of these cleaved ends to a new target DNA site. During Mu transposition, these reactions are catalyzed by a tetramer of four identical transposase subunits bound to the paired Mu DNA ends. To elucidate the organization of active sites within this tetramer, the subunit providing the essential active site DDE residues for each cleavage and joining reaction was determined. We demonstrate that recombination of the two Mu DNA ends is catalyzed by two active sites, where one active site promotes both cleavage and joining of one Mu DNA end. This active site uses all three DDE residues from the subunit bound to the transposase binding site proximal to the cleavage site on the other Mu DNA end (catalysis in trans). In addition, we uncover evidence that the catalytic activity of these two active sites is coupled such that the coordinated joining of both Mu DNA ends is favored during recombination. On the basis of these results, we propose that the DNA joining stage requires a cooperative transition within the transposase-DNA complex. The cooperative utilization of active sites supplied in trans by Mu transposase provides an example of how mobile elements can ensure concomitant recombination of distant DNA sites.

Bacteriophage mu↗
PubMed1999

The effects on siblings in families with a child with chronic fatigue syndrome.

Paediatric CFS/ME is a stressor, which affects not only the sufferer but also the whole family. The sibling bond exerts a great influence on all the children in the family. Healthy siblings are often overlooked as attention is focused on the child with CFS/ME or other chronic illness. Individual children react in different ways to serious illness in another sibling by adopting a variety of coping mechanisms. There is a need for health and education professionals to consider the whole family when caring for and working with a child with CFS/ME.

Adaptation, Psychological↗
PubMed1992

Filovirus clearance in non-human primates.

There has been concern in the USA and Europe about filovirus outbreaks in recently imported monkeys, and possible transmission to human beings. Healthy monkeys have been found to have low-titre immunofluorescence antibody (IFA) to Asian filoviruses (Reston and Pennsylvania viruses) as well as to the African filoviruses that caused fulminating human outbreaks in the 1970s (Ebola [Zaire] and Sudan viruses). We have assessed whether such monkeys are a risk to man. We studied 42 non-human primates; 31 were experimentally infected with African and Asian filoviruses, 6 were infected during a documented Reston filovirus outbreak, and 5 had serological evidence suggestive of recent filovirus infection. During the first 15 days after infection, virus could be routinely recovered from serum or biopsy or necropsy tissue, and Asian filovirus RNA could be detected by polymerase chain reaction. 20 to 600 days after challenge, filovirus could no longer be recovered nor viral RNA detected in 141 serum, liver, spleen, or kidney specimens. Animals surviving filovirus infection develop high-titre, cross-reacting filovirus-specific antibody 14 to 21 days after infection, and this coincides with virus clearance. Healthy monkeys with low-titre filovirus antibody may be regarded as uninfected.

Animals↗