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Oncogenic ras results in increased cell kill due to defective thermoprotection in lung cancer cells  Roger A Vertrees, PhD, Joseph B Zwischenberger, MD,

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Presentation on theme: "Oncogenic ras results in increased cell kill due to defective thermoprotection in lung cancer cells  Roger A Vertrees, PhD, Joseph B Zwischenberger, MD,"— Presentation transcript:

1 Oncogenic ras results in increased cell kill due to defective thermoprotection in lung cancer cells 
Roger A Vertrees, PhD, Joseph B Zwischenberger, MD, Paul J Boor, MD, Scot D Pencil, MD, PhD  The Annals of Thoracic Surgery  Volume 69, Issue 6, Pages (June 2000) DOI: /S (00)

2 Fig 1 The time course relating cell survival (percentage of starting number of cells) to heat dose revealed that there was no deleterious effect of heat stress on the BEAS2-B cell line. In contrast, the BZR-T33 cell line displayed a reduction in cell number after 1 hour of heat stress which eventually reduced this population by 50%. The Annals of Thoracic Surgery  , DOI: ( /S (00) )

3 Fig 2 Comparison between cell lines for the effect of heat stress on expression of three specific heat shock proteins. (A) More HSP70, p72 is present in the normal cell line (2C) before heat shock. Heat shock resulted in an increase in both cell lines; the increase in the BZR-T33 (T33H) was significantly greater. (B) More HSC70, p73 is present in the normal cell line (2C). Heat stress resulted in a significant increase in the expression of the transformed cell line (T33H). (C) Heat shock resulted in a significant increase in only the BEAS2-B (2H) cells. The Annals of Thoracic Surgery  , DOI: ( /S (00) )

4 Fig 3 Comparison of the time course for production of HSP70, p72. Cells were harvested and protein collected for each hour of heat stress (1, 2, and 3 hours) and recovery (1, 2, and 3 hours) and 18 hours later. Densimetric analysis of the Western blot showed two different responses to the heat stress treatment. Optical density (OD)/cell number was significantly (p < 0.05) higher in BEAS2-B cells. The results showed a delayed and more feeble heat stress response mustered by the BZR-T33 cell line at 1 to 5 hours which declined over the next 19 hours. In BEAS2-B cells, the response was immediate, prolonged, and maximal 24 hours later. The Annals of Thoracic Surgery  , DOI: ( /S (00) )

5 Fig 4 Results of survey technique revealed that in human lung cancer cell lines a mutant (mt.) ras was associated with a significant reduction (∗p < 0.05) in the number of cells surviving heat stress (43°C for 180 minutes). The ras status of ChagoK-1 and NCl-H596 cell lines is currently undetermined, however, their response to the heat stress was very similar to those cell lines with mutant ras. (wt = wild type.) The Annals of Thoracic Surgery  , DOI: ( /S (00) )


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