To show why, he pulls out a raft of study results collected in a large three - ring binder and points to several studies showing that mice subjected to stress developed more
cancers than normal mice.
Not exact matches
To their surprise, they found that these Th17 - deficient
mice experienced far more aggressive
cancer growth
than normal mice — with the
cancer completely smothering the lungs within 16 days.
Laboratory
mice that have received rapamycin have reduced the age - dependent decline in spontaneous activity, demonstrated more fitness, improved cognition and cardiovascular health, had less
cancer and lived substantially longer
than mice fed a
normal diet.
And because
mouse embryo cells with inactivated copies of BRCA2 are more sensitive to ionizing radiation
than normal cells are, «it's a reasonable extrapolation» that breast
cancers with mutated copies of the gene may be especially good candidates for radiation therapy.
Zeroing in on this kinase was encouraging, Goga said, because other researchers have shown that genetic - knockout
mice that lack the entire family of PIM kinases are slightly smaller
than normal mice, but «basically fine,» indicating that a drug targeting just PIM1 may have manageable levels of toxicity in breast
cancer patients.
It should be noted, however, that while a study on senescent cell ablation in genetically
normal mice would provide at least some evidence on the effect of senescent cells (and their ablation) on promoting
cancer, even such a study would likely show less effect
than could be anticipated in a large mammal model, since even normally - aging
mice rarely suffer metastatic disease to the extent of aging humans, as sheer primary tumor volume is generally sufficient to be fatal to
mice.
Experiments in Muc1 knockout
mice and
mice with Muc1 knockdown have shown that under Helicobacter infection,
mice deficient in Muc1 develop far more
cancer - promoting inflammation
than normal mice.