Why might long telomeres be selected for in laboratory mice?
Their arguments for increased telomere length in lab mice are:


Rate of tumour formation is dependent on the number of cells within an organism. Additionally, tumours take time to form. Therefore, small animals that only need to reproduce early in life, like lab mice, are less prone to tumours and there is then less selective pressure favouring telomere shortening. 
Senescence has a negative effect on reproductive success, even early in life, and there is therefore selective pressure favouring increased telomere length that reduces senescence.
While the lack of selection on senescence due to the short window for reproduction could have the opposite effect of reducing telomere length, point 2 is the dominant factor. 


To be frank, this all sounds extremely speculative to me and the supporting evidence they did provide was not entirely convincing (though I am far from an expert in the field). Keep in mind that it’s a hypothesis only. 

In case you don’t have access to their article, I quoted the relevant section below:


  The unusual telomere system of lab mice may be an unintended consequence of captive breeding. Retirement of breeders after 8 months eliminates selection on late-life effects. Tumor-forming mutations take time to occur, tumors take time to become lethal, and the likelihood of tumor initiation is presumably a function of the number of cells in the body, so in small bodied animals like mice, tumors may be rare and inflict minimal cost in the first eight months of life, even absent a telomeric fail-safe. Further, selection for sustained high reproductive output (beginning early and maintained for 8 months) should strongly favor a reduction in senescent effects occurring in that window. Selection acting to eliminate senescent effects and increase early reproductive output may tend to elongate telomeres. Because of the inextricable connection between tumor suppression and somatic maintenance, telomere elongation should dramatically increase the risk of eventual tumor formation, but any effects manifesting after the breeding cut-off will be selectively irrelevant. By our model, selection for early high rates of reproduction in the absence of selection for longevity or tumor suppression should produce long telomeres and a strong propensity for eventual tumor incidence. Despite diminished senescence, we expect these mice to have reduced maximum longevity compared to wild conspecifics. At all ages, lab mice (with elongated telomeres) should be more likely to die of tumors than wild mice. These mice should also be unusually resilient to somatic damage and show few signs of aging other than tumor formation. 
  
  ...
  
  The hypothesis that an 8 month breeding cut-off should select for non-senescent, tumor prone mice seems paradoxical. One might expect the elimination of selection on late life effects to accelerate senescence, not retard it. But in lab mice, selection for high, sustained rates of breeding appears to be the dominant factor. The tumor fail-safe has effectively been turned off, condemning these animals to form tumors, but leaving an early-life window of reproduction within which there is minimal senescent decline.