Correspondence re: Priskorn L, et al. Semen quality and lifespan: a study of 78 284 men followed for up to 50 years., Human Reproduction, Volume 40, Issue 4, April 2025, Pages 730–738.https://doi.org/10.1093/humrep/deaf023

The currently prevailing theory of a transmissible cancer cell lineage in Tasmanian devils was based on the discovery of apparently identical chromosomal aberrations in facial tumors of several animals. New findings of facial tumors that have no detectable cytogenetic similarities to previously published cancer karyotypes and the recent detection of varying portions of chromosome Y in all tumor cell lines of male devils (but none in tumors of females) cast doubt on the theory of a cancer transplant. Thus, I propose an alternative scenario in which similar chromosomal and genetic aberrations in individual cancers are a consequence of the low genetic diversity in populations of the Tasmanian devil resulting in a unique telomere length profile. Critically short telomeres on certain chromosome ends lead to chromosome-specific fusions and the activation of species-specific transposable elements that cause the observed karyotypic and molecular convergence. This new concept can explain the existence of genetic signs of tumor clonality within a population despite the independent origin of each facial cancer in these cancer-prone animals.

Correspondence re: Sandler, O., S. P. Mizrahi, N. Weiss, O. Agam, I. Simon, and N. Q. Balaban. 2015. “Lineage correlations of single cell division time as a probe of cell-cycle dynamics.” Nature no. 519 (7544):468-71. doi: 10.1038/nature14318.

Upon re-examination of large telomere datasets from healthy human populations, a downward secular trend in telomere length at birth was found. The authors theorized that relatively recent environmental stresses to female germ cells could have driven the observed intergenerational telomere erosion; otherwise, these trends would have pushed populations into pathological telomere length ranges within a few centuries. Strangely, the authors decided to disregard an 11-year-old theory of telomere-driven macroevolution that is based on progressive intergenerational telomere loss as the driving force behind species extinction and speciation. Additionally, Holohan and colleagues introduced a “new” interpretation of the old-father-long-telomered-offspring effect, namely as a consequence of intergenerational telomere erosion in the female lineage. Yet, an identical theoretical model has been published twice, several years before. To distinguish between a temporary trend caused by environmental pollution and a general evolutionary mechanism of intergenerational telomere erosion, we urgently need telomere length data from multigenerational studies on mammals with a short generation-time.

Correspondence re: Hung, C. M., et al. 2014. “Drastic population fluctuations explain the rapid extinction of the passenger pigeon.” Proc Natl Acad Sci U S A no. 111 (29):10636-41. doi: 10.1073/pnas.1401526111.

Correspondence re: Stringer, C. 2014. “Why we are not all multiregionalists now.” Trends Ecol Evol no. 29 (5):248-251

Correspondence re: Zimonjic et al. 2001. “Derivation of human tumor cells in vitro without widespread genomic instability.” Cancer Res no. 61 (24):8838-44. Submitted to Cancer Research 8/19/2002, rejected 8/29/2002

Correspondence re: Villeda et al. 2014.“Young blood reverses age-related impairments in cognitive function and synaptic plasticity in mice.” Nat Med no. 20 (6):659-63. doi: 10.1038/nm.3569.

Correspondence re: Forsberg, L. A., et al. 2014. “Mosaic loss of chromosome Y in peripheral blood is associated with shorter survival and higher risk of cancer.” Nat Genet 46 (6):624-8. doi: 10.1038/ng.2966.