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\title{Telomere-driven karyotypic and molecular convergence mimics the
transmissibility of cancer in the Tasmanian devil}



\author[1]{Reinhard Stindl}%
\affil[1]{Affiliation not available}%


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  \date{April 23, 2026}


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\begin{abstract}
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.%
\end{abstract}%



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