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Aneuploidy is the observation of an abnormal number of chromosomes per cell, differing from the normal karyotype (somatic number 2n, or n in gametes) by loss or gain of pairs of chromosomes, whole chromosomes or chromosome fragments. Chromosome missegregation in mitosis or meiosis can produce aneuploid cells or organisms respectively.
Information on the occurrence of aneuploidies in prehistory human populations are rare. Here, from a large screen of ancient human genomes and osteological examination, the authors find genetic evidence for six cases of trisomy 21 (Down syndrome) and one case of trisomy 18 (Edwards syndrome) in historic and prehistoric infants.
Girish et al. designed a method to genetically remove extra chromosomes from human aneuploid cancer cells to show that they are important for malignant growth and not just a bystander.
Two papers demonstrate that centrosome amplification can cause cancer in mammals and that a PIDDosome–p53-dependent control mechanism acts to prevent cell proliferation in the presence of extra centrosomes.
Sheltzeret al. find that single-chromosome gains can prevent tumorigenesis relative to genetically matched euploid cells, but that these aneuploid cells can evolve over time to have improved fitness.
Galluzzi and Kroemer take advantage of a large study of somatic copy number alterations to revisit the previously suggested idea that cancer aneuploidy frequently arises from genome duplication.
