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Hermann J. Muller (1890–1967)
Published in Krishna Dronamraju, A Century of Geneticists, 2018
With Julian Huxley’s help, Muller obtained a temporary position at the Institute for Animal Genetics at Edinburgh University. He was then 50 years old. Muller attracted several students during that period, including some who became well-known geneticists in their own right, such as Charlotte Auerbach, Guido Pontecorvo, and S.P. Ray Chaudhury. With Pontecorvo, Muller worked out the breakage–fusion–bridge cycle (dicentric chromosome formation), independently of Barbara McClintock, and used it to explain the curious dominant lethals he had observed in large numbers since his X-ray work in 1927. The dicentric chromosomes led to cell death and aborted embryos (Pontecorvo and Muller 1942). With his student S.P. Ray Chaudhury, Muller extended his radiation studies to chronic and acute doses. Another finding was that, for gene mutations, it made no difference whether a dose of 400 R was administered in a few minutes or drawn out over a month-long period. In either case, the mutation rate was the same, confirming Muller’s belief that gene mutations were punctiform events (Muller and Chaudhury 1939). The same observation got him embroiled in a dispute with British radiologists who considered it inappropriate it to extrapolate from flies to humans and that Muller’s view might unnecessarily alarm the public about the uses of radiation.
Chromosomal 1q21 abnormalities in multiple myeloma: a review of translational, clinical research, and therapeutic strategies
Published in Expert Review of Hematology, 2021
Kamlesh Bisht, Brian Walker, Shaji K. Kumar, Ivan Spicka, Philippe Moreau, Tom Martin, Luciano J. Costa, Joshua Richter, Taro Fukao, Sandrine Macé, Helgi van de Velde
Locus specific FISH and spectral karyotyping of patients with ≥4 copies of 1q21 revealed four types of chromosomal anomalies that distinguish this phenotype, namely, JT1q12 gains, deletion of the receptor chromosome including 17p, insertions into the receptor chromosome, and breakage-fusion-bridge cycle amplifications [2]. Such aberrant chromosomes undergo multiple rounds of breakage and fusion cycles and mitotic segregation errors, which finally result into either whole-chromosome arm or segmental duplications [2,31,44]. The epigenetic factors responsible for driving the pericentromeric heterochromatin de-condensation in MM are still unknown. In solid tumors, aberrant expression of histone lysine demethylase 4A (KDM4A) and hypoxic stress induce aberrant amplification of 1q21 [48,49].