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Profile

Profile of Haig H. Kazazian Jr.

Beth Azar
PNAS December 22, 2020 117 (51) 32185-32188; first published December 3, 2020; https://doi.org/10.1073/pnas.2023398117
Beth Azar
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When geneticist Haig H. Kazazian Jr. was 16, he overheard a conversation between his father and a family friend. “What do you think? Is he going to be a doctor?” asked his father. “I think he’ll be a scientist,” replied the friend. Kazazian went on to become both. Trained in pediatrics, he developed a love of genetics early on and took up research. At first, he focused on blood disorders, with an eye toward characterizing the molecular basis of thalassemia and hemophilia. Then, a discovery in his laboratory on human jumping genes shifted his focus to questions that have taken him on a 30-year journey to understand what mobile pieces of DNA do in the human genome and how they work. Elected to the National Academy of Sciences in 2018, Kazazian is Professor of Pediatrics, Molecular Biology, and Genetics at the Johns Hopkins University School of Medicine. His Inaugural Article (1) reports the search for jumping genes in gastrointestinal tumor cells.

Haig H. Kazazian Jr. Image credit: Courtney J. Barbour.

Fulfilling a Father’s Dreams

Kazazian’s success is all the sweeter because of the hardships his parents endured. They were Armenian immigrants fleeing the Turkish genocide. His mother arrived in Racine, Wisconsin in 1920. His father was the only member of his immediate family to survive life in a concentration camp in northeastern Syria after a forced march from Anatolia. In 1917 his father escaped, via Damascus and Cuba, to Toledo, Ohio, where an uncle owned an oriental rug store. The elder Kazazian, having lost his opportunity for an education, worked alongside his uncle, eventually taking over the business when his uncle died in 1951.

“My father was very smart, and he had wanted to become a physician,” recalls Kazazian. “I feel like I was fulfilling his dreams in the next generation. I wasn’t pressured, …

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References

  1. ↵
    1. K. Yamaguchi et al
    ., Striking heterogeneity of somatic L1 retrotransposition in single normal and cancerous gastrointestinal cells. Proc. Natl. Acad. Sci. U.S.A. 117, 32215–32222 (2020).
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  2. ↵
    1. H. H. Kazazian Jr.,
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    , X-linked 6-phosphogluconate dehydrogenase in drosophila: subunit associations. Science 150, 1601–1602 (1965).
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    1. H. H. Kazazian Jr.,
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    , Studies on the quantitative control of polypeptide synthesis in human reticulocytes. J. Biol. Chem. 243, 2048–2055 (1968).
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    , Prenatal diagnosis using polymorphic DNA restriction sites: Report on 95 pregnancies at risk for sickle cell disease or β-thalassemia. N. Engl. J. Med. 308, 1054–1058 (1983).
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    1. S. E. Antonarakis,
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    , Nonrandom association of polymorphic restriction sites in the β-globin gene cluster. Proc. Natl. Acad. Sci. U.S.A. 79, 137–141 (1982).
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    1. S. H. Orkin et al
    ., Linkage of β-thalassaemia mutations and β-globin gene polymorphisms with DNA polymorphisms in human β-globin gene cluster. Nature 296, 627–631 (1982).
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    1. H. H. Kazazian Jr. et al
    ., Molecular characterization of seven β-thalassemia mutations in Asian Indians. EMBO J. 3, 593–596 (1984).
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    1. T. C. Cheng et al
    ., β-Thalassemia in Chinese: Use of in vivo RNA analysis and oligonucleotide hybridization in systematic characterization of molecular defects. Proc. Natl. Acad. Sci. U.S.A. 81, 2821–2825 (1984).
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    ., Molecular heterogeneity of beta-thalassemia in Mestizo Mexicans. Genomics 11, 474 (1991).
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    ., The molecular basis of β thalassaemia in Punjabi and Maharashtran Indians includes a multilocus aetiology involving triplicated α-globin loci. Br. J. Haematol. 86, 372–376 (1994).
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    ., Evolution of a genetic disease in an ethnic isolate: β-thalassemia in the Jews of Kurdistan. Proc. Natl. Acad. Sci. U.S.A. 88, 310–314 (1991).
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    ., Characterization of β-thalassaemia mutations using direct genomic sequencing of amplified single copy DNA. Nature 330, 384–386 (1987).
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    ., Haemophilia A resulting from de novo insertion of L1 sequences represents a novel mechanism of mutation in man. Nature 332, 164–166 (1988).
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    ., High frequency retrotransposition in cultured mammalian cells. Cell 87, 917–927 (1996).
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    ., Evidence consistent with human L1 retrotransposition in maternal meiosis I. Am. J. Hum. Genet. 71, 327–336 (2002).
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    , SVA elements are nonautonomous retrotransposons that cause disease in humans. Am. J. Hum. Genet. 73, 1444–1451 (2003).
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  20. ↵
    1. H. Kano et al
    ., L1 retrotransposition occurs mainly in embryogenesis and creates somatic mosaicism. Genes Dev. 23, 1303–1312 (2009).
    OpenUrlAbstract/FREE Full Text

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Profile of Haig H. Kazazian Jr.
Beth Azar
Proceedings of the National Academy of Sciences Dec 2020, 117 (51) 32185-32188; DOI: 10.1073/pnas.2023398117

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Beth Azar
Proceedings of the National Academy of Sciences Dec 2020, 117 (51) 32185-32188; DOI: 10.1073/pnas.2023398117
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