Juan Manuel Vazquez

Juan Manuel Vazquez

Postdoctoral Researcher

Sudmant Lab, University of California - Berkeley

Biography

I am a Puerto Rican biologist studying the evolution of longevity and healthspan in expectional animals such as bats, elephants, and whales. I use a combination of computational and empirical approaches in my work, using a complete functional genomics pipeline to identify and characterize genetic changes between long- and short-lived species in primary cell culture systems. In addition to my work in aging, I strive to promote transparency, diversity, and inclusivity in STEM, and am actively involved in various outreach and training programs.

My current research focus is the role of genomic stability in longevity differences between species, and the feedback loops between chromatin organization and lifespan. In the Sudmant Lab at UC Berkeley, I use single-cell genomics to study the within-species relationship between chromatin and aging in vivo using mice; and I use primary cell culture samples from various Myotis species of bats to study genomic stabilty and lifespan between species.

Pedagogy and inclusivity are at the heart of my academic program. Science only has meaning when its fruits are widely and openly shared with all; furthermore, science is only beneficial and benevolent when its fruits are available equally to all. As such, I am always seeking more opportunities to reach out and promote STEM to any and all groups and identities!

Interests

  • Pedagogy and Teaching
  • Aging
  • Peto’s Paradox
  • Comparative Biology
  • Transhumanism and the Ethics of Lifespan Extension

Education

  • PhD & MSc in Human Genetics, 2020

    University of Chicago

  • BSc in Biology, Molecular Genetics, 2015

    University of Rochester

  • BA in Chemistry, 2015

    University of Rochester

Skills

Pedagogy

99%

R

99%

Python3

99%

Functional Genomics

99%

Single Cell Genomics

10%

Comparative Biology

99%

Molecular Biology

99%

English, Spanish, French

100%

Projects

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Peto’s Paradox

Are cases of individual tumor suppressor duplications in Peto’s Paradox lineages one-off events, or part of a general mechanism

Recent & Upcoming Talks

The Role of Gene Duplication in Mediating Peto's Paradox in Afrotheria and Chiroptera

Based on emperical studies of humans, mice, and various other species, an individual’s cancer risk is directly proportional to their cell count (body size) and lifespan. This leads to a theoretical prediction that large and/or long-lived species would possess a higher predisposition to cancer compared to smaller, shorter-lived species; compounding this risk is the fact that body size and lifespan are strongly correlated. However, in a phenomenon known as Peto’s Paradox, cancer risk between species does not correlate with either their body sizes or lifespans. This implies that enhanced cancer resistance mechanisms must co-evolve with increases in body size and lifespan; however, there are many ways this can come about. Rather than reinventing the wheel, species can carry an increased load of cancer risk by increasing the number of wheels they have. My thesis focuses on the role tumor suppressor gene duplications play in Peto’s Paradox: Chapter 1 explores whether or not tumor suppressor genes are especially enriched among duplicated genes in large, long lived species, while Chapters 2 and 3 functionally characterize two such duplications. Overall, my work here highlights the vital role that tumor suppressor gene duplicates play in lowering the cancer risk of large, long-lived species, while also highlighting new questions for future work, especially regarding antagonistic pleitropy and growth-suppression paradoxes with these duplicates.

Recent Publications

The Role of Gene Duplication in Mediating Peto's Paradox in Afrotheria and Chiroptera

Based on emperical studies of humans, mice, and various other species, an individual’s cancer risk is directly proportional to their cell count (body size) and lifespan. This leads to a theoretical prediction that large and/or long-lived species would possess a higher predisposition to cancer compared to smaller, shorter-lived species; compounding this risk is the fact that body size and lifespan are strongly correlated. However, in a phenomenon known as Peto’s Paradox, cancer risk between species does not correlate with either their body sizes or lifespans. This implies that enhanced cancer resistance mechanisms must co-evolve with increases in body size and lifespan; however, there are many ways this can come about. Rather than reinventing the wheel, species can carry an increased load of cancer risk by increasing the number of wheels they have. My thesis focuses on the role tumor suppressor gene duplications play in Peto’s Paradox: Chapter 1 explores whether or not tumor suppressor genes are especially enriched among duplicated genes in large, long lived species, while Chapters 2 and 3 functionally characterize two such duplications. Overall, my work here highlights the vital role that tumor suppressor gene duplicates play in lowering the cancer risk of large, long-lived species, while also highlighting new questions for future work, especially regarding antagonistic pleitropy and growth-suppression paradoxes with these duplicates.