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Sunday Science by Go_UnPro Episode 1: 2025_11_02

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Manage episode 517493691 series 3677756
Content provided by Go UnPro and Brent W. Laartz. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by Go UnPro and Brent W. Laartz or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://podcastplayer.com/legal.

In this first episode of Sunday Science, we explore a few articles showing the carcinogenic potential of a strain of E coli (pks+ or colibactin-producing) that produces a DNA mutational toxin. Evidence from the discussed articles shows that this bacteria could be responsible for a high percentage of early onset (under age 50) colorectal cancer (CRC). CRC at this age is increasing and now encompasses 10% of all CRC, which percentage is growing by 2% per year. Up to 68% of these cancers have evidence of the hallmark mutations and presence of the pks+ E coli above. Diets high in fiber decrease and diets low in fiber increase the presence of this bacteria. As we elucidate the particular mutations associated with this and other carcinogens, we can detect these mutations within the DNA of each cancer patient. The data shows evidence of this bacteria being present in those with CRC under age 50, and it is more prevalent in countries that have a higher incidence of CRC under age 50, and likely has been present since an early age, such as the first 10 years of life.

A simple arithmetic problem of subracting 40 years from 2015 when these early-onset CRC began their increase, yields the year 1975 which is when we began to incorporate processed foods and refined sugar and high-fructose corn syrup into our diet. This and the data of onset at age 10 and before, begs us to consider what we are doing to our children and the possibility that there are a whole 40 years of children that are increasing their processed food intake. How many early-onset CRC patients will there be 40 years from now? MIcrobiome and genetic mutational research into other cancers such as oropharyngeal, bladder, and anal carcinoma could soon provide these answers.

References

    • Insights into the role of the intestinal microbiota in colon cancer. Sofia Oke and Alberto Martin. Ther Adv Gastroenterol 2017, Vol. 10(5) 417 –428

    • Microbiome and colorectal cancer: Unraveling host-microbiota interactions in colitis-associated colorectal cancer development. lMingsong Kang, Alberto Martin. Seminars in Immunology. Volume 32, August 2017, Pages 3-13

    • Gut Microbial Metabolism Drives Transformation of Msh2-Deficient Colon Epithelial Cells. Antoaneta Belcheva1 . Cell. Volume 158, Issue 2p288-299July 17, 2014
    • Oliero M, Hajjar R, Cuisiniere T, Fragoso G, Calvé A and Santos MM (2023) Inulin impacts tumorigenesis promotion by colibactinproducing Escherichia coli in ApcMin/+ mice. Front. Microbiol. 14:1067505.

    • Dietary fibre counters the oncogenic potential of colibactin-producing Escherichia coli in colorectal cancer. Alberto Martin. Nature Microbiology 10: 855-870.

  continue reading

2 episodes

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Manage episode 517493691 series 3677756
Content provided by Go UnPro and Brent W. Laartz. All podcast content including episodes, graphics, and podcast descriptions are uploaded and provided directly by Go UnPro and Brent W. Laartz or their podcast platform partner. If you believe someone is using your copyrighted work without your permission, you can follow the process outlined here https://podcastplayer.com/legal.

In this first episode of Sunday Science, we explore a few articles showing the carcinogenic potential of a strain of E coli (pks+ or colibactin-producing) that produces a DNA mutational toxin. Evidence from the discussed articles shows that this bacteria could be responsible for a high percentage of early onset (under age 50) colorectal cancer (CRC). CRC at this age is increasing and now encompasses 10% of all CRC, which percentage is growing by 2% per year. Up to 68% of these cancers have evidence of the hallmark mutations and presence of the pks+ E coli above. Diets high in fiber decrease and diets low in fiber increase the presence of this bacteria. As we elucidate the particular mutations associated with this and other carcinogens, we can detect these mutations within the DNA of each cancer patient. The data shows evidence of this bacteria being present in those with CRC under age 50, and it is more prevalent in countries that have a higher incidence of CRC under age 50, and likely has been present since an early age, such as the first 10 years of life.

A simple arithmetic problem of subracting 40 years from 2015 when these early-onset CRC began their increase, yields the year 1975 which is when we began to incorporate processed foods and refined sugar and high-fructose corn syrup into our diet. This and the data of onset at age 10 and before, begs us to consider what we are doing to our children and the possibility that there are a whole 40 years of children that are increasing their processed food intake. How many early-onset CRC patients will there be 40 years from now? MIcrobiome and genetic mutational research into other cancers such as oropharyngeal, bladder, and anal carcinoma could soon provide these answers.

References

    • Insights into the role of the intestinal microbiota in colon cancer. Sofia Oke and Alberto Martin. Ther Adv Gastroenterol 2017, Vol. 10(5) 417 –428

    • Microbiome and colorectal cancer: Unraveling host-microbiota interactions in colitis-associated colorectal cancer development. lMingsong Kang, Alberto Martin. Seminars in Immunology. Volume 32, August 2017, Pages 3-13

    • Gut Microbial Metabolism Drives Transformation of Msh2-Deficient Colon Epithelial Cells. Antoaneta Belcheva1 . Cell. Volume 158, Issue 2p288-299July 17, 2014
    • Oliero M, Hajjar R, Cuisiniere T, Fragoso G, Calvé A and Santos MM (2023) Inulin impacts tumorigenesis promotion by colibactinproducing Escherichia coli in ApcMin/+ mice. Front. Microbiol. 14:1067505.

    • Dietary fibre counters the oncogenic potential of colibactin-producing Escherichia coli in colorectal cancer. Alberto Martin. Nature Microbiology 10: 855-870.

  continue reading

2 episodes

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