echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Medical News > Medical World News > Nature Sub-Journal: Pregnancy Reduces Breast Cancer Risk Through Epigenetic Reprogramming

    Nature Sub-Journal: Pregnancy Reduces Breast Cancer Risk Through Epigenetic Reprogramming

    • Last Update: 2020-06-15
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    Previous studies have shown that women who become pregnant before the age of 25 are 30 percent less likely to develop breast cancerPregnancy causes a series of cellular and molecular changes in the breast epithelial cells (MEC) in adult womenA new study of mice has revealed how pregnancy reduces the mechanism of breast cancerThe researchers found that pregnancy reprogrammed chromatin enhancers in the MEC in mice and affected the transcription altimeron (cMYC)The findings were published in the journal Nature CommunicationsThe paper's author, DrCamila dos Santos, an assistant professor at Cold Spring Harbor Laboratory in the United States, is working on how signals that appear during pregnancy alter gene expression, how these changes affect normal and malignant breast development, and provide molecular details of pregnancy protectionDr Camila dos Santos said: "The pregnancy itself changes the way the DNA area is opened or closedLike a yo-yo, the center is what we call a nuclear bodyIt is a bundle of protein that protects DNAWhen you release a melodious ball, you get a string that represents a portion of the DNA that is openAnd because it is open, transcription factors can bind and turn genes on or offIf you pull the yo-yo back, everything goes into the yo-yoThis is what we call closed chromatin, so transcription factors cannot be combined there"The team over-expressed the cMYC gene and found that MEC after pregnancy was resistant to the cancer of the geneIn contrast, pre-pregnancy MEC is not resistant to cMYC and is still susceptible to cancerBasically, pregnancy prevents breast cells from interacting with cancer-causing genes, and doing so does not change the normal epigenetics of pregnancyDrDos Santos's research also showed that cMYC overexpression drives post-pregnancy MEC into an aging state, which stops cells from growing and prevents cancer from developingAccording to DrDos Santos, senescent cells are "in a gray area and do not grow or die," meaning they can remain aging, dead, or cancerousThe cancer gene is turned off, and at the same time, the gene that causes the cell's death is turned onThese signals are a key factor in the number of these cells that do not turn into cancerDrDos Santos and his team are now determining whether human breast cells work in the same way as miceThey also transplanted the cells that changed the pregnancy to mice that had never been pregnant, hoping to find out whether the altered cells affected non-pregnancy environmentsIn summary, this study provides useful insights into the protection of pregnancy and may lead to new drug targets.
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.