BioPharmaTrend
Latest News
All Topics
  • AI in Bio
  • Tech Giants
  • Next-Gen Tools
  • Biotech Ventures
  • Industry Movers
Interviews
Companies
  • Company Directory
  • Sponsored Case Studies
  • Create Company Profile
More
  • About Us
  • Our Team
  • Advisory Board
  • Citations and Press Coverage
  • Partner Events Calendar
  • Advertise with Us
  • Write for Us
Newsletter
Login/Join
  • AI in Bio
  • Tech Giants
  • Next-Gen Tools
  • Biotech Ventures
  • Industry Movers

The Key Role Of Stem Cells In Lethal Gastric Cancer Revealed

by Caroline Green  (contributor )   •   Feb. 6, 2020  

Disclaimer: All opinions expressed by Contributors are their own and do not represent those of their employers, or BiopharmaTrend.com.
Contributors are fully responsible for assuring they own any required copyright for any content they submit to BiopharmaTrend.com. This website and its owners shall not be liable for neither information and content submitted for publication by Contributors, nor its accuracy.

   Biopharma insight   
Share:   Share in LinkedIn  Share in Bluesky  Share in Reddit  Share in Hacker News  Share in X  Share in Facebook  Send by email   |  

In a recent study published in Nature Communications, scientists from Cornell University made new findings in common and fatal gastric cancer research. In the United States, the incidence of gastroesophageal cancer increased 2.5-fold from the 1970s to the early 2000s, however, from the 1950s, the number of all patients with gastric cancer decreased by more than 80%; despite this, gastric cancer is still the fifth most common cancer and the third leading cause of cancer death worldwide.

#advertisement
AI in Drug Discovery Report 2025

In this study, the researchers identified a novel pathway in gastroesophageal cancer that may be expected to serve as a potential target to help develop novel therapies; a type of stem cell offspring called Lgr5 + may gather in large numbers, thereby promoting the development of cancer at the encounter between the two gastric tissues. Professor Alexander Nikitin, a researcher, said that at the global level, gastric squamous columnar junction cancer (gastroesophageal cancer) is a frequent disease and the prognosis of patients is poor, so it is essential to study the mechanism of this type of cancer formation and how it is treated.

In this study, the researchers developed experimental mouse models carrying two tumor suppressor genes that can become inactivated under specific conditions, a model that meets a number of parameters necessary to perform accurate studies of cancer, and previous researchers have certain limitations in mouse studies, that is, mice golden glow produce specific types of tumors or premature death, which undoubtedly inhibits the conduct of the study, but in this study, the mouse model developed by the researchers was able to develop a related form of metastatic gastric columnar junction cancer.

Previously, researchers have found that Lgr5 + stem cells are involved in many types of cancer, said researcher Nikitin. This study suggests that this may not necessarily be applicable to all types of cancer, but there is no evidence that Lgr5 + stem cells themselves induce gastric columnar junction cancer. In this study, through the study of mouse models and organoids, the researchers found that a large number of offspring called Lgr5-CD44 + cells (not Lgr5 + stem cells) accumulate at junctions, and when stem cells undergo classification, they differentiate into specialized cells. But early in division, these cells are not mature, and they have not yet differentiated, and the researchers can detect the presence of these offspring cells in the earliest identifiable lesions and advanced cancers. And after using organoids for research, the researchers found that these cells can be easily transformed.

The results suggest that the cancer-prone characteristics of other transition zones may also be due to the presence of a large number of immature cells, and the researchers also revealed a special protein called osteopontin, which can bind to the receptor of CD44 + cells and turn on a series of downstream effects; the osteoponti –CD44 + complex can control the balance between stem cells and differentiated cells, and produce more stem cells and cells with stem cell characteristics, such as Lgr5-CD44 + cells.

The presence of osteopontin signaling can maintain cells in an immature state, which may be one of the key mechanisms that can help explain why the body has a large pool of immature cells (Lgr5-CD44 + cells), the researchers said. The researchers studied two groups of human patients and found that the results were consistent with those obtained from studies in mouse models, that is, low levels of osteopontin and CD44 cells were directly associated with higher survival status of patients, while late overexpression was directly associated with poorer prognosis in human gastric scale-columnar junction cancer patients.

Later, researchers need to conduct more in-depth studies to investigate and analyze whether osteopontin inhibitors and CD44 + cell antibodies can be used to inhibit the accumulation of Lgr5-CD44 + cells, so as to better treat cancer.

Share:   Share in LinkedIn  Share in Bluesky  Share in Reddit  Share in Hacker News  Share in X  Share in Facebook  Send by email

You may also be interested to read:

How Pharma Reacts To Wuhan Coronavirus Outbreak
by Andrii Buvailo
The Evolution Of Pharmaceutical R&D Model
by Andrii Buvailo

 

#advertisement
ThermoFisher Scientific: Integrated genetic technologies for cell therapy development

BiopharmaTrend.com

Where Tech Meets Bio
mail  Newsletter
in  LinkedIn
x  X
rss  RSS Feed

About


  • What we do
  • Citations and Press Coverage
  • Terms of Use
  • Privacy Policy
  • Disclaimer

We Offer


  • Newsletter
  • BioTech Scout
  • Interviews
  • Partner Events
  • Case Studies

Opportunities


  • Advertise
  • Submit Company
  • Write for Us
  • Contact Us

© BPT Analytics LTD 2025
We use cookies to personalise content and to analyse our traffic. You consent to our cookies if you continue to use our website. Read more details in our cookies policy.