This study explores a new approach to fighting cancer and extending lifespan through genetic engineering of the blood system. The researchers conducted experiments on mice and observed promising results. They genetically modified the blood cells of donor mice to produce a specific protein that has anti-cancer properties and the ability to increase lifespan. These modified blood cells were then transferred into recipient mice with cancerous tumours.
The results showed that the transferred blood cells effectively suppressed tumor growth and improved the overall lifespan of the recipient mice.
This research has significant implications for the development of potential treatments for cancer and extending human lifespan.
By manipulating the genetic makeup of blood cells, scientists may be able to enhance the body’s natural defenses against cancer and potentially increase longevity.
While further studies are needed to confirm these findings and assess their applicability to humans, this study presents a promising step towards innovative therapies in the future.
Promising findings: genetically altered blood cells show potential against cancer and ageing
Here are our key takeaways from the study, Hematopoietic Transfer of the Anti-Cancer and Lifespan-Extending Capabilities of A Genetically Engineered Blood System.
Anti-cancer capability of Eklf(K74R) mice
The study introduces a genetically engineered mouse model called Eklf(K74R) that carries a mutation in the KLF1/ EKLF transcription factor.
This mutation leads to extended lifespan and healthy characteristics, including resistance to cancer.
The anti-cancer capability of Eklf(K74R) mice was found to be independent of gender, age, and genetic background. It implies that these mice have enhanced mechanisms to prevent or suppress the development and progression of cancer.
Transfer of anti-cancer and lifespan-extending characteristics via bone marrow transplantation (BMT)
The researchers conducted experiments to investigate whether the anti-cancer capability and extended lifespan characteristics of Eklf(K74R) mice could be transferred to wild-type (WT) mice through transplantation of bone marrow mononuclear cells (BMMNC).
The results showed that when WT mice received BMT from Eklf(K74R) mice, their lifespan was extended by approximately 5 months compared to WT mice receiving BMT from WT mice.
This finding suggests that the beneficial effects associated with the genetically engineered blood system can be transferred to recipient mice through BMT.
Inhibition of tumour growth by Eklf(K74R) BMMNC
The study also examined the effect of BMT using BMMNC from Eklf(K74R) mice on tumour growth.
It was observed that the growth of tumours with B16-F10-luc cells was significantly slower in mice that received BMT from Eklf(K74R) mice compared to those receiving BMMNC from WT mice.
This indicates that the BMMNC from Eklf(K74R) mice possess an inherent capability to inhibit tumour growth more effectively than BMMNC from WT mice.
Expression of immune checkpoint genes and anti-cancer capabilities
The researchers investigated the expression levels of immune checkpoint genes (ICGs), specifically Pd-1 and Pd-l1, in Eklf(K74R) mice compared to WT mice. It was found that the expression levels of these ICGs were reduced in the leukocytes (PB, B, and T cells) of Eklf(K74R) mice. Lower expression of ICGs, such as Pd-1 and Pd-l1, is associated with enhanced anti-cancer capabilities. The study suggests that the anti-cancer capabilities of Eklf(K74R) mice may be attributed, at least in part, to the downregulation of these immune checkpoint genes.
These findings contribute to a better understanding of the genetic factors and mechanisms that influence cancer resistance and lifespan extension in the context of the genetically engineered blood system represented by Eklf(K74R) mice.
However, it’s important to note that this article is a preprint and has not undergone peer review, so further validation and scrutiny by the scientific community are necessary before drawing definitive conclusions.
Reference: Jing-Ping Wang, View ORCID ProfileChun-Hao Hung, Yao-Huei Liou, Ching-Chen Liu, Kun-Hai Yeh, Keh-Yang Wang, Zheng-Sheng Lai, Tzu-Chi Hsu, Tung-Liang Lee, Yu-Chiau Shyu, Pei-Wen Hsiao, Liuh-Yow Chen, Trees-Juen Chuang, Chen-Hsin Albert Yu, Nah-Shih Liao, Che-Kun James Shen. doi: https://doi.org/10.1101/2023.04.21.537849. This article is a preprint and has not been certified by peer review.