According to creationists, genes don't evolve but are intelligently designed, so presumably their intelligent designer should be given the credit for designing a gene which has been shown to help cancer cells disseminate and set up colonies of secondaries throughout the body. The gene, Gstt1, is responsible for 90% of cancer-related deaths.
Gstt1 has a key role in eliminating toxins from the body so blocking it as a prophylactic treatment to prevent cancer metastases may not be a straightforward option.
The gene's role in helping cancer to metastasize was discovered by a team of investigators from the Massachusetts General Cancer Center, Boston, USA, who have just published their findings in the journal Nature Cell Biology and explained it in a press release from Massachusetts General Hospital:
What can you tell me about the gene Gstt1? The GSTT1 gene (Glutathione S-Transferase Theta 1) is part of the glutathione S-transferase (GST) family, which plays a crucial role in the detoxification process of the body. GST enzymes are involved in the conjugation of the antioxidant glutathione to various endogenous and exogenous compounds, facilitating their removal from the body.
Here are some key points about the GSTT1 gene:
Function
- Detoxification: GSTT1 encodes an enzyme that helps detoxify reactive electrophilic compounds, including carcinogens, therapeutic drugs, environmental toxins, and products of oxidative stress.
- Conjugation Activity: The enzyme catalyzes the conjugation of glutathione to substrates, making them more water-soluble and easier to excrete.
Polymorphisms and Gene Variants
- Gene Deletion: One notable polymorphism of GSTT1 is a null variant, where the entire gene is deleted. This deletion results in a complete lack of functional enzyme, which can impact an individual's ability to detoxify certain compounds.
- Population Variability: The frequency of the GSTT1 null genotype varies among different populations. For example, it is more common in Asian populations compared to European or African populations.
Clinical Significance
- Disease Association: The GSTT1 null genotype has been studied in relation to various diseases, including cancer, asthma, and other conditions linked to oxidative stress and exposure to toxins.
- Cancer Risk: Some studies suggest that individuals with the GSTT1 null genotype may have an increased risk of certain cancers, possibly due to reduced ability to detoxify carcinogens.
- Drug Response: Variations in GSTT1 may influence the efficacy and toxicity of certain drugs, affecting pharmacogenetic responses.
Research and Testing
- Genetic Testing: Testing for GSTT1 polymorphisms, particularly the null genotype, can be part of pharmacogenetic panels or studies investigating susceptibility to environmental toxins and disease risk.
- Functional Studies: Research continues to explore the specific substrates and mechanisms by which GSTT1 and its variants impact health and disease.
Environmental and Lifestyle Factors
- Exposure to Toxins: Individuals with the GSTT1 null genotype may be more susceptible to the harmful effects of environmental toxins such as cigarette smoke, pollution, and occupational chemicals.
- Diet and Lifestyle: Antioxidant-rich diets and lifestyles that minimize exposure to toxins may be particularly beneficial for individuals with reduced GSTT1 activity.
Understanding the role and implications of the GSTT1 gene can provide insights into an individual’s detoxification capacity and potential risk factors for certain diseases. Genetic testing and personalized medicine approaches can help tailor preventive and therapeutic strategies based on GSTT1 genotype.
Key Takeaways
- Investigators have identified a gene whose expression confers a growth advantage to metastatic cancer cells, which cause 90% of cancer-related deaths
- The team showed that silencing this gene in lab models of cancer prevented metastatic cells from growing and spreading
- The findings could lead to new strategies to treat metastatic cancer and would be particularly impactful for patients with pancreatic cancer
Metastatic cancer cells, which cause 90% of cancer-related deaths, must overcome numerous hurdles to spread from a primary tumor through the bloodstream.
A new study led by investigators from the Mass General Cancer Center has identified a gene whose expression confers a growth advantage to these cells.
Mechanistically, the gene’s expression allows metastatic cancer cells to cause changes to their surrounding environment so that they can grow in new locations in the body. The findings are published in Nature Cell Biology.
Our results point to potentially novel therapeutic avenues to specifically target metastatic cancer.
Professor Raul Mostoslavsky, MD, PhD, senior author
Scientific Director
Krantz Family Center for Cancer Research
Mass General Cancer Center, Boston, USA.
Mostoslavsky and colleagues first compared gene expression patterns in primary versus metastatic tumors in mice with pancreatic cancer or breast cancer. After identifying various genes whose expression increased in metastatic tumor cells, the researchers silenced each gene individually.
In these experiments, silencing the Gstt1 gene had no effect on primary tumor cells from mice, but it stripped metastatic cancer cells of their ability to grow and spread. It also blocked cell growth in two metastatic-derived human pancreatic cancer cell lines.
Gstt1 encodes an enzyme that is a member of a superfamily of proteins involved with protecting cells from toxins, among other functions. Mechanistic studies indicated that the Gstt1 enzyme causes metastatic cancer cells to modify and secrete a protein called fibronectin, which is important for helping cells to attach themselves to the extracellular matrix, a large network of proteins and other molecules that surround, support, and give structure to cells and tissues in the body.
Gstt1 alters the matrix surrounding the metastatic cells so they can grow in these foreign niches. Our results could lead to new strategies for the treatment of metastatic disease. This would be especially impactful for pancreatic cancer, in which most patients present with metastases when initially diagnosed.
Professor Raul Mostoslavsky.
Authorship: Christina M. Ferrer, Ruben Boon, Hyo Min Cho, Tiziano Bernasocchi, Lai Ping Wong, Murat Cetinbas, Elizabeth R. Haggerty, Irene Mitsiades, Gregory R. Wojtkiewic, Daniel E. McLoughlin, Reem Aboushousha, Hend Abdelhamid, Sita Kugel, Esther Rheinbay, Ruslan Sadreyev, Dejan Juric, Yvonne M. Janssen-Heininger, and Raul Mostoslavsky.
Dr. Mostoslavsky is a professor of Medicine at Harvard Medical School, the Laurel Schwartz Professor in Medicine in the Field of Oncology at Massachusetts General Hospital and the Kristine and Bob Higgins MGH Research Scholar 2012-2017.
AbstractIn the context of their world in which nothing happens unless an intelligent designer so wills it, perhaps a creationist could explain why the Gstt1 gene seems to be designed to make it easier for cancer to metastasize and to be responsible for 90% of cancer deaths.
Identifying the adaptive mechanisms of metastatic cancer cells remains an elusive question in the treatment of metastatic disease, particularly in pancreatic cancer (pancreatic adenocarcinoma, PDA). A loss-of-function shRNA targeted screen in metastatic-derived cells identified Gstt1, a member of the glutathione S-transferase superfamily, as uniquely required for dissemination and metastasis, but dispensable for primary tumour growth. Gstt1 is expressed in latent disseminated tumour cells (DTCs), is retained within a subpopulation of slow-cycling cells within existing metastases, and its inhibition leads to complete regression of macrometastatic tumours. This distinct Gstt1high population is highly metastatic and retains slow-cycling phenotypes, epithelial–mesenchymal transition features and DTC characteristics compared to the Gstt1low population. Mechanistic studies indicate that in this subset of cancer cells, Gstt1 maintains metastases by binding and glutathione-modifying intracellular fibronectin, in turn promoting its secretion and deposition into the metastatic microenvironment. We identified Gstt1 as a mediator of metastasis, highlighting the importance of heterogeneity and its influence on the metastatic tumour microenvironment.
Ferrer, C.M., Cho, H.M., Boon, R. et al.
The glutathione S-transferase Gstt1 drives survival and dissemination in metastases. Nat Cell Biol (2024). https://doi.org/10.1038/s41556-024-01426-7
Copyright: © 2024 The authors.
Published by Springer Nature Ltd. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
In fact, it would be interesting to hear why their putative designer designed cancer in the first place, let alone going to these lengths to ensure it kills people and why any decent person should regard this designer as an all-loving god who cares for its creation and not a sadistic monster.
The Unintelligent Designer: Refuting The Intelligent Design Hoax
ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.
Available in Hardcover, Paperback or ebook for Kindle
The Malevolent Designer: Why Nature's God is Not Good
This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.
Illustrated by Catherine Webber-Hounslow.
Available in Hardcover, Paperback or ebook for Kindle
Illustrated by Catherine Webber-Hounslow.
The creator of cancer is a cruel, sadistic, malevolent monster and could not possibly be all good. It's not even close to being all good. Anyone who thinks its an all good being is woefully delusional and wrong, which would describe nearly all creationists. Cancer is a crime and the creator of cancer is a criminal. Science needs to work hard and find a cure to this devilish disease. We need to rid the world of this disease from hell. Life and the world would be a better place without this disease to say the very least. Our priorities should be to rid the world of all diseases and especially this scourge known as cancer, which is the worst cruelty the Devil has created.Thank you for reading and let's all support the scientists in their fight to rid the world of this horrific disease.
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