The beneficial effects of metformin on cancer prevention

-


The scientific journal "The beneficial effects of metformin on cancer prevention and therapy: a comprehensive review of recent advances" explores the potential of metformin, a drug commonly used to treat type 2 diabetes, in cancer prevention and therapy. The article delves into recent research findings to evaluate metformin's impact on various aspects of cancer.

Here's a concise breakdown of the key points addressed in the journal:

  • Metformin's Potential Benefits: The review analyzes studies suggesting that metformin may influence several cellular processes linked to cancer development and progression. These processes include insulin signaling, cell growth, metabolism and epigenetics.

  • Metformin in Cancer Prevention: The article explores research on metformin's potential to reduce cancer risk. Studies in patients with type 2 diabetes indicate that metformin use might be associated with a lower incidence of certain cancers.

  • Metformin in Cancer Therapy: The review examines how metformin might enhance the effectiveness of conventional cancer therapies like chemotherapy. Studies suggest that metformin may improve treatment response and outcomes in some cancers.

  • Mechanisms of Action: The article explores the mechanisms by which metformin might exert its anti-cancer effects. These mechanisms likely involve epigenetic regulating cellular metabolism and signaling pathways that influence cancer cell proliferation and survival.

  • Limitations and Future Directions: The review acknowledges limitations in current research, including the need for larger and more robust clinical trials. The article highlights the importance of further investigations to elucidate the potential of metformin in cancer prevention and therapy.


Overall, the journal provides a comprehensive analysis of the growing body of research on metformin's potential role in combating cancer. While promising findings exist, more extensive studies are needed to confirm these observations and determine the optimal use of metformin in cancer management.


The review points to the exciting area of epigenetics, a mechanism that regulates gene expression without altering the DNA sequence itself as with evolution, as a possible explanation for metformin's anti-cancer effects.

Epigenetics plays a crucial role in cancer development. Abnormal epigenetic modifications can lead to uncontrolled cell growth, a hallmark of cancer. Metformin's ability to influence epigenetic processes has emerged as a promising avenue for cancer therapy.

The journal explores how metformin might target epigenetic mechanisms:

  • DNA methylation: Metformin may affect enzymes involved in DNA methylation, a process that can silence genes. By regulating DNA methylation, metformin could potentially reactivate tumor suppressor genes silenced in cancer cells.

  • Histone modifications: Histones are proteins that package DNA. Metformin might influence enzymes that add chemical groups to histones, altering how tightly DNA is coiled. This can influence gene accessibility and expression. By affecting histone modifications, metformin could potentially block the expression of genes promoting cancer growth.


The review highlights the need for further research to fully understand the interplay between metformin, epigenetics, and cancer. However, the initial findings are encouraging and warrant further investigation into metformin's potential as a cancer preventive or therapeutic agent.


The research delves into recent progress in understanding how metformin might influence cancer development and progression.

Epigenetics, however, is a separate field of study that focuses on how gene expression can be altered without changes in the underlying DNA sequence. This field sheds light on mechanisms beyond the neo-Darwinian model of evolution, which emphasizes genetic mutations as the sole drivers of heritable traits.


Epigenetic modifications can influence gene activity and play a role in cancer development. Metformin's potential impact on cancer is explained by its influence on epigenetic pathways. However, the specific details of this interplay are still being actively explored.


Neo-Darwinian theory, which emphasizes "survival of the fittest," doesn't explain the potential anti-cancer effects of metformin. This theory focuses on the evolution of traits that enhance an organism's ability to survive and reproduce within its environment. Metformin's influence on cancer, however, deals with cellular mechanisms within an organism, impacting how cells divide and respond to signals.

The concept of "survival of the fittest" applies more to the organism's adaptation to its external environment over generations. Metformin's potential impact on cancer lies in its influence on cellular processes within an individual organism.

In Darwinian theory living longer without cancer should be a part of the “survival of the fittest.”



Comments

Post a Comment

Popular posts from this blog

No, the EES is not just a add on to Neo-Darwinism aka the Modern Synthesis

-
Image
" The summary of the state of affairs on the 150th anniversary of the Origin is somewhat shocking: in the post-genomic era, all major tenets of the Modern Synthesis fthe theory of evolution) are, if not outright overturned replaced by a new and incomparably more complex vision of the key aspects of evolution (EES). So, not to mince words , the Modern Synthesis is gone" -Eugene Koonin, an evolutionary biologist (Cited by over 270,000 evolutionary scientists.) The Extended Evolutionary Synthesis (EES) represents a significant departure from the traditional neo-Darwinian framework, also known as the Modern Synthesis . While both theories aim to explain evolutionary change, they differ fundamentally in their underlying mechanisms and the roles they assign to various biological processes. A crucial point of divergence lies in the interpretation and application of the term " evolutionary ," particularly concerning the incorporation of epigenetic mechanisms....
Read more

Is the random mutational model of evolution on its way out?

-
Image
While the random mutational model of evolution has long been a cornerstone of evolutionary biology, the Extended Evolutionary Synthesis (EES) and the study of epigenetics are challenging its core assumptions. The Random Mutational Model and Its Limitations The traditional view of evolution, often called the Modern Synthesis or neo-Darwinism , emphasizes random genetic mutations as the primary source of variation. Natural selection then acts upon this variation, favoring individuals with advantageous traits. This model has been successful in explaining some evolutionary phenomena, but it also has limitations: It struggles to explain complex adaptations: The idea that complex features like the eye or the immune system arose solely through random mutations seems statistically improbable. It overlooks the role of the environment: The traditional model treats the environment as a selective force, but it doesn't fully consider how organisms can actively respond to and s...
Read more

ERVs and Common Descent: A Reassessment in Light of Recent Findings

-
Image
Endogenous retroviruses (ERVs) have long been considered strong evidence for the common descent of humans and chimpanzees. These remnants of ancient viral infections, embedded in the genomes of both species, were once thought to be non-functional "junk DNA." The premise was that the shared presence of these seemingly random insertions in corresponding genomic locations could best be explained by a shared evolutionary history. However, recent research, such as the "Switching Sides" article published in May 2021, has challenged this assumption by demonstrating that ERVs play a functional role in the development of the human embryo and immune system. This discovery raises questions about the validity of using ERVs as primary evidence for common descent. The Traditional Argument for Common Descent The traditional argument for common descent based on ERVs rests on the following points: Random Insertion: Retroviral insertions are thought to occur randomly in...
Read more