tumor suppressors – BioQuakes

Is there a cure for cancer?

MIT researchers have developed a novel technique using prime editing, a variant of CRISPR genome-editing, to screen thousands of mutations in cancer genes, such as the tumor suppressor gene p53, more efficiently. This method allows for the identification of harmful mutations previously overlooked, shedding light on their role in tumor development and response to treatment. Unlike previous approaches, which introduced artificial versions of mutant genes, this technique edits the genome directly, providing more accurate insights into mutation effects.

The researchers demonstrated the effectiveness of their approach by examining over 1,000 mutations in the p53 gene found in cancer patients, revealing previously unknown harmful mutations. By enabling the generation of various mutations seen in cancer patients and testing their response to therapy, this technique holds promise for precision medicine, potentially revolutionizing cancer treatment strategies. With further exploration into other cancer-linked genes, the researchers aim to uncover new therapeutic targets and eventually personalize cancer therapies based on individual genetic makeup, marking a significant advancement in cancer research and treatment.

In AP Bio’s Unit 6 on Cell Cycle and Mendelian Genetics, we briefly touched upon the topic of cancer, but I found myself captivated and eager to delve further into its complexities and implications. In learning about cancer, I discovered that its development stems from cells breaking free of normal controls, leading to unregulated division and tumor formation. Unlike normal cells, cancer cells disregard signals that regulate division, perpetuating their growth indefinitely. Furthermore, cancer spreads through a process called metastasis, where tumors manipulate blood vessels to obtain nutrients and travel to distant parts of the body, contributing significantly to cancer-related deaths. Treatments target the diverse population of cancer cells, aiming to eliminate them; however, the high mutation rate often leads to drug resistance and tumor recurrence.

Growing up, I heard stories of my family’s experiences with cancer, especially the loss of my mother’s birth father to a rare liver cancer when she was just a child. His passing at such a young age left an indelible mark on our family. Unfortunately, his story isn’t the only one. Cancer has touched other members of my family too, reminding me of the importance of understanding this disease. Instead of feeling weighed down by sadness, I’ve chosen to embrace curiosity and become proactive in learning about cancer. It’s my way of honoring their memories and empowering myself to make a difference. As I prepare for college this Fall, I’ve been reflecting on my career aspirations. My goal is to make a meaningful and purposeful impact in the field of medicine, so I’ve decided to pursue a career in nursing. This path resonates with me as it aligns with my passion for helping others and allows me to realize my professional ambitions.

The innovative technique developed by MIT researchers, along with my personal journey, has inspired me to join the fight against cancer. With a newfound understanding and determination, I eagerly look forward to pursuing a nursing career, driven by the belief that every effort contributes to better treatments and outcomes for those impacted by cancer.What’s your take on CRISPR genome-editing? Share your thoughts or any interesting facts you know!

Cancer most commonly is defined as a “perpetuating mass of dystregulated cells growing in an uncontrolled manner”, however the meaning can be further related to epigenetics, for they appear to be very much interconnected. Another definition of cancer goes on to note this relationship as the “dynamic genetic and epigenetic alterations that contribute to cancer initiation and progress.” Recent research shows that if epigenetics is disrupted, it might switch to oncogenes or shut down tumor suppressors. Either way, this would lead to the development of tumor cells that would cause cancer. We are already aware of the fact that chemical modification affecting the packaging of our DNA can switch genes on and off. The first time that became aware of an epigenetic code, we learned that that code chemically labels active or inactive genetic information. The focus of epigenetics is on the change caused by the modification of gene expression, not the alteration of the code itself. With recent discoveries through research on epigenetics and its relation to cancer, we learned that there must be a balance of “writers” and “erasers” for the cells. Recent data has shown that methyltransferase EZH2 is an epigenetic writer that is hyperactivated in many cancers, specifically melanomas and lymphomas. This recent research also shows KDM3A (member of the jumonji histone lysine demthylase family) as an epigenetic eraser. KDM3A fulfills an oncogenic role by activating a network of tumor promoting genes. Epigonomic changes also allow tumor cells to evade the immune system so that these cells can thrive and divide without the disruption of the immune system. Ultimately, there are two potential pathways that epigenomic regulators can cause cancer. The first is the result of too much epigenetic activation, which can lead to oncogenes. The second is too much epigenetic protection that conversely blocks tumor suppressor genes. DNA hypermethylation causes the silencing of tumor suppressor genes.

Both of these methods would lead to the development of cancer. Epigenetic regulation involves methods including histone regulation, DNA methylation, and changes in noncoding RNAs such as miRNAs. One of the challenges of studying cancer and researching possible vulnverabilities in pathways is that they are often disrupted by epigenetics. The recent studies also have shown that there are close ties between epigenomic (analysis of global epigenetic changes across many genes) changes and metabolites, or human cellular chemistry. Metabolites initiate, target, or maintain epigenetic factors with the transcriptional complex, and cooperation with them metabolites can target, amplify or mute these coded responses. Since the fields of both epigenetics and metabolism are still developing a great deal, there is hope that these insights with regards to cancer and regulating gene expression to prevent the development of cancer will allow for more precision in targeting cancer, specifically when existing methods of therapy fail to work sufficiently.

BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: tumor suppressors

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