EPIGENETICS IN CANCER INITIATION 🎗️

“𝓐𝓰𝓮-𝓪𝓼𝓼𝓸𝓬𝓲𝓪𝓽𝓮𝓭 𝓮𝓹𝓲𝓰𝓮𝓷𝓮𝓽𝓲𝓬 𝓬𝓱𝓪𝓷𝓰𝓮𝓼 𝓶𝓪𝔂 𝓹𝓻𝓲𝓶𝓮 𝓬𝓮𝓵𝓵𝓼 𝓯𝓸𝓻 𝓶𝓪𝓵𝓲𝓰𝓷𝓪𝓷𝓽 𝓽𝓻𝓪𝓷𝓼𝓯𝓸𝓻𝓶𝓪𝓽𝓲𝓸𝓷 𝓵𝓸𝓷𝓰 𝓫𝓮𝓯𝓸𝓻𝓮 𝓶𝓾𝓽𝓪𝓽𝓲𝓸𝓷𝓼 𝓪𝓬𝓬𝓾𝓶𝓾𝓵𝓪𝓽𝓮.” - Professor Anne Brunet

🧬 Epigenetics (heritable changes in gene expression without DNA sequence alteration) is increasingly recognized as a driver of early cancer initiation, not just a downstream effect. It shapes cellular identity, yet its dysregulation can quietly reprogram cells toward malignancy.

          🔹 Aberrant hypermethylation silences tumor suppressor genes, while global hypomethylation promotes genomic instability and oncogene activation. These early shifts often precede detectable mutations, suggesting epigenetic “priming.”

          🔹 Altered acetylation and methylation reshape chromatin accessibility, tipping the balance toward proliferation and away from apoptosis (key hallmarks of early tumorigenesis).

         🔹 Dysregulated miRNAs disrupt post-transcriptional control, weakening tumor suppression and amplifying oncogenic signaling networks.

➡️ Environmental exposures (e.g., tobacco, diet, pollutants) further accelerate these changes, linking lifestyle and aging to cancer risk through cumulative epigenetic drift.

⚠️ In an Oystershell, unlike genetic mutations, epigenetic alterations are potentially reversible; making them powerful targets for early detection, prevention, and precision therapy.

Abubakar Abubakar ✍🏻

• Jones, P.A., & Baylin, S.B. (2007). The epigenomics of cancer. Cell.

• Feinberg, A.P., & Tycko, B. (2004). The history of cancer epigenetics. Nat Rev Cancer.

• Baylin, S.B., & Jones, P.A. (2016). Epigenetic determinants of cancer. Cold Spring Harb Perspect Biol.

• Esteller, M. (2008). Epigenetics in cancer. N Engl J Med.


#Epigenetics #CancerBiology #Oncology #PrecisionMedicine #Genomics #Research #NGS #IVF #PGT #CRISPR ⚕️

Comments

Post a Comment

Popular posts from this blog

GENE DUPLICATIONS IN EVOLUTIONARY INNOVATION

Image
"𝔾𝕖𝕟𝕖 𝕕𝕦𝕡𝕝𝕚𝕔𝕒𝕥𝕚𝕠𝕟 𝕡𝕣𝕠𝕧𝕚𝕕𝕖𝕤 𝕒 𝕣𝕖𝕕𝕦𝕟𝕕𝕒𝕟𝕔𝕪 𝕥𝕙𝕒𝕥 𝕗𝕣𝕖𝕖𝕤 𝕠𝕟𝕖 𝕔𝕠𝕡𝕪 𝕗𝕣𝕠𝕞 𝕤𝕖𝕝𝕖𝕔𝕥𝕚𝕧𝕖 𝕔𝕠𝕟𝕤𝕥𝕣𝕒𝕚𝕟𝕥, 𝕒𝕝𝕝𝕠𝕨𝕚𝕟𝕘 𝕚𝕥 𝕥𝕠 𝕖𝕩𝕡𝕝𝕠𝕣𝕖 𝕟𝕖𝕨 𝕗𝕦𝕟𝕔𝕥𝕚𝕠𝕟𝕒𝕝 𝕤𝕡𝕒𝕔𝕖." - Dr. Richard Lewontin 🧬 Gene duplications are a driving force in evolution, offering raw material for innovation. They arise through mechanisms like unequal crossing over, retroposition, or whole-genome duplication (WGD). Once a gene is duplicated, one copy can conserve its original role, while the other diverges; fueling new functions, adaptations, or even nonfunctionalization (pseudogenes).           🔹 The evolutionary fates of gene duplications includes: Subfunctionalization: split ancestral functions across duplicates. Neofunctionalization: gain of new roles, which is vital for innovation. Pseudogenization: loss of function. A classic case is the globin gene family: duplications enabled the evolution of h...
Read more

MUTATIONAL SIGNATURES IN CANCER GENOMES 🎗️

Image
“𝕋𝕙𝕖 𝕘𝕖𝕟𝕠𝕞𝕖 𝕠𝕗 𝕖𝕧𝕖𝕣𝕪 𝕔𝕒𝕟𝕔𝕖𝕣 𝕡𝕣𝕠𝕧𝕚𝕕𝕖𝕤 𝕒 𝕜𝕚𝕟𝕕 𝕠𝕗 ‘𝕒𝕣𝕔𝕙𝕒𝕖𝕠𝕝𝕠𝕘𝕚𝕔𝕒𝕝 𝕣𝕖𝕔𝕠𝕣𝕕,’ 𝕨𝕣𝕚𝕥𝕥𝕖𝕟 𝕚𝕟 𝕥𝕙𝕖 𝔻ℕ𝔸 𝕔𝕠𝕕𝕖 𝕚𝕥𝕤𝕖𝕝𝕗, 𝕠𝕗 𝕥𝕙𝕖 𝕖𝕩𝕡𝕠𝕤𝕦𝕣𝕖𝕤 𝕥𝕙𝕒𝕥 𝕔𝕒𝕦𝕤𝕖𝕕 𝕥𝕙𝕖 𝕞𝕦𝕥𝕒𝕥𝕚𝕠𝕟𝕤 𝕥𝕙𝕒𝕥 𝕝𝕖𝕒𝕕 𝕥𝕠 𝕥𝕙𝕖 𝕔𝕒𝕟𝕔𝕖𝕣.” - Sir. Mike Stratton 🧬 Cancer arises from the accumulation of somatic mutations, each carrying clues about the biological and environmental forces that shaped the tumor’s evolution. With the advent of high-throughput sequencing and large-scale projects like TCGA and ICGC, we have uncovered distinct mutational signatures; recurring patterns of DNA alterations that reflect specific mutagenic processes. 🔹 What are mutational signatures? They are characteristic patterns of nucleotide substitutions, insertions, or deletions, shaped by mechanisms such as aging, tobacco exposure, UV light, or defective DNA repair. For example, Signature 1 correlates with age-related deamin...
Read more