(5)FU Don’t Call Me Cil-ly

 I really had to stretch that title to make it work. Or not make it work, you decide, there are only so many ways to make the mouthful that is fluorouracil work in a title. To bypass that landmine, I’ll refer to it as FU. Much easier to say. Anyways, fluorouracil/FU, what is it?

FU is used to treat many cancers both topically and intravenously, warts and keloid scars via intralesional injection, skin cancer prevention, and ocular malignancies. Pretty versatile drug. So how does it work? Without getting in the weeds,  FU inhibits the creation of deoxythymidine monophosphate to prevent DNA replication by double strand breakage. FU also acts as a pyrimidine analog, and sneaks into the place of uricil and thymine, essential parts of DNA and RNA. 

Fast dividing cells naturally go through more of these compounds. FU also selectively inhibits the deoxythymidine stuff in sun damaged skin which is why when applied topically, it doesn’t melt all of your skin off. Just the bad stuff. Which for some of us is a lot. Anyways, pretty cool. It replaces the bricks for a new building with pillows so it can’t get more than a few feet high, at least that is how I think of it. 

The versatility of the drug is very interesting but makes sense to me, as I said above, it seems logical (to me, please correct me if I am wrong) that faster divided cells will take up the FU faster. Something I did not realize before reading an excellent book I have mentioned before, The Emperor of All Maladies, is that cancer can be resistant to chemotherapy drugs (and radiation). Similar to antibiotics. I had probably learned it in school but stored that next to the information on South Korean politics, the stuff I don’t need often. 

How does this work? The cells just tell the FU to F off and that’s it. No but that would be almost funny if it wasn’t cancer, cells giving the finger to molecules. I just melted my brain trying to understand resistance, I can only understand the gist of it. Cancer cells of various types can move drugs out of the cell (like bacteria), produce compounds that negate FU, develop ways to produce the products that FU Fs with and many more. Actually, it’s all kinda like bacteria. And yes, you can tell me “or course dummy, they’re both cells and collections of cells trying to spread into the future” and you’re right. But I just made the leap in my mind. See? I learn gooder when I talk with letters. I’m the smartiest. 

Anyway, super cool. FU can be used alone or in combination to treat cancers and is a staple oncology and dermatology drug. As I start my nursing career in oncology I hope to really build out my understanding of many of the various anti-cancer molecules we have. I hope y’all learned a thing. Love ya. 

PS, check out the podcast and share this. Thanks. 
References 

Fluorouracil from StatPearls at the NIH: National Library of Medicine by Casale & Patel

5-Fluorouracil: Mechanisms of Resistance and Reversal Strategies from Molecules 2008 by Zhang et al.

5-Fluorouracil resistance mechanisms in colorectal cancer: From classical pathways to promising processes by Blondy et al., in Cancer Science September 2020. 

Four Decades of Continuing Innovation with Fluorouracil: Current and Future Approaches to Fluorouracil Chemoradiation Therapy from the Journal of Clinical Oncology Volume 22, Issue 11 by Rich et al.

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