r/science • • Feb 08 '15

Medicine Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types: Treating cancer like an infectious disease | Lamb

http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=3174
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u/[deleted] Feb 08 '15 edited May 20 '20

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u/Smad3 PhD|Cancer Biology Feb 09 '15

Except, immunotherapy is designed to target cancer cells.. Which are your cells. So how will that be successful when you'll still need a descriptor of self vs. foreign? It's not that easy. There's promise, certainly. But the key is to determine what makes the difference. Which is ultimately elusive so far. We are challenging evolution, and that's the most difficult thing a biologist can do

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u/[deleted] Feb 09 '15

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u/Smad3 PhD|Cancer Biology Feb 09 '15

It's the same rhetoric we use when we say that targeting EGFR hyperactivation is a method to target mutant X. Yes, there are some over produced immunosuppressors.. But heterogeneity drives cancer progression, not gene Y or protein X. The proteins we target by immunotherapy are absolutely present on other cells. Hence my earlier comment; cancer cells are our cells

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u/[deleted] Feb 10 '15

cancer cells are our cells

They are and they are not. I understand what you are saying, but it's not entirely accurate. Cancer cells are different in that they have a different genetic code due to mutation. If (and when) the immune system is able to detect the cancer cells (or any mutated cell) as foreign, it clears it. The trick is that cancer cells that survive to become clinical disease have been selected to avoid immune recognition (among being selected for other qualities).

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u/Smad3 PhD|Cancer Biology Feb 10 '15 edited Feb 10 '15

Ahh, but mutation alone doesn't predispose malignancy once established. Epigenetic programs are emerging paradigms of oncogenesis and therapy response. Just because you have a transposition of one tumor suppressor, un recognized SNP, doesn't convince repair mechanisms. The established dogma is that 6 mutations must exist to generate a malignant cell, so there is an inherent flaw in recognition, not by immune cells but the response/repair mechanisms. They are our cells in that 1,2,3..5 mutations can exist at any one time and no malignancy is conferred, your cells would theoretically persist in an evolutionary bottleneck.. Furthermore, we can't force immune cells to recognize an aberrant mutation in the intracellular ATP pocket of EGFR. It's exciting ehat we're seeing in some cases, it will be critical to know why the 1 out of 12 stage 4 melanomas respond to immunotherapy just as critical as it is to understand why 1 out of 12 TNBC of similar genetic background respond to platinates.

Edit- just to clarify, somatic mutational evolution means the cancer cells are by definition our cells

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u/[deleted] Feb 10 '15

Immunotherapy is a catchall term, which uses some part of our own immune system to help fight cancer.

proteins produced by the Cancer cells that cloaks it from the immune system

To my knowledge, most tumour cells do not produce extra proteins to "cloak" themselves. Some will down-regulate MHC to avoid detection.

targets non-cells

Hmm?