Timeline for If Tumors have lots of mutations in them how is it the immune system can't detect them?
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10 events
| when toggle format | what | by | license | comment | |
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| Nov 25, 2015 at 3:57 | comment | added | 201044 | Since a malignant tumour cell used to be 'normal' or still functioning with its mutations ; as a 'former' normal cell it would have a lot of 'in-built' strategies to avoid attack from the immune system . Then when it changes into malignancy it would still have these immune avoidance strategies to use to be 'hard to detect'. If some of these natural immune avoidance abilities that must be in all normal cells were targeted or 'temporarily shut off' by a designer virus or some special chemicals then the tumour might be made apparent and attacked by the immune system. | |
| Sep 29, 2015 at 22:10 | comment | added | 201044 | Do 'regular' non-cancerous cells have many traits or strategies within their genes or epigenetics or whatever ,that allows them to be unharmed by the immune system? ( assuming no auto-immune problems. ) | |
| Sep 14, 2015 at 5:39 | comment | added | 201044 | A 'regular' human cell has a lot of inherent 'strategies' for 'avoiding' immune system 'attacks' unless of course there is an auto-immune disease 'situation' involved. So if such a 'regular cell' becomes cancerous with a lot of mutations , does it and it's daughter cells retain all the immune avoidance abilities it had before it became cancerous? Do the 'acquired mutations it has in fact not interfere with the immune avoidance 'abilities' it has? | |
| Aug 16, 2015 at 0:54 | comment | added | CDB | Yes, quite a bit actually. Since this is a comment and I have limited characters, I would point you to this link: ncbi.nlm.nih.gov/pmc/articles/PMC3489746 From the first paragraph after the abstract; "Moreover, many tumors downregulate the expression of MHC molecules..." read on. I would also suggest the paragraph labeled " Why Does Antitumor T-cell Responses Often Prove Defective?" located further into the article. Basically, it's a more complex version of my answer above. | |
| Aug 16, 2015 at 0:10 | comment | added | 201044 | If a cell's apoptosis mechanism is not functioning would this disrupt or cause to malfunction the MHC in the cell? | |
| Aug 15, 2015 at 20:35 | comment | added | CDB | I apologize for not explaining this concept very well. It would seem, if you were that confused, I have failed completely at explaining it. I have done my best to explain and it is understandable to me, so I do not know how to clarify. Please, if you can explain more efficiently, feel free to edit my answer. | |
| Aug 15, 2015 at 20:17 | comment | added | InactionPotential | It reads as if you completely misunderstand how the MHC-T-cell interaction works. MHC class I molecules on the cell-surface are loaded with the peptide fragments from intracellular proteins degraded by the proteasome. In infection, this can be proteins from viruses or microbes that are recognized as foreign. In cancer, this can be mutations that generate a peptide with novel structure. Many mutations, especially deletions, but also many oncogenic point mutations do not necessarily generate novel immunogenic peptides. | |
| Aug 15, 2015 at 19:45 | comment | added | CDB | Did I fail to convey this? Perhaps my wording was confusing. I meant that most main CANCER causing genes do not cause a major change in the surface molecules of the cell. However you are correct, some genes that are not considered MHC linked genes can affect this, but most are not cancer causing. | |
| Aug 15, 2015 at 19:25 | comment | added | InactionPotential | This is very wrong. T-cells recognize MHC + peptide combinations. Immunogenic mutations in non-MHC genes can drive an anti-tumor response. | |
| Aug 15, 2015 at 18:42 | history | answered | CDB | CC BY-SA 3.0 |