Just thinking

Prostate Cancer

This is probably an idiotic idea, but please hear me out and then tell my why I'm wrong. Assuming a drug like atezolizumab works in only a small percentage of patients. Let's say we know that if patient A has success with the drug and we juxtapose him with a patient B who failed to respond can we assume that the difference in these patients is in their immune systems and not the biology of their cancers.

If blood types could be matched why couldn't you remove enough immune cells, on the order of say the provenge model and then replicate and infuse them into patient B.

6 Replies

oldestnewest
  • Interesting ....reminds me of stem cell therapy/ bone marrow transplants. Seems feasible

  • i would like to follow this idea

  • I think biology of their cancers could be a significant reason for the lack of response because PCa is a genetic malfunction and the mutations of the DNA with different genetical properties can vary from one individual to another easily in addition to the PCa being heterogeneous. Atezolizumab is a programmed death-ligand 1 blocking antibody ( PD-L1 ) which is indicated for the treatment of metastatic cancer but is not yet established to the level of Provenge as an immunotherapy for advanced metastatic PCa. Your line of thinking too is meaningful in comparative terms but it has to go a long way in trials to establish the facts.

    I appreciate, we can learn from this type of thinking. Not at all idiotic!

  • My thinking was based on the probability that the biology of the cancers would be similar considering that they've all been exposed to basically the same treatments and acquired modes of resistance.

  • The biology of the tumors in each cancer patient is likely to be different. Even within a single patient there can be significant differences between tumor cells, for example some being highly dependent on testosterone while others are less dependent or not dependent at all.

    The reason for this is that human beings are thought to have something like 19-20,000 genes. A large number of those genes, perhaps hundreds of them, affect cell division and replication, or affect the ability of cells of one type to metastasize into areas of the body where they don't belong. Hundreds of other genes affect the body's response to cancer. Mutations in any of them can contribute to the development of cancer.

    Given the number of genes that can cause or prevent cancer, and the random character of gene mutation, the number of different possible combinations of genes that are involved in creating cancer is huge. The chances of any two patients having the same exact combination is small.

    "Targeted therapies" typically work by looking for a specific gene that is often involved in cancer and either destroying it or stimulating it to work again, or replacing its effects by inserting a chemical into the body that that gene would normally synthesize but can't because it's damaged. But they only work if the patient has the right specific gene value (called an "allele".)

    Alan

  • Well then targeted therapy seems to be the way to go. I'm just stuck looking for where I can sign up. I still think my idea has some value. I believe a trial like that could at least narrow the possibilities if not work with another subset of patients.

You may also like...