Bird shot mets after response; any familiarity with this?

DAMN! Melanoma DOES suck great big green hairy stinky wizard balls, doesn’t it? I have known of others with this response. I will cross fingers and toes that your lesions are BRAF positive. Meantime and in conjunction with – I would certainly pursue intralesional therapy!!! No, you wouldn’t inject EVERY lesion. Nor should you have to!!! No matter the poison picked, all have shown responses in the injected lesions as well as “by-stander” lesions that were not injected. I mean – what the heck! I would go for it.

Here are posts I have on the subject: https://chaoticallypreciselifeloveandmelanoma.blogspot.com/search?q=intralesional&max-results=20&by-date=true

There is also this: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7066689/

Hope that helps at least on the intratumoral/intralesional front. Hang tough. Yours, celeste

I think the following article will explain the mixed response you are experiencing. Unfortunately, I was unable to copy the figures however you can clearly see them when you go to the posted link on the bottom of my post. Here is the abstract and Figure 6 explaination for the mixed response melanoma patient following immumotherapy. One can clearly see how tumors respond differently to identical therapy and why various different therapies are required to combat melanoma.

Abstract
Tumours can escape T-cell responses by losing major histocompatibility complex (MHC)/ human leucocyte antigen (HLA) class I molecules. In the early stages of cancer development, primary tumours are composed of homogeneous HLA class I-positive cancer cells. Subsequently, infiltration of the tumour by T cells generates a vast diversity of tumour clones with different MHC class I expressions. A Darwinian type of T-cell-mediated immune selection results in a tumour composed solely of MHC class I-negative cells. Metastatic colonization is a highly complex phenomenon in which T lymphocytes and natural killer cells play a major role. We have obtained evidence that the MHC class I phenotype of metastatic colonies can be highly diverse and is not necessarily the same as that of the primary tumour. The molecular mechanisms responsible for MHC/HLA class I alterations are an important determinant of the clinical response to cancer immunotherapy. Hence, immunotherapy can successfully up-regulate MHC/HLA class I expression if the alteration is reversible (‘soft’), leading to T-cell-mediated tumour regression. In contrast, it cannot recover this expression if the alteration is irreversible (‘hard’), when tumour cells escape T-cell-mediated destruction with subsequent cancer progression. This review summarizes clinical and experimental data on the complexity of immune escape mechanisms used by tumour cells to avoid T and natural killer cell responses. We also provide in-depth analysis of the nature of MHC/HLA class I changes during metastatic colonization and contribute evidence of the enormous diversity of MHC/HLA class I phenotypes that can be produced by tumour cells during this process.

Keywords: CD8 cell; antigen presentation/processing; cancer; cytotoxicity; immunotherapy.

If you look at Figure 6 it shows the results of a mixed responder melanoma patient to immunotherapy with the following explaination

Figure 6 Different human leucocyte antigen (HLA) class I expression in metastases from the same patient. This figure shows two metastatic lesions analysed in a ‘mixed responder’ to immunotherapy (a). One lesion is capable of up‐regulating HLA class I to induce a T‐cell response and regresses. The other lesion cannot up‐regulate HLA class I and eventually progresses. The type of molecular alteration (hard or soft) responsible for the HLA class I down‐regulation plays a pivotal role in these different responses.

https://pubmed.ncbi.nlm.nih.gov/31509607/