Posted on 11/08/2022 9:31:07 AM PST by ConservativeMind
A treatment may significantly enhance the efficacy of chemotherapy in breast cancer patients, reducing the risk for lung metastasis following chemo from 52% to only 6%. The study identified the mechanism that generates a cancer-promoting inflammatory environment in response to chemotherapy. Moreover, the researchers found that by adding an anti-inflammatory agent to the chemotherapy, metastasis can be prevented.
To this end, the researchers created an animal model for breast cancer metastasis. The animals received the same treatment as human patients: surgical removal of the primary tumor, then chemotherapy, followed by monitoring to detect metastatic relapse as early as possible. The disturbing results: metastatic tumors were detected in the lungs of a large percentage of the treated animals—similar to the percentage found in the control group.
To decipher these adverse effects, the researchers examined the animals' lungs at an intermediate stage—when tiny micro-metastases may have already developed, but even advanced imaging technologies like CT cannot detect them.
Prof. Erez says, "We discovered a previously unknown mechanism: the chemotherapy generates an inflammatory response in connective tissue cells called fibroblasts, causing them to summon immune cells from the bone marrow. This in turn creates an inflammatory environment that supports the micro-metastases, helping them grow into full-fledged metastatic tumors. In this way, the chemotherapy, administered as a means for combating cancer, achieves the opposite result."
To combat this newly discovered process, the researchers combined the chemotherapy administered to the animals with a drug that blocks the activity of complement proteins. The results were very encouraging: following the combined treatment the percentage of animals developing no metastases rose from 32% to 67%; and the percentage of those with extensive cancer colonization in their lungs decreased from 52% with regular chemotherapy to 6% when the inflammation inhibitor was added.
(Excerpt) Read more at medicalxpress.com ...
Doxorubicin was used against triple-negative breast cancer. It caused an increase in metastasis to occur in a number of mice. However, they found an option to do this without much issue, providing solid chemo outcomes without lingering metastasis concern.
The first was to add in C3a and C5a inhibitors, and these stopped the Doxorubicin from encouraging metastasis. Unfortunately, I couldn’t find quick information showing this class of medicine was approved for use, so it likely can’t help “immediately,” which is one of the things I look for with our “Take Charge” lists. I guess you could pass on the chemo or take it, knowing you have a definitely chance of metastasis, or consider an immunotherapy with surgery, with or without this form of chemo.
The other opportunity is what the study found, but also wasn’t stated in the write up. Cisplatin seems to have behaved somewhat similar to Doxorubicin before metastasis, but when applied after metastasis, it did far better at reducing the cancer load than Doxorubicin (“…cisplatin at the same setting significantly hindered both the metastatic load and incidence compared to either control or doxorubicin.”).
Again, I’m not a doctor, so do feel free to sanity check what I offer.
There is some hope with an inhibitor applied with Doxorubicin, and knowing a form of chemo helps trigger cancer spread, perhaps surgery, radiation, and/or immunotherapy could be emphasized.
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A timely article for me. We have a surgeon’s appt this afternoon for my ward (former sis in law who is mentally challenged) to see what kind of surgery for breast cancer in her left breast. Getting biopsy tomorrow on the other one because they have found something there also. She is almost 61 y.o. but mentally a naive teenager...sigh Prayers welcomed for MJ!
Get her on a very low carb diet, as cancer feeds on high blood sugar and is stimulated by insulin. This can help shrink the tumor.
Two red flags.
No information as to what the complement protein inhibitor is.
Animal model.
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