Dear Mr. Rob578

Thanks for alerting us to another potential treatment for melanoma. This one was discover at Michigan State University as part of an NIH funded research project. After independent confirmation it will need alot of further research to bring it to the point of clinical trials with humans. That can be a while. The time for Anti-PD1 to get to clinical trials was at least 10 years. I am sure that Michigan State University has one or more patents on it already. Therefore it will not fit into the usual  theory of "BIG PHARMA" failing to fund further research because there is no potential for BIG profit. If you have actual information otherwise or can give reasons to believe the development of this potential treatment has been blocked please let us know. Perhaps you should contact Dr. Neubig and ask him. Please remember that sometimes university PR departments like to "hype" the research being done to promote themselves.

Meanwhile back at MPIP, we will have to carry on with the people and the treatments that we have now. Melanoma is not a theory nor a conspiracy. It is reality. That is what we should pay attention to, really.

Dear Mr. Rob578: These articles are some of the 29 from Pubmed that I referenced for you on a previous thread. They are studies of melanoma cells in a test tube. Interesting, but far from proof of effect in real people with melanoma. If you follow the links that Bubbles provided you (more than once) – you can find many more substances that are effective in a test tube, like extracts from seaweed and shrimp.   As a medical professional I must state that your perspective on the import of basic research needs further development. Please try to realize that persistence in this matter is a waste of time and energy. Unlike YouTube videos touting the benefits of baking soda for skin cancer, MRF and this forum are committed to providing relevant, scientific information to real people in real need of help.

There must be a flight of ducks about. I hear quacking.

Dear Jules

There is no connection between your melanoma , your thyroid levels and lymph nodes. If a lymph node is palpable(one that you can feel) in this setting spread by melanoma is a possiblity. However other causes are possible like post surgical inflammation, infection and other unrelated causes. The absense of palpable nodes is good but does not rule out spread to the lymph nodes that is not grown enough yet to be felt. That is the reason for a sentinel node biopsy. A sentinel node biopsy can be important because it gives information about the risk of progression and thus figures into treatment decisions. What node is the site for tumor spread varies from person to person and requires a study. It's hard but this is the time for gathering as much information as you can. Good Luck 

Exactlty

Dear Mr. Rob578:

You are right about the approach to the treatment of melanoma when you characterize it as "show me the clinical trials and hard evidence or move on." That is a good way to state the scientific approach to medicine. Without that criterion we would be reduced to voodoo and magical thinking. And yes, anyone can give valid opinions if they have the ability to understand the science and provide reproducible and verifiable data. You can have differences regarding what the data means, but you have to start with the data. Your claims, that your assertions in regard to propolis for instance, must be shown to be untrue or else accepted – has the cart before the horse. If you are claiming that propolis helps with melanoma then you have to show the evidence that it does. Evidence is not simply testimonials by those who believe it works. That can be a place to start, but it is not the place to end. To find out when and if a treatment works requires a well designed clinical trial, often more than one. That is very frustrating. It is especially tough for those on the raw end of the statistics. Still, many with melanoma are tougher. They have sacrificed money, suffered, and even given their lives to make possible the science needed to allow clinical trials that provide answers for themselves and others. To call into question the scientific approach is to insult them. I think you should keep that in mind. Finally, I want to commend you for recognizing the fact that the fellow melanoma victims on this forum are here for you as well. They are not seeking confrontation but support. Bees do have the right idea. You will attract more support with honey than with vinegar.

There are a number of issues to address Mr. Rob578:

1) There are only 29 articles in Pubmed that you can find with a search for melanoma and bee propolis in a data base that spans decades. None of the articles is more than a report of bee propolis on cells in a dish except for one on cytokine levels in mice. There is no data relating melanoma to the use of bee propolis in the treatment of melanoma in humans. I believe one would be hard pressed to bet one's life on this data. This is not a personal attack on you. It is a characterization of the data. 

2) To that point, your vituperative and personally abusive response to anything not entirely positive about the information you post is destructive and self defeating. It also detracts from the function of this forum. These are people with real problems seeking real solutions. This forum can be incredibly supportive. However I don't think it will tolerate your temper tantrums. 

Here is a link to the full article:http://stm.sciencemag.org/content/10/426/eaan4488.full

and here is the text of the discussion{DISCUSSION

We have developed a practical strategy for immunotherapy of cancer. It takes advantage of the preexisting T cell immune repertoire within the tumor microenvironment. The combination of a TLR agonist and an activating antibody against OX40 amplifies these antitumor T cells and induces their action throughout the body against tumor at nontreated sites. This in situ vaccination does not require knowledge of the tumor antigens. Potential drawbacks include reliance on adequate immune infiltrates and the availability of a suitable injectable site of tumor.

After screening a series of immune activators and checkpoint antibodies, we identified the combination of CpG oligodeoxynucleotide (TLR9 ligand) and anti-OX40 antibody to be the most potent form of in situ vaccination in multiple mouse models. TLR7/8 agonists could substitute for CpG, but checkpoint antibodies against PD1, PDL1, or CTLA4 could not substitute for anti-OX40.

The synergistic therapeutic effect between locally injected CpG and anti-OX40 antibodies is explained by the fact that CpG induced the expression of the OX40 target on CD4+ T cells in the tumor microenvironment. CpG also induced OX40 in CD4+ T cells in the tumor microenvironment of human lymphoma tumors, and therefore, our results are likely to translate to human cancer.

It has been reported that local intratumoral administration of CpG together with systemic antibody against IL-10R leads to rejection of the injected tumor and distant metastases (17, 18). This combination was shown to deflect M2 to M1 macrophages in the tumor microenvironment (19). Therefore, we examined the requirement for induction of OX40 expression on CD4 T cells by CpG in our system. We found that it was dependent on cytokines secreted by myeloid cells, including IL-12, IFN-γ, or TNF-α but not IL-2, IL-4, IL-10, and GM-CSF.

The therapeutic effect at the distant sites was specific for antigens expressed by the tumor at the injected site that were shared with the tumor cells at the distant sites. This result not only established the tumor specificity of the immunization but also proved that it was the local effect of the injected agents in the tumor microenvironment rather than their systemic delivery that triggered the systemic antitumor immune response.

Autoimmune toxicities are a common complication of systemically administered immune checkpoint antibodies (20–24). In contrast, direct injection of the antibodies into the tumor at very low doses can avoid these side effects (25, 26). In our experiments, in situ injection of microgram quantities of immune stimulants and checkpoint antibodies proved to be sufficient to induce the required local immune modulation, resulting in a systemic antitumor immune response.

A major challenge in tumor immunotherapy lies in breaking tumor immune tolerance. In a previous report, we showed that depletion of tumor-specific Tregs by the addition of anti-CTLA4 antibody was associated with enhanced antitumor efficacy (27). However, we find here that activating antibody against OX40 is sufficient. It is known that OX40 is expressed on both Tregs and Teffs in the tumor microenvironment, and as we now realize, OX40 can be further induced on CD4+ T cells in response to CpG. Modulating both Teffs and Tregs is essential to obtain therapeutic effect (28–30). Antibodies to OX40 costimulate Teffs (31–37), and they also inhibit the function of Tregs (12, 27, 38–40).

Having demonstrated the potent therapeutic efficacy of in situ immunotherapy in several different transplanted tumor types, we assessed this form of therapy in a spontaneous arising tumor. The MMTV-PyMT mouse model recapitulates several of the characteristics of virulent human breast cancer, among them showing histology similarity, having loss of estrogen and progesterone receptors, and overexpressing ErbB2/Neu and cyclin D1 (6, 41, 42). Although the tumors within a mouse arise independently in different mammary glands, they all share the expression of the PyMT antigen (43). Injection of CpG and anti-OX40 antibody into the first tumor to occur in each mouse resulted in reduced tumor load in the other mammary fat pads and prevented lung metastases. These results demonstrate the potency of the in situ vaccine maneuver in a situation of spontaneous cancer-driven by a strong oncogene, suggesting the possibility of a direct application to human cancer. By analogy to the genetically prone mice, we can imagine administering an in situ vaccine at the site of the primary tumor before surgery in patients at high risk for the occurrence of metastatic disease and/or in patients genetically prone to develop second primary cancers, such as those with inherited mutation in the BRCA genes.

The CpG used here, SD-101, is currently being tested in patients as a single agent and in combination with other therapeutic modalities (NCT02927964, NCT02266147, NCT01745354, NCT02254772, and NCT02521870). Anti-OX40 antibody is also currently being studied in phase 1 clinical trials (NCT02559024, NCT01644968, NCT02221960, NCT02318394, NCT02274155, NCT01862900, NCT01303705, and NCT02205333). The results from our current preclinical studies provide strong rationale for combining CpG with agonistic anti-OX40 antibodies in a therapeutic format of in situ vaccination in patients with lymphoma and solid tumors. As we have shown, CpG and anti-OX40 antibodies work locally at very low doses that should provide the advantage of avoiding toxicities that occur with their systemic administration.

Good results in mice (a total of 90). Nice proof of concept. A while to go before humans can get it.Maybe a little premature pr work.

Just for the record John Beard's theories of cancer being caused by pancreatic enzymes have no basis in reality and are ,in fact, the framework upon which many "cancer treatment " scams are based.We need real science for real people with real cancer.

Just for the record John Beard's theories of cancer being caused by pancreatic enzymes have no basis in reality and are ,in fact, the framework upon which many "cancer treatment " scams are based.We need real science for real people with real cancer.

Just for the record John Beard's theories of cancer being caused by pancreatic enzymes have no basis in reality and are ,in fact, the framework upon which many "cancer treatment " scams are based.We need real science for real people with real cancer.

Charlie 

Just for you information the data about interferon and ulceration is from 2009. Here is a report from 2012.

Long-term results of the randomized phase III trial EORTC 18991 of adjuvant therapy with pegylated interferon alfa-2b versus observation in resected stage III melanoma.