Myxoma virus is a decidedly nasty customer, particularly if you’re a rabbit. Or, it turns out, a human melanoma cell.

However, recent studies have shown the virus is not known to infect human cells, raising the prospect of conscripting it in the battle against skin cancer.

That said, not everyone is going to be happy having a virus injected into them in order to treat their melanoma, particularly as viruses are known to mutate in unpredictable ways.

As such, a team at RMIT has used an advanced new technique to synthesise a key peptide from the myxoma virus that is responsible for its cancer killing clout, and have found this peptide can do its dirty work without harming healthy cells.

The team, led by Dr Taghrid Istivan, used a new technology designed by fellow RMIT researchers, Professor Irena Cosic and Dr Elena Pirogova, to design the peptide.

This technology, called the resonant recognition model (RRM), is used to design therapeutic peptides from scratch. It uses complex computer modelling to analyse protein structure and function effectively based on looking at the resonant frequencies of the peptide.

This enables the researchers to predict which amino acids will contribute to the protein function, and then to design a new peptide with just the components required to give the desired function.

This process is also a darn sight easier than producing the virus protein in other ways.

“A virus protein is big, expensive to synthesise and has inherent risks when used in medical treatments, because all viruses can mutate,” said Dr Istivan. “By synthesising a small peptide that mimics the action of a protein, we can offer a stable, safe, targeted and cost-effective alternative.”

The researchers tested the synthetic peptide on melanoma cells and found it had a dose-dependent toxic effect, as expected. They also found that it didn’t harm human cells.

It is hoped the peptide can be developed into a treatment for melanoma, which has proven a challenging cancer to treat.

“Currently the only effective treatment for early stage melanoma is surgery to cut out the tumour and healthy skin surrounding the affected mole,” said Dr Istivan.

The next step is to begin conducting clinical trials to determine how effective the peptide is in vivo and whether it has any undesirable side effects or can consistently batter down melanoma without resistance emerging.

“With further work, including clinical trials, we hope our research could lead to the development of a cream to painlessly and efficiently treat early stage melanoma.”

The researchers will be presenting their results at the 40th Congress of the International Society of Oncology and Biomarkers, in October in Jerusalem, and have published on their synthetic peptide in the Journal of Biomedical Science.

VIENNA (IMNG) - Combination therapy with a BRAF inhibitor and a MEK inhibitor extended progression-free survival by more than 3 months in patients with BRAF V600 mutated metastatic melanoma, early clinical findings suggest."This is the first kinase-kinase combination to show enhanced antitumor activity over the single agent," and the first to show that specific oncogenic toxicities may be reduced with combination therapy, said Dr. Georgina Long of the Melanoma Institute Australia in Sydney.In a phase... Read More

  1. * Corresponding Author:
    F. Stephen Hodi, Medical Oncology, Dana-Farber Cancer Inst., 450 Brookline Aveneue, Boston, MA, 02215, United States This email address is being protected from spambots. You need JavaScript enabled to view it.


Purpose: Selective BRAF inhibition (BRAFi) provides a paradigm shift for melanoma treatment. The duration of benefit is typically limited before resistance develops. Interest remains in combining targeted and immune therapies to overcome resistance and improve durability of clinical benefit. One mechanism of evading immune destruction is PD-L1 expression by tumors that results in potent anti-tumor immune suppression. Experimental Design: BRAFi resistant melanoma cells were examined for changes in PD-L1 expression by immunoblot and flow cytometry. Signaling pathways involved in altering PD-L1 expression were examined. Strategies to maximize the effect of the BRAFi therapy were studied including MEKi, MEKi combinations, and additional pathways including PI3K. Results: Melanoma cells resistant to BRAFi exhibit increased MAPK signaling and promotion of PD-L1 expression. PD-L1 expression is transcriptionally modulated by c-Jun and augmented by STAT3. MEK inhibition (MEKi) regains down regulation of MAPK signaling and suppresses the production of PD-L1. MEKi in melanoma cells demonstrates duel therapeutic effects with simultaneous suppression of PD-L1 expression and induction of apoptosis. By combining MEKi with BRAFi, an additive effect on the inhibition of PD-L1 expression results. Conclusions: We report a novel mechanism that suppresses pre-existing immune responses in melanoma patients receiving BRAFi therapy. BRAFi resistance leads to increased expression of PD-L1 in melanoma cells, mediated by c-Jun and STAT3. MEKi may be feasible to counteract BRAFi resistance of MAPK reactivation and also for the additive effect of PD-L1 suppression. Potential therapeutic benefits of combining targeted inhibitors and immune modulation to improve patient outcomes should be investigated.

  • Received August 20, 2012.
  • Revision received September 27, 2012.
  • Accepted October 18, 2012.

/PRNewswire/ -- Specialised Therapeutics Australia Pty Ltd today announced that abstracts for the upcoming Society for Melanoma Research meeting have been published online in the organization's official journal at

The publication includes an abstract reviewing results from a phase III metastatic melanoma study with ABRAXANE® (nanoparticle albumin-bound paclitaxel).

In the randomised, open-label, international study (CA033), ABRAXANE showed a statistically significant improvement in progression-free survival (PFS) in chemotherapy-naïve patients with metastatic melanoma compared to patients receiving dacarbazine chemotherapy (4.8 vs. 2.5 months, respectively (HR:0.792; 95.1% CI: 0.631, 0.992; P=0.044).
Read more here:

SATURDAY, Sept. 29 (HealthDay News) -- Researchers say they've discovered a two-drug combination that delays treatment resistance in patients with advanced melanoma.

By targeting different points in the same growth-factor pathway, the kinase inhibitor drugs dabrafenib and trametinib postponed the development of drug resistance in patients with BRAF-positive metastatic melanoma, the study authors said.

Melanoma is the most serious, and often deadly, form of skin cancer. In about half of patients with melanoma that has spread, tumor growth is caused by genetic mutations that keep the BRAF protein -- part of the MAPK cell growth pathway -- constantly activated. Drugs that inhibit BRAF activity can rapidly stop and reverse tumor growth in about 90 percent of patients. But the response is temporary in most cases, and tumor growth resumes in six or seven months, the researchers explained.

Previous research suggested that this drug resistance develops because the MAPK pathway gets turned back on through activation of MEK, another protein that is part off the MAPK pathway.

"We investigated this (drug) combination because of research we and others have conducted into the molecular underpinnings of resistance to BRAF inhibitor therapy," study lead author Dr. Keith Flaherty, of the Massachusetts General Hospital Cancer Center, said in a hospital news release.

The phase 1 and 2 study was sponsored by GlaxoSmithKline, which developed both drugs.

"We found that adding the MEK inhibitor trametinib to BRAF inhibitor dabrafenib clearly delays the emergence of resistance. In fact, the combination was at least twice as effective as BRAF inhibition alone," he said.


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