Method for better treatment of breast cancer 

diabetes, chronic wounds, magnetism, intestinal tumours, molecular scissors, disease, genetic, immune cells, drug development, Diabetes, Antibiotic, hydrogen generation, chronic obstructive pulmonary disease, malaria, photosynthesis, kidney failure, Brain tumours, mental health, blood cancer, cancer, dementia, cancer treatment, antibiotic resistance, blood vessel leakage, quantum simulations, atrial fibrillation, batteries, goiter treatment, terahertz radiation, organic materials , Guild of European Research Intensive Universities, gene copies, social anxiety, blue light screens, ‘Our hope is that these findings will make it possible to discover a way to selectively inhibit the TGF-beta signals that stimulate tumour development without knocking out the signals that inhibit tumour development, and that this can eventually be used in the fight against cancer,’ says Eleftheria Vasilaki, postdoctoral researcher at Ludwig Institute for Cancer Research at Uppsala University and lead author of the study. TGF-beta regulates cell growth and specialisation, in particular during foetal development. In the context of tumour development, TGF-beta has a complicated role. Initially, it inhibits tumour formation because it inhibits cell division and stimulates cell death. At a late stage of tumour development, however, TGF-beta stimulates proliferation and metastasis of tumour cells and thereby accelerates tumour formation. TGF-beta’s signalling mechanisms and role in tumour development have been studied at the Ludwig Institute for Cancer Research at Uppsala University for the past 30 years. Recent discoveries at the Institute, now published in the current study in Science Signaling, explain part of the mechanism by which TGF-beta switches from suppressing to enhancing tumour development. Uppsala researchers, in collaboration with a Japanese research team, discovered that TGF-beta along with the oncoprotein Ras, which is often activated in tumours, affects members of the p53 family. The p53 protein plays a key role in regulating tumour development and is often altered – mutated – in tumours. TGF-beta and Ras suppress the effect of mutated p53, thereby enhancing the effect of another member of the p53 family, namely delta-Np63, which in turn stimulates tumour development and metastasis.

A new study shows that a novel imaging-based method for defining appropriateness of breast cancer treatment is as accurate as the current standard-of-care and could reduce the need for invasive tissue sampling. The results suggest that the method might lead to more optimal treatment of individual patients.

Measuring the growth factor HER2 (human epidermal growth factor receptor type 2) is an important tool for deciding correct treatment in breast cancer. Treatments targeting HER2 are expensive but save the lives of many women. Targeted treatments have no effect if the metastases do not express HER2. The current diagnosis of elevated HER2 expression in metastatic cancer is based on examination of tissue samples obtained by surgery or needle biopsies from the liver, bones and other organs.

The aim of the current study, published in the Open-Access journal Theranostics, was to develop a simpler and non-invasive technique, based on whole-body PET/CT imaging, and compare the results of image analysis to the invasive measurements in the same patients. The study included 16 women with on-going treatment of metastatic breast cancer. Twelve had been diagnosed with a HER2-positive primary tumor and four were HER2-negative. All patients were scanned using combined PET/CT and a novel tracer molecule, ABY-025 Affibody, labeled with the short-lived radioactive isotope gallium-68.

The results showed that the amount of HER2-expression in the metastases was accurately measured with the new method. In addition, the amount of HER2-expression in the metastases was frequently found to be different from the primary tumor, leading to a change in therapy in several patients.

– The new method might substitute invasive tissue sampling in the near future. Our study resulted in two patients starting therapy and one patient ending therapy with HER2-targeting drugs says Jens Sörensen, PET-reseacher and adjunct professor at the Institution of Surgical Sciences, Uppsala University.

The research group now plans a larger study with more participating hospitals to confirm the results with the intention of making the new method more widely available to patients.

The study was conducted as an academic clinical trial with funding from The Swedish Cancer Foundation (Cancerfonden) and BRO, The Swedish National Organization of Breast Cancer Societies.

Reference: Measuring HER2-Receptor Expression In Metastatic Breast Cancer Using [68Ga]ABY-025 Affibody PET/CT, Theranostics 2016; 6(2):262-271. Doi:10.7150/thno.13502