In the first article in this series, we looked at how HMGB1 has taken an increasingly important position as a key mediator in the immune response, playing a major role in many diseases, from cancer to coronavirus. There is now significant evidence that HMGB1 is essential for SARS-COV-2 replication, as well as potentially being a therapeutic target in severe cases of COVID-19.1 In this article we examine how we can effectively measure HMGB1 accurately in serum and other samples and begin the journey from research to clinic.
Photodynamic Therapy (PDT) is being increasingly recognized as having potential for the treatment of tumors, especially dermatological. But using conventional manual methods of recording the metabolic processes that occur as a result of adding the photosensitizer to target cells has major limitations.
HMGB1 is a key mediator in the immune response and increased levels can be important indicators of disease. In this, the last in our series on HMGB1, we will look at the performance of the IBL HMGB1 ELISA Kit, which has been used to demonstrate the value of total HMGB1 as a clinical biomarker in a wide range of sample types and diseases. This kit is regarded by key opinion leaders as the gold standard in the field and has been used in more than 800 publications.
In the first article in this series, we looked at how HMGB1 has taken an increasingly important position as a key mediator in the immune response and as such plays a major role in a large number of diseases – from sepsis to cancer. As Professor Helena Erlandsson Harris, a pioneer in HMGB1 research, says, “I am convinced that the next step will be even better data to demonstrate the usefulness of HMGB1 as a prognostic/diagnostic biomarker. This has been hampered by the need to understand the isoforms that control different functions and also the methods for measuring HMGB1. It would be even better if HMGB1 detection were included in larger biomarker panels.” HMGB1 has indeed been included as a necessary biomarker in consensus guidelines for the detection of immunogenic cell death. The question is how to measure it. In this article, we will look at the development of increasingly sensitive, reliable and easy-to-use assays for clinical research and routine use and how this has been complicated by the need to resolve the isoforms, and also overcome interference caused by auto-antibodies and other proteins that naturally interact with HMGB1 to modulate its function.
As a nuclear protein present in most cell types, HMGB1 (high mobility group box 1) is a key mediator of the immune system in health and disease. Interest in HMGB1 has increased dramatically as the protein has been shown to be critical to the cell’s response to stress and plays a major role in many disease states, including infectious diseases, ischemia, immune disorders, neurodegenerative diseases, metabolic disorders, and, not least, cancer. Highly conserved in mammals, HMGB1 (also known as HMG-1 and amphoterin) is primarily located in the chromatin where it stabilizes chromosome structure and plays a key role in controlling gene expression.
We may well be on the threshold of a new hope for oncology. Shorthanded to ctDNA, circulating cell free tumor DNA is sloughed off from tumors. It can be detected in liquid biopsies of just a few milliliters of blood. This could revolutionize what oncology can achieve by diagnosing cancers earlier and more efficiently.
How can we improve upon the completely artificial situation that we have today for screening drugs? We spoke to Dr. Christopher Millan, Co-Founder and CTO of the up-and-coming company, CellSpring. Based in Zürich, Christopher Millan with his business partner, CEO Kramer Schmidt, are both Americans. We also asked Chris how two Americans end up establishing a biotech start-up company in Switzerland.
Next-generation sequencing (NGS) is poised to become a decisive tool in diagnostic, therapeutic, and prognostic applications in oncology. In the first part of this two-part series, we saw that sequencing tumor-derived DNA alone can risk incorrect diagnosis by misinterpreting somatic alterations as being tumor-specific. This pinpoints the need to sequence normal tissue in parallel to map out the somatic alterations already present in the patient, which clearly has implications for the future of NGS-based diagnosis and workflows in the clinical laboratory.
Massively parallel sequencing has rapidly become a must-have tool of the trade in molecular biology and drug discovery research. In recent years, the cost of next-generation sequencing (NGS) has declined exponentially, while throughput, accuracy, and read lengths have soared, and multiple regulatory-compliant sequencing technologies have achieved commercial success.
(Part 2 of 2. Read Part I). In 1948, Bill Koster of the Variety Club of New England and Dr. Sidney Farber working at the Children’s Hospital Boston had launched The Children's Cancer Research Fund, aimed at supporting a hospital dedicated to the research of childhood leukemia. But they needed a poster child to boost fundraising.
In his book, The Emperor of All Maladies, Siddhartha Mukherjee tells the story of one of the turning points in the history of cancer medicine. A turning point that he dates to May 1947. In this two-part article we will look at how cancer research has been transformed by fundraising.
(Part 3 of 3: Read Part 2)In the first part of this series, we introduced you to imatinib (Gleevec). This drug was originally launched in 2001 as a potent treatment for chronic myeloid leukemia (CML). It also proved to be effective against a number of other cancers. Here we look at possibilities for individualized treatment.
(Part 2 of 3: Read part 1) 'The so-called ‘War against Cancer’ started with US President Richard Nixon’s National Cancer Act of 1971. It turned out to be many battles on many fronts as cancer was confirmed to be not one but a myriad of diseases. Not only that, but each cancer cell in a given patient has a different genetic make-up.
In 1996, Dr. Charles Sawyers at Memorial Sloan Kettering Cancer Center, USA, became involved in the initial testing of a drug for the treatment of chronic myeloid leukemia (CML). The drug, imatinib (later to be launched as Gleevec), could be taken once a day with few side effects and had a dramatic clinical result. Even patients in advanced stages of the disease, reliant on oxygen and with only a few weeks to live, became symptom-free almost immediately. The trouble was, those same patients quickly developed a resistance to the drug and suffered a relapse.