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Wellcome Trust Research Round-up: 18.05.15

18 May, 2015

Our fortnightly round-up of news from the Wellcome Trust Community

Two new targets for cancer treatment

B0004178 Illustration of a cell in telophaseTwo studies published in the Journal of Cell Biology have identified potential new targets for the treatment of a wide range of cancers.

The research looks at advancing our understanding of cell division in normal cells, how this goes wrong in cancer, and how this may be targeted in a cancer-specific way.

Wellcome Trust-funded researchers found a role for two enzymes, Nek5 and Nek6, in the regulation of cell division. Nek5 functions to ensure an essential structure of cell division, the ‘scaffold’ upon which genetic material is separated, forms at the correct time. Nek6 is then able to recruit ‘chaperone proteins’ to this scaffold to ensure proteins are folded correctly. These chaperones also help to protect the cells from environmental stresses.

The enzymes are attractive targets for anti-cancer therapies – inhibiting chaperone proteins or preventing the scaffold from assembling correctly will disrupt cell division.

Professor Andrew Fry, from the University of Leicester, said: “Together, these two papers provide exciting new insights on how cells ensure that they faithfully pass on the right amount of genetic material to their offspring when they divide. They also highlight potential new targets for the development of novel cancer treatments.”

You can read the two papers here: (1) (2)

Targeting the root cause of asthma

C0015484 Asthma InhalerA potential new target for asthma therapy has been identified by researchers at the Wellcome Trust Sanger Institute.

A specialised type of immune cell, the innate lymphoid cell 2 (ILC2), is involved in the regeneration of lung tissue following damage caused by diseases such as influenza. However, if your body produces too many of these cells it can cause inflammation and, subsequently, asthma.

Researchers have found that the activity of a gene called BCL11B is required to mature newly-produced ILC2 cells and also regulates the number of these mature cells in your body.

Ensuring the levels of these ICL2 cells are high enough to help prevent influenza infection, but not so high that they can cause asthma is essential. Therefore researchers are hopeful that the manipulation of the activity of this BCL11B gene could offer a potential for target for therapy.

“Before now, asthma treatment has focussed on treating symptoms,” says Professor Gordon Dougan, a senior author and group leader at the Wellcome Trust Sanger Institute. “Now that we have joined the dots between the development of ILC2 cells and the expression of BCL11B, we can begin looking for drug targets that will tackle asthma’s root cause.”

This research is published in the Journal of Experimental Medicine.

Immune response silenced by Hepatitis B virus

B0009950 Hepatitis B virus (HBV) particle, illustrationThe body’s immune cells are left starved of essential nutrients by Hepatitis B infection, leaving them unable to control the disease, a new Wellcome Trust-funded study has found.

Although the adult immune system is usually able to control acute hepatitis B infection within a year, chronic infection lasts throughout life and causes liver damage and cancer. By controlling suppressor cells in the liver the virus can silence immune responses by starving cells of their essential ‘food source’.

Current hepatitis treatments are rarely effective at clearing the disease and although a vaccine does exist, it does not work after infection. Researchers are therefore hoping that by understanding the mechanism by which the virus is able to control the immune system, they may be one step closer to finding a suitable therapy.

Wellcome Trust Senior Investigator Professor Mala Maini said: “If we could boost the immune system and counteract the liver’s suppressive effect, then the infection could potentially be cleared after a large ‘burst’ of immune activity. This might cause short-term damage to the liver, but would prevent the long-term damage from scarring and liver cancers that we see in chronic patients.”

The research, published in Nature Medicine, may also offer an insight into controlling harmful immune responses following organ transplantation.

Spread of drug resistant typhoid

5279772517_d5b81fba0e_zThe global spread of antibiotic resistant typhoid is driven by a single family of typhoid bacteria, according to a new large scale genomics study.

In research led by the Wellcome Trust Sanger Institute, scientists collected data from more than 24 countries to create one of the most comprehensive data sets for a single infectious agent.

This data is an essential step in developing global surveillance of this public health threat. The results showed that this new family of bacteria, H58 Typhi, is displacing other typhoid strains and subsequently completely altering the genetic landscape of the disease.

Resistant to most front line drugs, H58 Typhi is continuing to evolve and acquire mutations as it spreads. These new mutated genes, which give the typhoid bacteria their resistance to new antibiotics, are becoming stable parts of the H58 genome and therefore creating a multi-drug resistant pathogen.

“H58 is an example of an emerging multiple drug resistant pathogen which is rapidly spreading around the world,” says Professor Gordon Dougan, senior author from the Sanger Institute. “In this study we have been able to provide a framework for future surveillance of this bacterium, which will enable us to understand how antimicrobial resistance emerges and spreads intercontinentally, with the aim to facilitate prevention and control of typhoid through the use of effective antimicrobials, introduction of vaccines, and water and sanitation programmes.”

This study is published in Nature Genetics.

Other Wellcome Trust-funded research news

Researchers have identified a crucial pathway involved in the suppression of immune attacks on our own tissues. The study, published in Immunity, highlights the role of regulatory T cells in preventing damage and suggests that this pathway could be targeted to promote suppression of inflammation in human diseases such as inflammatory bowel disease

In other news…

Congratulations to Professor Lalita Ramakrishnan who has been elected to the US National Academy of Science. A Wellcome Trust Principal Research Fellow, Lalita works on the pathogenesis of tuberculosis and identifying potential therapeutic targets.

The Royal Society and the Academy of Medical Sciences have recently elected their newest Fellows and 19 members of the Wellcome Trust community have been honoured.  Those elected work across the breadth of the biomedical sciences and the Fellowships recognise their contribution to society through the advancement of research. You can see the full list of new Fellows on the Royal Society and Academy of Medical Sciences website.

Image credits: (from top to bottom) Illustration of cell in telophase, Benedict Campbell, Wellcome Images; Asthma inhaler, Wellcome Library; Hepatitis B virus particle illustration, Pete Jeffs, Wellcome Images; Typhoid bacteria by Sanofi Pasteur via Flickr, CC-BY-NC-ND

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