But until now
how the tumour cells affect and influence the surrounding tissue between dogs and humans has been unknown.
We are investigating
how tumour cells can disseminate from the primary tumour and remain alive but clinically undetectable for many years, and how they start expanding into life threatening cancers in some patients.
Not exact matches
Researchers at the University of Gothenburg are focusing on
how HAMLET can be taken up into
tumour cells.
This early stage research will explore
how the virus targets stem
cells and provide the starting point to develop new treatments that seek out the
tumour and spare the surrounding healthy brain tissue.
The Lund University research team has looked at
how cancer
cells communicate with surrounding
cells and
how this encourages the development of malignant
tumours.
How do the genetically diverse
cells in a
tumour interact, for example, and what is the role of the cellular environment that they inhabit?
But at the time, they thought it might take years to pinpoint the precise position of the gene, sequence it, and understand
how it causes mutations to accumulate in
tumour cells (This Week, 15 May).
Breast cancer researchers have mapped early genetic alterations in normal - looking
cells at various distances from primary
tumours to show
how changes along the lining of mammary ducts can lead to disease.
For the first time ever, we could make a really comprehensive comparison of individual normal and
tumour cells from the exact same type of tissue, taken at the same time, from the same person, and see
how the cancer had developed.»
To carry out the study, the team has analysed
how different carbohydrates act on the surface of silver nanoparticles (Ag - NP) of around 50 nanometres, which have been introduced into cultures of liver
cells and
tumour cells from the nervous system of mice.
So if biologists can discover
how to disable cancer
cells» DNA repair proteins, it may be possible to destroy
tumours using lower doses of radiation or drugs.
After testing if the
cells remained viable, or alive, after printing, the researchers examined
how the
cells proliferated,
how they expressed a specific set of proteins that help
tumours spread, and
how resistant the
cells were to anti-cancer drugs.
This bank of living
tumour cells allowed the team to study not only the genetics of the
cells, but also
how genetic mutations in the mitochondria — which drive energy production in the
cell — caused changes in the
cell's metabolism.
Putting together their analyses of the mitochondrial DNA in each
tumour cell line and the metabolic pathways at work, the team were able to deduce
how each
cell line's genetics directly affected its ability to multiply.
The researchers, working with
cell cultures, first observed
how individual
tumour cells kill specific
cells in the vascular wall, called endothelial
cells.
A key question in cancer research has been
how cancer
cells are able to survive once they break away from a
tumour to spread around the body.
«Our research focuses particularly on the activity of this gene and
how it relates to neuroblastoma,» says Professor Marie Arsenian - Henriksson at the Department of Microbiology,
Tumour and
Cell Biology, Karolinska Institutet.
We believe that each dog breed may correspond to one type of B - or T -
cell lymphoma and so studies within and between breeds gives us a unique possibility to understand
how the genetic background affects what type of
tumour develops, and
how its progression is regulated», says Ingegerd Elvers.
Dr Claus Jorgensen, who led the research at The Institute of Cancer Research, London, and at Cancer Research UK's Manchester Institute at the University of Manchester, said: «The next step is to figure out
how to keep this receptor switched on, so that the
tumour cells can't leave the blood vessels — stopping breast cancer spreading and making the disease easier to treat successfully.»
«It suggests to us that targeting the pathways used in regulating
cell fate decisions —
how stem
cells choose between
cell proliferation and differentiation — could be a more effective way of halting
tumours in their tracks and lead to potential new therapies.»
In this film Professor Sir Mike Stratton (director of the Wellcome Trust Sanger Institute) describes
how mutations in DNA can cause a
cell to grow out of control and develop into a cancerous
tumour.
We target
tumours by exploring
how the proteins found on the cancer
cell surface can be utilised to inhibit growth or kill
tumours.
Understanding the processes that restrain mutant
cells from developing into
tumours, and
how they are breached when cancers do form will guide the development of strategies to reduce the chance of cancer development in individuals who have acquired a high level of mutations.
«It tells you about the ecosystem of the
tumour», Simona says, «using fluorescent markers, we can label many specific
cell types and structures within the brain in the vicinity of the
tumour, and look not just at the
tumour cells but
how they interact with their surroundings.
Professor Dive's exhibit was designed to introduce visitors to the concept of circulating
tumour cells (CTCs) and
how liquid biopsies could hold the key for better diagnosis and treatment of lung cancer.
Here Steve tells us
how his interest in stem
cells led him into cancer research and
how he believes this angle of brain
tumour research has unique potential for tackling cancers which are currently difficult to treat.
Steve tells us
how his interest in stem
cells led him into cancer research, and the potential for breakthroughs in brain
tumour research and treatment.
Recent evidence indicates that non-cancerous support
cells within
tumours, referred to as the stroma are emerging as key sources of
tumour - promoting inflammation, but little is known
how or when in
tumour evolution these functions are acquired.
A better understanding of
how the immune system works to fight cancer and a detailed characterisation of the different immune
cells that infiltrate a particular patient's
tumour, would enable more efficient treatments.
Cancer
cells multiply quickly and in a way that is out of control; this is
how tumours are formed.
Kelley, lead investigator on the study published today in Nature Chemistry, explained
how her team has advanced a completely new approach using magnetic nanoparticles with DNA capture probes on their surface that can target circulating
tumour cells (CTCs) in blood samples to see if the
cells contains biomarkers associated with drug resistance.
Areas of focus include: understanding
how tumour - reactive T
cells and B
cells promote patient survival in cancer; defining the effects of standard treatments on tumor immunity; and using genomic approaches to identify novel
tumour mutations that can serve as target antigens for immunotherapy.
The first step is to understand
how a small fraction of the
tumour cells often escape therapy while becoming more malignant.
The same thing happens (the inhibition of stated growth factors) with hyperbaric oxygen therapy so it makes sense
how all this fits together in powerful synergy to increase metabolic stress on
tumour cells.
· Cancer Growth and Spread — Healing Angiogenesis and Metastasis, discussing blood vessel development and growth factors, dysregulation including hypoxia and other blood supply stress responses in cancer and other diseases and
how cancer
cells travel and invade — metastasis via the complex
tumour microenvironment — TME — comprised of immune
cells, cytokines, growth factors, reactive oxygen species (ROS) and cancer - associated fibroblast (CAF);
Lectures provided on: Canine and Feline Lymphoma, What's new in Oncology,
How to read a histopathology report; Canine mast
cell tumours and TKIs; Canine Hemangiosarcoma.