While our understanding and treatment of cancer has advanced significantly in recent years, most specialists would readily admit that the dynamics of tumor growth are poorly understood.

It’s easy to see why. Tumor growth is a multifaceted process  that involves complex interactions between many types of cells and their surrounding tissue.

So it’s interesting to see a multidisciplinary group of mathematicians, cell biologists, cancer specialists and chemists take on the task of modeling tumor growth and the effect that drug treatments have on it. Their results are startling, counterintuitive and frightening.
Such a model has to reproduce a number of important behaviors. For example, the availability of nutrients is the most important factor in tumor growth. When tumors reach 2 mm across, diffusion of oxygen and other nutrients is no longer enough to sustain them and so they enter a new phase in which they grow their own blood vessels to keep them nourished.

It is this that Peter Hinow at the University of Minnesota and buddies say they’ve captured in detail for the first time.

They also looked at the way in which drug treatments effect tumor growth. We know that endothelial cells that line blood vessels  play a dual role in tumor growth. On the one hand, blood vessels supply the tumour with the nutrients needed to help it grow. Many chemotherapy treatments target endothelial cells on the assumption that killing them will cut off the tumor’s lifeblood.

But on the other hand, blood vessels are also the channel along which cancer drugs must pass to reach the tumor.

So what is the effect of killing endothelial cells? That all depends on how they are applied, say Hinow and colleagues. Their frightening  conclusion is that, applied to the tumor in the right way, chemotherapy treatments can dramatically reduce the size of  a tumor.

But applied in the wrong way, without due consideration for the structure of the tumor, chemotherapy treatments can cut off the supply of cancer-fighting drugs to a tumor, causing it to grow.

So chemotherapy can end up making tumors bigger rather than smaller.

That’s a shocking and important result.

Ref: arxiv.org/abs/0810.1024: A Spatial Model of Tumor-Host Interaction: Application of Chemotherapy

The distinctive sensation of tannins on the tongue will be familiar (overfamiliar, perhaps?) to many arXivblog readers.

And if you’ve ever wondered what causes that mouth-puckering dryness, you now have an answer thanks to the dedicated and selfless work of Drazen Zanchi and colleagues at the Laboratoire de Physique Théorique et Hautes Energies in Paris.

Tannins are large molecules with aromatic rings and OH groups which naturally bind to each other and to proteins, while repelling water. So the presence of tannins causes proteins to aggregate together. From the biological point of view, that makes good sense. Tannins are part of plants’ defence systems against the proteins that bacteria, viruses and higher herbivores secrete when invading. It takes these proteins out of action be forcing them to aggrgegate together.

Zanchi says exactly this process is responsible for the mouthfeel of tannins. Tannins bind to salivary proteins in the mouth making them aggregate and this causes a rapid and immediate drop in the viscosity of saliva. That’s why your mouth feels dry as you gulp sip your favourite oak-matured cab before after work every day.

Obviously, the strength of this effect and the size of the aggregates that form determine the mouthfeel of the wine.

So feel free to raise a glass to Zanchi and his pals next time you get a chance (which shouldn’t be too long now). Not least because this effect may turn out to have other uses.

The team say that attaching tannins to a surface could force proteins to aggregate at that site. Sounds handy. And they’re convinced they have only scratched the surface of a rich, untapped and largely undiscovered chemistry of tannin behaviour.

Ref: http://arxiv.org/abs/0810.1136: Colloidal Stability of Tannins: Astringency, Wine Tasting and Beyond