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Cutting Edge

Science and Religion News

 Dr Gregory Farrelly FAITH Magazine November-December 2013

Cancer Biology and Physics

Most adults will find that they know someone who has had a brush with cancer, sometimes tragically, although medical advances continue to be made. As a physics teacher, I teach the therapeutic effects of gamma radiation in radiotherapy, along with the associated dangers (radiation can cause cells to become cancerous as well as kill cells that are already cancerous), but a common misconception among students is that cancer cells are rather like viruses or bacteria, a sort of alien cell that has entered the body, growing out of control with little relation to the surrounding cells.

The July 2013 edition of Physics World (Vol 26, No.7) was devoted to cancer and the physics of cancer. A fascinating article by the polymath British theoretical physicist Professor Paul Davies considers the evolutionary characteristics of cancer cells. These cells, in the view of Davies and the Australian scientist Charles Lineweaver, show a sort of atavism, a reversion to an ancient evolutionary stage.

Most GCSE biology students will recall that mitosis is the type of cell division used for growth, repair and asexual reproduction, producing cells identical to the parent cell, whereas meiosis is the cell division used in sexual reproduction, containing genetic material from both mother and father cells and giving rise to genetic variation. Single-celled organisms reproduce by mitosis, whereas multi-cellular organisms reproduce by meiosis, using specialised sex cells, the germ line. Germline cells are labelled “immortal”: they have reproduced indefinitely since the beginning of life. The other (somatic) cells differentiate into brain cells, muscle cells, etc. These somatic cells die when damaged or after a certain time (ageing). This occursaccording to a sort of biochemical programme, for the overall good of the organism.

Cancer cells, in contrast, continue to live and multiply instead of dying when they should; they behave in a purely selfish way (I sometimes joke that this is rather like some students – a joke that is not always appreciated).
Once triggered, the “subroutine” of cancer results in a neoplasm (a group of new, cancerous cells) becoming mobile; this is metastasis, responsible for most deaths from cancer. The cells move via the bloodstream or the lymphatic system and the way they do so depends on their physical properties (described below). Primary cancer cells also prepare further biological sites chemically, something Davies regards as “a carefully orchestrated and pre-programmed strategy”.

Darwinian evolution suggests that cancer cells result from random mutations, surviving the attacks by the body’s antibodies, etc. However, if the cells are random mutations, why are they so adapted for survival and why do dormant cancers awaken? Also, why do cancer cells transplanted into healthy organs often not develop into tumours.

Once started, cancer cells show accelerated growth, mobility, spread and colonisation. The most malignant cells represent the most ancestral forms, a sort of reversal of the evolutionary arrow of time. For example, cancer cells tend to use glycolysis in the cell cytoplasm in their metabolism, an ancient system, whereas healthy cells use oxidation-phosphorylation. Glycolysis flourishes in low-oxygen conditions, characteristic of cancerous tumours and characteristic of conditions on the ancient Earth.

As differentiation continues, various genes are “switched off” but stem cells, even in adults, retain a certain pluripotency in order to produce fully differentiated cells lost by damage or ageing. Ancestral genetic imprints are evident in embryogenesis. For example, even fish and humans have proto-gills in the early stages; these cells have a very ancient genetic code. Embryonic cells are pluripotent, having the full genetic code enabling them to become any type of cell; they differentiate into particular cells in their later development. Davies and Lineweaver suggest that genes active in embryogenesis and switched off later may be reactivated because of damage, causing the accelerated cell division of these rogue cancer cells. In this view, the cancercells have the dynamic changeability of embryonic cells, being able to quickly adapt and undergo metastasis. The survival of these cancer cells is, then, a remnant of billions of years of evolution.

Elsewhere, Philip Ball, an English science writer, reports on research into the mechanical properties of cancer cells. An atomic force microscope has been used to examine the stiffness of cancer cells. There is evidence to suggest that cancer cells are softer than normal cells (although tumours are stiffer). And a histogram of stiffness showed that as tumours become “pre-malignant”, two peaks appear on the graph, rather than the single one observed for normal cells.

This could offer a technique to help in the prognosis of metastases, the spreading of cancer cells to other regions of the body, responsible for 90 per cent of deaths from cancer. Metastasis involves clumps of cancer cells becoming detached and moving through the blood stream or the lymphatic system to other areas, where they become attached to a new site and continue growing. It is too early to be certain, but the softness of cancer cells may be what enables them to pass through blood vessel walls, etc. If so, this could mark a cheap and effective diagnostic tool in cancer treatment.

Faith readers will be able to identify in this analysis some familiar themes: the interdependence of material reality within a coherent Unity-Law, a dynamic environment, purposive (not “random”) evolution and the “goodness” of life itself. Why is it that nature behaves as it does? Why do cells have “laws” of reproduction, development, growth and decay? As a Catholic scientist, I have to ask myself why there is science at all – why nature is not truly random, disordered, arbitrary, etc.

The answer? “In the beginning was the Word… All things were made through Him.” (John 1:1-3)

Faith Magazine

November - December 2013