SATURN SPOTTING:

The planet Saturn is presently making one of its retrograde motions and passing from the constellation of Leo westward to the faint constellation of Cancer. It previously passed to Leo from cancer last fall in Sept and Oct.. Looking down the alley from her city location Molly cannot distinguish any of the stars of Cancer, but she can easily make out most of the stars of Leo and at least Castor, Pollux, Tejat and Alhena in Gemini (the constellation immediately to the west of Cancer). Saturn is about 15 degrees to the west of Algiebra(the second star in the "hook" of Leo, and a bit further towards the zenith than the bright star Regulus (the beginning of the "hook"). Viewing is a bit restricted because of the light of the first quarter Moon. Tonight, at about 11:00 pm Central Standard Time, Leo and Saturn are a bit to the east of due south. Orion has begun to advance towards the horizon in the southwest. Sirius, the brightest star in the sky, is almost due south.

For further information on the planet Saturn go to the Wikipedia article and the Nine Planets site. The two sites complement each other.

A little interesting Saturn factoid. The actual length of a Saturnian day is uncertain. The gaseous nature of the planet leaves no firm "handle" to measure the period of rotation. Astronomers have relied on radio measurements of the planet's magnetic field to make their estimates, but recent findings have shown that geyser activity on the small Saturnian moon Encaledus inhibits the rotation of the planet's magnetic field to a speed less than that of the actual rotation. The most recent measurements place Saturn's "day" as about 10 hours and 47 minutes. Interestingly enough comparative measurements have shown that this is about 6 to 8 minutes longer than the time Saturn took to rotate in the 1980s when the first measurements were taken.

Anyways, more on Saturn, Leo and the other constellations mentioned later.

Molly

Transmissible tumours:
The September 7th edition of Nature Magazine has an article under the News and Views section entitled 'Infectious Tumour Cells' (Vol 443, pp35-36). This article discusses the two types of cancer that are directly transferable from individual to individual under normal conditions. These are the canine transmissible venereal tumour (CTVT) and the devil facial tumour disease (DFTD) of Tasmanian Devils. I have read articles on the latter, but, like most veterinarians, I have been familiar with CTVT for much longer. So my memory lapse can perhaps be forgiven when I quoted to a client recently that CTVT was the only cancer known to be directly infectious "as a cancer". My stock of Tasmanian devil faces in memory is exactly zero, so the second fact easily slips my mind.
In any case the article presents the evidence that these tumours are in fact infectious clones of original tumour cells that arose in animals other than those infected rather than being malignant transformations of the cells of the present host animal. The evidence is much stronger in the case of CTVT. Murgis et al (Cell 126 ,477-487-2006) show that the tumours from dogs across 5 continents are closely related genetically and distinct from the genome of the host dog. They use a combination of techniques [dog leukocyte antigens (dla similar to the human hla), haplotyping (chromosome analysis), microsatellite DNA and mitochondrial DNA sequencing]. The various tumours, "had less genetic variability than that observed within even the most inbred breed of dog".
The evidence for the facial tumours of Tasmanian Devils is less robust. It consists merely of consistent patterns of chromosome abnormalities.
The authors of this review (David Dingli and Martin A. Novak) go on to discuss the limited ways in which tumours are transmitted directly in humans. These include mother to fetus transfer, interfetal transfer in multiple pregnancies and transmission via organ donation. Mercifully such events are quite rare. In the case of organ transplants the rate is 0.04% of solid organ transplants and 0.06% of haematopoietic stem cell transfers.
The reason why cancer generally is not transferable is graft rejection due to the MHC antigens that distinguish self from non-self. CTVT cells reduce their expression of MHCs (the DLA previously mentioned) and thereby avoid graft rejection on the part of killer T cells. They do not, however, totally inhibit the expression of such antigens as this would stimulate attack by the NK (natural killer cells), a less specific form of the cellular immune defenses.
The authors go on to say that this phenomenon is evidence of the theory that the MHC evolved mainly as a defense against tumours.