Cells exfoliated from colorectal cancers may only be implicated in local recurrence if they are proven to be viable and capable of growth. Thirty patients with primary colorectal cancer were studied. Cells were obtained from primary tumour, uninvolved mucosa, mesorectum, lumen of the bowel, luminal mucus, serosal surface of the bowel and from washings of the tumour bed after dissection. Colonies grew in vitro in monolayer culture from 21/30 primary tumours; 11/41 mesorectum specimens; 11/27 luminal washings; 14/29 luminal mucus specimens; 1/27 serosal surface washings and 3/13 post-dissection washes. Colonies stained positively for the epithelial markers cytokeratin and desmosomes and also for carcinoembryonic antigen. Cells capable of in vitro growth are present in these various sites and, if spilled at operation, may well be implicated as one of the factors leading to local recurrence.

In the past, it has been noted that experimental tumour cells inoculated into the peritoneal cavity or into the lumen of the bowel will grow at a recently formed colonic anastomosis. However, it has previously been unclear whether the healing process enhances tumour growth or whether the presence of a suture line merely allows the tumour cells to gain access to the tissues. In the present study, using the hooded Lister rat, we have confirmed these findings by showing that growth of the syngeneic MC28 sarcoma and OES5 breast carcinoma occurs preferentially at colonic anastomoses and laparotomy wounds after intraperitoneal injection, and at colonic anastomoses after intraluminal injection. In previous studies using the MC28 sarcoma and the OES5 breast carcinoma injected by the intracardiac route (so that tumour cells reach normal and healing tissues in approximately equal numbers) we have shown that tumour growth is enhanced in healing wounds but not in the surrounding normal tissues when cells reach a healing colonic anastomosis or laparotomy wound within 2 h of its formation. Furthermore, by studying the distribution of radiolabelled tumour cells after intracardiac injection, we have calculated that the probability of a tumour cell leading to a deposit in a healing anastomosis or laparotomy wound is increased 1,000 fold compared to normal tissue. No previous studies have combined the data for intracardiac, intraluminal and intraperitoneal injection of tumour cells using the same animal model. We conclude that the same phenomenon of tumour growth enhancement in colonic anastomoses and laparotomy wounds reported after intracardiac injection of tumour cells may well be enhancing tumour growth after intraperitoneal and intraluminal injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Caffeine and taurine are two major neuromodulators present in large quantities in many popular energy drinks. We investigated their effects on sleep-wake control in constant darkness using the fruit fly Drosophila as a model system. It has been shown that caffeine, as the most widely used psychostimulant, can boost arousal through the dopamine pathway in the mushroom bodies of flies. Taurine is a GABA receptor agonist, which is inhibitory to neuronal firing. We show here that flies receiving a low dose of caffeine (0.01%) increase locomotor activity by 25%, and decrease total sleep by 15%. Treatment with taurine at 0.1% to 1.5% reduces locomotor activity by 28% to 86%, and shifts it from diurnal to nocturnal. At 0.75%, taurine also increases total sleep by 50%. Our results show that taurine increases sleep, while caffeine, as previously reported, attenuates sleep. Flies treated with both caffeine and taurine exhibit two differential effects which depend upon the ratio of taurine to caffeine. A high taurine:caffeine ratio promotes sleep, while a low ratio of taurine:caffeine inhibits sleep to a greater extent than the equivalent amount of caffeine alone. This intriguing enhancement of caffeine action by low doses of taurine may account for the presence of both compounds in energy-promoting drinks such as Red Bull® and Monster®.

Summary Intracardiac injection, in hooded Lister rats, of syngeneic MC28 sarcoma cells never induced tumour growth in normal bowel. Tumour growth occurred at the site of a colonic anastomosis if surgery preceded tumour injection but not if it followed tumour injection, even by as little as 1h. Maximum enhancement of tumour growth occurred when the healing process had progressed between 2 and 8 days, with a peak at 5 to 7 days. The enhancing effect was largely over by the time the healing had progressed 14 days. The syngeneic OES5 breast carcinoma also grew at colonic anastomoses when surgery preceded tumour injection by 5 days, but not in normal colon. The MC28 sarcoma also grew at ileal anastomoses but not in the normal ileum after intracardiac injection. By injecting radiolabelled sarcoma cells, an estimate of the probability of a single bloodborne tumour cell lodging at a colonic anastomosis and leading to a tumour deposit was calculated to be of the order of 1:43 whereas the probability of the cell lodging in normal colon and causing a deposit is < 1:4 x 104.When cells from the transplantable syngeneic sarcoma and carcinoma used in this study are injected into the left ventricle of a rat, they distribute to all organs in proportion to the fraction of the cardiac output they receive (Murphy et al., 1986). However, some organs (e.g., adrenals and bone), commonly develop deposits, other organs (e.g., skin and lungs), occasionally develop deposits, whilst others (e.g., spleen and intestines), never develop deposits. This effect is reproducible with different tumours and appears to be a feature of the behaviour of the recipient tissue rather than the tumour (Murphy et al., 1986). The resistance of the colon to growth of these experimental tumours is paralleled by the clinical observation that the large bowel is a rare site for bloodborne secondary deposits from primary malignancies elsewhere in the body.Trauma to a tissue is known to enhance the ability of that tissue to support growth of tumour either from locally implanted cells (Jones & Rous, 1914), or from cells that reached the site of injury via the circulation (Robinson & Hoppe, 1962;Alexander & Altemeier, 1964;Fisher & Fisher, 1965).Following intracardiac injection of the two tumours used in this investigation, Murphy et al. (1988) found that growth occurred much more readily in healing laparotomy wounds than in the surrounding normal skeletal muscle. There have been no studies to investigate the effect of surgical trauma on the ability of the large bowel to support growth of tumour cells delivered by the circulation. The aims of this investigation were firstly to determine whether surgical trauma to the colon would enhance its ability to support growth of bloodborne cancer cells; and secondly, if enhancement did take place, to determine at which stage in the healing process the enhancement is at a maximum. experiments, and the OES5 breast carcinoma. MC28 is a methylcholanthrene-induced sarcoma and OES5 is an oestrogen-induced breast carcinoma (Senior et...

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