Trauma and the localization of tumor cells

Fisher, Bernard; Fisher, Edwin R.; Feduska, Nicholas J.

doi:10.1002/1097-0142(1967)20:1<23::aid-cncr2820200103>3.0.co;2-p

Cited by 146 publications

(49 citation statements)

References 14 publications

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“…If so, the high initial incidence, and greater extent of spread of LMC1 after combined treatment might be accounted for by a failure of surveillance. If, however, rejection responses to this kind of tumour do not occur (Hewitt, 1976) other explanations for the effect of CP must be sought; for example, greater lodgement of metastatic cells in tissues which have been subjected to non-specific trauma (Fisher, Fisher and Feduska, 1967).…”

Section: Discussionmentioning

confidence: 99%

Metastasis of a transplantable mammary tumour in rats treated with cyclophosphamide and/or irradiation

Moore¹,

Dixon²

1977

Br J Cancer

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Summary.-We report observations on the spread by metastasis and infiltration of a transplantable tumour in rats treated by 6OCo y-irradiation of the primary, irradiation plus parenteral cyclophosphamide, or parenteral cyclophosphamide alone. The proportion of animals with overt disseminated disease and the extent of spread were measured with respect to the time elapsed after implantation and treatment of the primary tumour. The incidence of metastatic disease was broadly similar for all treatment groups, but the extent of dissemination was greater in rats whose treatment included cyclophosphamide.

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Section: Discussionmentioning

confidence: 99%

Metastasis of a transplantable mammary tumour in rats treated with cyclophosphamide and/or irradiation

Moore¹,

Dixon²

1977

Br J Cancer

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“…In the second series (Table II) (Fisher et al, 1967), hepatic trauma (Fisher & Fisher, 1965), and splenic trauma (Alexander & Altemeier, 1964) to enhance development of metastases in these organs from bloodborne tumour cells. The normal colon and ileum are refractory to growth of bloodborne tumour cells used in this study (Murphy et al, 1986) and the colon and ileum are clinically very rare sites for secondary deposits from tumours elsewhere in the body.…”

Section: Resultsmentioning

confidence: 99%

“…Fisher et al (1967) showed that trauma to a hind limb increased the trapping of arterially injected tumour cells by 1.9-3 times for mechanical trauma, 3.6-9.8 times for chemical trauma and 1.6-2.5 times for surgical incision and suture. The figures of Fisher et al (1967) for increased cell trapping after surgery agree well with the present study where cell trapping was increased by 1.5-1.6 times in the 1.5 cm of colon bearing the anastomosis, compared to an equal length of normal colon. However, a cell arriving at the anastomosis stands a 1:43 chance of forming a deposit whereas for a cell arriving in normal colon the chance is less than 1:4 x 104.…”

Section: Resultsmentioning

confidence: 99%

Preferential growth of bloodborne cancer cells in colonic anastomoses

Skipper

Jeffrey²,

Cooper³

et al. 1988

Br J Cancer

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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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“…On the contrary, several experimental studies have shown that rejection of thyroid-parathyroid grafts does occur. [8][9][10] Parathyroid grafting during immunosuppression has not previously been attempted in man. Our patient was receiving immunosuppressive drugs after renal transplantation.…”

Section: Discussionmentioning

confidence: 99%

Survival of a Homologous Parathyroid Implant in an Immunosuppressed Patient

Groth¹,

Hammond²,

Iwatsuki³

et al. 1973

The Lancet

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SummaryA patient who had undergone subtotal parathyroidectomy while on chronic haemodialysis became severely hypocalcaemic after receiving a well-functioning cadaveric renal graft. After a homologous parathyroid implant, there was a biochemical improvement in the patient, and at biopsy 6 months later the parathyroid graft was histologically normal. 21 months after the implant, serum calcium and phosphorus remain normal without calcium supplementation.

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Trauma and the localization of tumor cells

Cited by 146 publications

References 14 publications

Metastasis of a transplantable mammary tumour in rats treated with cyclophosphamide and/or irradiation

Metastasis of a transplantable mammary tumour in rats treated with cyclophosphamide and/or irradiation

Preferential growth of bloodborne cancer cells in colonic anastomoses

Survival of a Homologous Parathyroid Implant in an Immunosuppressed Patient

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