Local Recurrence and Metastasis of Excised Breast Carcinoma in the Rat

Dixon, B.; Speakman, H.

doi:10.1177/014107687907200806

Cited by 6 publications

(9 citation statements)

References 19 publications

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“…Although a metachronous cascade process is also implicated in implanted LMC tumors in rats (Dixon and Bagnall, 1986), the fact that in this case "there was also significant incidence of rats with positive regional nodes with no metastases in local nodes," at first sight, casts doubts on the validity of the cascade mechanism. However, it is difficult to critically assess these latter observations because lymph-node involvement was apparently determined by gross inspection only (Dixon and Speakman, 1979), which raises the possibility of false-positive reports. This is reinforced by the present observations of grossly enlarged, hyperplastic lymph nodes which did not contain detectable cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Lymphogenous and hematogenous metastasis of Lewis lung carcinoma in the mouse

Weiss

Ward

1987

Intl Journal of Cancer

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Quantitative and temporal comparisons were made between lymphogenous and hematogenous metastasis in the non-immunogenic model system of mice bearing transplanted 3LL tumors in their hind feet. The experimental evidence indicates that cancer cells disseminate from clinically detectable primary cancers by non-exclusive routes in the blood-stream and in the lymphatics. Following a delay of approximately 2 weeks after injection of 3LL cancer cells into the foot, local lymph-node micrometastases occur, together with the first appearance of overt hematogenous metastases in the lungs. The anatomic extent of lymph-node involvement, determined by bioassays of orthotopic grafts, of ipsilateral popliteal, inguinal and lumbar nodes, provides an accurate indicator of hematogenous metastasis, even though lymphogenous and hematogenous metastasis are operationally independent in this tumor/host system.

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Section: Discussionmentioning

confidence: 99%

Lymphogenous and hematogenous metastasis of Lewis lung carcinoma in the mouse

Weiss

Ward

1987

Intl Journal of Cancer

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“…When transplanted subcutaneously, in the form of a tumour pellet enclosed within a capsule of everted gut [26], it metastasizes after about 10 days to inguinal and axillary lymph nodes and as few as 100, otherwise occult metastatic cells, may be detected in the nodes by their transplantation to fresh isogenic hosts [34]. In rats with 8-10 mm diameter 'primary' turnouts, about 50 70 per cent of animals have widespread but occult lymphatic metastases in local, regional and distant nodes which may be detected by their growth in situ after curative local irradiation and or excision of the subcutaneous tumour [9,10]. These metastases have the same cellular and macroscopic growth characteristics as the untreated primary tumour [3,10].…”

Section: Introductionmentioning

confidence: 99%

The pattern and timing of lymphatic metastasis of the rat carcinoma LMC1

Dixon¹,

Bagnall²

1986

Clin Exp Metast

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The distribution pattern and latency of lymphatic metastases naturally disseminated by the Leeds Mammary Carcinoma (LMC1) when transplanted subcutaneously in isogeneic Johns' Strain Wistar rats has been determined. After the curative local irradiation and excision of the primary tumour in 210 rats, 55 +/- 3 per cent developed either local (26 +/- 3 per cent), and/or regional (28 +/- 3 per cent) and/or distant (37 +/- 3 per cent) lymph node metastases. Analysis of their pattern of distribution suggests that metastasis to local (inguinal and lumbar) and distant (axillary and mediastinal) nodes results mainly from the radial dissemination, trapping and nodal proliferation of cells released by the primary tumour. Although direct metastasis to the para-aortic node may have occurred, in the main seeding of this site and thence to other, regional, i.e. iliac and/or adrenal nodes, resulted from the dissemination of tumour cells from the local nodes. The latency of metastases appearing at different sites after primary tumour ablation, although highly variable, was site dependent and for local, regional and distant nodes was 30 +/- 14, 48 +/- 16, 56 +/- 17 days respectively. In addition, the latency of metastases at regional and distant nodes was directly correlated with the latency of local metastases. The latency of adrenal and iliac metastases also correlated with para-aortic node metastasis, as did mediastinal with axillary lymph node metastasis. From the data, a semi-quantitative model of lymphatic metastasis has been developed for further evaluation and adjuvant chemotherapy testing.

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“…Lymph nodes in situ Rats were implanted, randomized, and their growing primary tumours excised (Dixon & Speakman, 1979) up to 26 days later. After surgery, all animals were scored for up to 100 days to record the incidence of ipse-lateral inguinal, axillary and para-aortic lymph node metastases.…”

Section: Animalsmentioning

confidence: 99%

“…After surgery, all animals were scored for up to 100 days to record the incidence of ipse-lateral inguinal, axillary and para-aortic lymph node metastases. Although metastases may also occur at other sites (Moore & Dixon, 1979b;Dixon & Speakman, 1979), positive inguinal, axillary and para-aortic nodes, develop earlier and adrenal and iliac lymph node metastases do not occur without seeding of the para-aortic node (Dixon & Bagnall, 1986).…”

Section: Animalsmentioning

confidence: 99%

The lymphnodal clonogenicity and kinetics of metastatic cells disseminated by a transplanted rat carcinoma

Dixon¹,

Bagnall²,

Speakman³

1986

Br J Cancer

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In contrast to the wealth of data on the cellular transplantation of experimental tumours there are few concerning the further seeding of cells that may be released once tumour growth is established in situ. In particular, the lack of an in vivo clonogenic assay for spontaneous metastatic cells has limited therapeutic studies of this aspect of the cancer problem to the experimental use of clinical endpoints, e.g. prolonged survival or increased survival rates (Van de Velde et al., 1977;De Ruiter et al., 1982;Wondergem et al., 1985). In the 1950s methods for assaying the clonogenicity and transplantation kinetics of primary tumour cells were developed (Hewitt, 1958;Berry & Andrews, 1961) and this produced rapid progress in quantifying the principal factors governing the clinical outcome of primary tumour therapy (Steel, 1977). A similar development in experimental tumour metastasis could be just as important, e.g. in defining the basic principles of adjuvant treatment of patients at significant risk from occult metastases (Salmon, 1977).As indicated by Porter et al. (1973), a limiting dilution (TD50) assay would be helpful in the study of tumour metastasis but, presumably due to the previous lack of a suitable animal model (Carr & Carr, 1981;Fidler & Hart, 1982;Kim, 1984;Vandenris et al., 1985) . More importantly the method adopted was similar to a dilution assay but to avoid the need to isolate metastatic cells from a node, their numbers were assayed by determining the latency of the tumour it formed after transplantation to a fresh host. From the latency and incidence of tumour positive nodes, it is also possible to derive a TD50 curve for metastatic cells and thus provide the basis of an in situ cell survival assay after therapy (Speakman, 1986). In this paper we present and discuss our data on the lymphnodal clonogenicity of untreated metastatic cells. All the data were derived from only a few LMC1 generations using liquid-N2 stored material and no changes in tumour transplantability or growth characteristics were observed. Three types of experiment were performed. The first to determine the TD50 of LMC1 cells derived directly from the primary tumour. The second involved the transfer of axillary, inguinal and para-aortic lymph nodes from tumour-bearing to fresh hosts to determine from the incidence and latency of tumours formed the TD50 of transplanted metastatic cells. In the third, the subcutaneous primary tumour was excised at various times after its implantation, leaving the nodes to form overt metastases and thus determine their incidence and latency in the primary host.

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Local Recurrence and Metastasis of Excised Breast Carcinoma in the Rat

Cited by 6 publications

References 19 publications

Lymphogenous and hematogenous metastasis of Lewis lung carcinoma in the mouse

Lymphogenous and hematogenous metastasis of Lewis lung carcinoma in the mouse

The pattern and timing of lymphatic metastasis of the rat carcinoma LMC1

The lymphnodal clonogenicity and kinetics of metastatic cells disseminated by a transplanted rat carcinoma

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