Enhancement by drugs of metastatic lung nodule formation after intravenous tumour cell injection

Putten, L.M. van; Kram, L. K. J.; Dierendonck, H. H. C. Van; Smink, T.; Füzy, M.

doi:10.1002/ijc.2910150408

Cited by 95 publications

(46 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Three cytotoxic agents were investigated for their ability to enhance lung colony formation by the Lewis lung tumour: cyclophosphamide (CY) (the agent that in the hands of van Putten et al (1975) gave the greatest enhancement with the C22LR osteosarcoma) local thoracic or whole-body irradiation (found by Brown (1973) to enhance colony formation by the KHT sarcoma) and bleomycin (because of its tendency to enhance radiation-induced lung damage). The experiments were designed to measure the "enhancement factor" due to pretreatment of the recipient mice (i.e.…”

Section: Resultsmentioning

confidence: 99%

“…injected cells has been used as a method of assaying the clonogenic capacity of cells removed from treated murine tumours. This approach was first described by Hill and Bush (1969) using the KHT sarcoma, and since that time it has been applied to a number of other mouse tumouirs including the C22LR osteosarcoma (van Putten et al, 1975) and the Lewis lung tumour and B 16 melanoma (Hill and Stanley, 1975). A high cloning efficiency in the lungs for i.v.…”

mentioning

confidence: 99%

“…injected cells is important in reducing the possibility that the colonies are formed by a selected group of tumour cells and also because the higher the cloning efficiency the greater the sensitivity of the assay. Brown (1973) showed that local thoracic irradiation increased the lung-cloning efficiency of the KHT sarcoma, and more recently van Putten et al (1975) have shown that a variety of systemically administered cytotoxic agents enhance the lung-cloning efficiency of the C22LR osteosarcoma.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Enhancement by cytotoxic agents of artificial pulmonary metastasis

Steel¹,

Adams²

1977

Br J Cancer

View full text Add to dashboard Cite

Summary.-The formation of lung colonies by i.v. injected Lewis lung-tumour cells in syngeneic recipients was greatly enhanced by prior treatment of the mice with cyclophosphamide. The lung-cloning efficiency was linearly related to cyclophosphamide dose and the optimum time of treatment was 2-4 days before the injection of tumour cells. The resulting lung colonies had a similar size distribution to colonies in untreated recipients. Bleomycin, local thoracic irradiation and wholebody irradiation were much less effective in enhancing the lung-cloning efficiency.Cyclophosphamide also enhanced the take probability of i.m. implanted tumour cells.

show abstract

Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Enhancement by cytotoxic agents of artificial pulmonary metastasis

Steel¹,

Adams²

1977

Br J Cancer

View full text Add to dashboard Cite

show abstract

“…28,29 Using the method of Teicher et al, 27 Mitsumoto et al 30 established 2 CPTresistant mouse epithelial tumour cell lines with enhanced metastatic capabilities associated with higher levels of cell adhesion to ECM components, such as fibronectin, laminin, collagen type IV and Matrigel; enhanced MMP-2 activity; and higher levels of cell motility. Van Putten et al 31 showed that treatment of animals bearing a transplantable osteosarcoma with cyclophosphamide or CCNU resulted in a significant increase in lung metastases compared to controls. Following these initial observations, enhancement of metastases was also obtained in other tumour systems with cyclophosphamide 32,33 and bleomycin.…”

Section: Discussionmentioning

confidence: 99%

Enhanced in vitro invasiveness and drug resistance with altered gene expression patterns in a human lung carcinoma cell line after pulse selection with anticancer drugs

Liang

O’Driscoll

McDonnell

et al. 2004

Intl Journal of Cancer

View full text Add to dashboard Cite

The human lung carcinoma cell line DLKP was exposed to sequential pulses of 10 commonly used chemotherapeutic drugs (VP-16, vincristine, taxotere, mitoxantrone, 5-fluorouracil, methotrexate, CCNU, BCNU, cisplatin and chlorambucil); resulting cell lines exhibited resistance to the selecting agents (ranging approx. 1.5-to 36-fold) and, in some cases, cross-resistance to methotrexate (approx. 1.4-to 22-fold), vincristine (1.6-to 262-fold), doxorubicin (Adriamycin, approx. 1.1-to 33-fold) and taxotere (approx. 1.1-to 36-fold). Several of the variants displayed collateral sensitivity to cisplatin. A marked increase in in vitro invasiveness and motility was observed with variants pulsed with mitoxantrone, 5-fluorouracil, methotrexate, BCNU, cisplatin and chlorambucil. There was no significant change in invasiveness of cells pulsed with VP-16, vincristine, taxotere or CCNU. All of the pulseselected variants showed elevated levels of MDR-1/P-gp protein by Western blot analysis, although mdr-1 mRNA levels were not increased (except for DLKP-taxotere). In DLKPtaxotere, MRP1 protein levels were also greatly elevated, but mrp1 mRNA levels remained unchanged. BCRP was upregulated in DLKP-mitoxantrone at both the mRNA and protein levels. Gelatin zymography, Western blot and RT-PCR showed that DLKP and its variants secreted MMPs 2, 9 and 13. MMP inhibition assays suggested that MMP-2 plays a more important role than MMPs 9 and 13 in cell invasion of these DLKP drug-resistant variants in vitro. Reducing intracellular drug levels, often associated with overexpression of P-gp, 3 members of the MRP family 4 and the BCRP/ MXR protein, 5 is an important and frequent mechanism of MDR.Invasion through basement membrane is believed to be a critical step in metastasis. There are 4 main classes of proteases involved in proteolytic degradation of the ECM: serine-, cysteine-and aspartyl-proteases as well as MMPs. 6 The MMPs are a family of more than 20 members produced by tumour cells, connective tissue cells and inflammatory cells. MMPs are secreted as latent proenzymes and activated by proteolytic removal of an aminoterminal domain. 7 A large body of evidence shows that MMPs play a crucial role in cancer invasion and metastasis. Based on sequence homology and substrate specificity, MMP-2 and MMP-9 are classified as type IV collagenases that degrade the major component (type IV collagen) of basement membrane; 8 MMP-13, also called "collagenase-3", belongs to a group known as interstitial collagenases, which degrade collagen types I, II, III, VII, VIII and X. 9 The possibility of a relationship between drug resistance and invasion/metastasis phenotypes has been raised by 2 types of observation: 10 firstly, some tumour cells selected for resistance to drugs are invasive/metastatic relative to nonresistant parental cells; secondly, in some cases, secondary (more metastatic) tumours are more resistant to chemotherapeutic drugs than their primary counterparts. In support of this, Osmak et al. 11 reported a study of drug-resistant cervical and ...

show abstract

“…He thus proved that reduction of TD50 for tumour cells, in mice recently exposed to WBI, was not, in this case, an immunological phenomenon. Van Putten et al (1975) demonstrated a significant decrease of RNM and increase of pulmonary metastasis, following intratesticular injection of non-immunogenic sarcoma cells, if the mice received a single dose (250 mg/kg) of cyclophosphamide 2 h after injection of tumour. In their system, pre-exposure of mice to WBI increased pulmonary metastases but not RNM (a notable distinction from our finding).…”

Section: Discussionmentioning

confidence: 99%

Facilitation of nodal metastasis from a non-immunogenic murine carcinoma by previous whole-body irradiation of tumour recipients

Hewitt¹,

Blake²

1977

Br J Cancer

View full text Add to dashboard Cite

Summary.-Of 193 CBA mice kept under prolonged observation after excision of small intradermal transplants of a non-immunogenic tumour (CBA Carcinoma NT), 27 (14%) presented with local recurrence, 19 (10%) with regional lymphnodal metastasis (RNM) and 72 (37o%), with pulmonary metastasis + other systemic metastases.When mice were exposed to sublethal whole-body irradiation (WBI) before tumour transplantation, the incidence of RNM rose to -80% and the latent period was reduced fronm 60 days to -40 days after tumour transplantation. This enhancement of RNM by WBI was undiminished when the interval between WBI and tumour transplantation was increased from 1 to 90 days. An explanation for this effect in terms of immunosuppression by the WBI is unlikely for the following reasons: the tumour was non-immunogenic by standard quantitative tests; the effect persisted long after the expected time for recovery of immune reactivity; and i.v. injection of normal marrow and lymphoid cells after WBI failed to reduce the effect. That the effect was systemic was proved by failure of local pre-irradiation of the tumour bed or regional node to enhance RNM. The effect was not observed when WBI was given 4 days after excision of tumours. These and other experiments failed to indicate the mechanism of the effect of WBI, but its long persistence suggests that it may relate to stored lethal radiation damage in migrating cells of slow turnover tissues.IT HAS been commonly reported over the past decades that preliminary wholebody irradiation (WBI) of rodents enhances the growth of transplanted tumours and/or metastases from them. In the great majority of reports, the information was obtained from tumours which were frankly immunogenic in the hosts, and it is reasonable to conclude, as most authors do, that the enhancement was attributable to suppression of immunity by the WBI. Indeed, the demonstration of enhancement by WBI has now come to be regarded as evidence that a tumour is immunogenic. In the case of enhancement of metastasis by preliminary local irradiation, the site most commonly studied has been the lung. It has been shown that local pre-irradiation of the lung increases the yield of tumour nodules in the lung following i.v. injection of tumour cells (Milas and Withers, 1970; Withers and Milas, 1973;Brown, 1973). Because these authors found no greater enhancement after WBI than after local irradiation, they were inclined to dismiss immunosuppression as contributing to their findings.We report here a powerful and longlasting enhancing effect of pre-WBI on the incidence of regional nodal metastases from intradermal (i.d.) implants of a syngeneic carcinoma for which there is no evidence of immunogenicity. Local pre-irradiation of the tumour bed or regional node did not enhance nodal metastasis. Thus, the phenomenon we are to describe is clearly distinct both from enhancement by immunosuppression and from enhancement by local pre-irradiation independent of immunosuppression. We also describe a number of experiments

show abstract

Enhancement by drugs of metastatic lung nodule formation after intravenous tumour cell injection

Cited by 95 publications

References 15 publications

Enhancement by cytotoxic agents of artificial pulmonary metastasis

Enhancement by cytotoxic agents of artificial pulmonary metastasis

Enhanced in vitro invasiveness and drug resistance with altered gene expression patterns in a human lung carcinoma cell line after pulse selection with anticancer drugs

Facilitation of nodal metastasis from a non-immunogenic murine carcinoma by previous whole-body irradiation of tumour recipients

Contact Info

Product

Resources

About