Metastatic properties of murine sarcomas and carcinomas I. Positive correlation with lung colonization and lack of correlation with s.c. tumor take

Volpe, John P.; Hunter, Nancy; Basić, Ivan; Milas, Luka

doi:10.1007/bf01585082

Cited by 47 publications

(27 citation statements)

References 15 publications

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“…Growing in the C3H/HeN mice were KHT sarcoma (Kallman et al, 1967), fibrosarcomas RIF (Twentyman et al, 1980), FsaR and FsaN (Volpe et al, 1985), and SCC models SCCVII (Suit et al, 1985) and AT17. Mice strains Balb/c and C57BL were used for the EMT6 mammary sarcoma (Rockwell et al, 1972) and Lewis lung carcinoma (LLC) (Sugiura and Stock, 1955) respectively.…”

Section: Materials and Methods Tumour Modelsmentioning

confidence: 99%

Photofrin accumulation in malignant and host cell populations of various tumours

Korbelik

Krosl²

1996

Br J Cancer

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Summary Photofrin accumulation in malignant and host cell populations of various tumours was studied by flow cytometry analysis of cells dissociated from the tumour tissue. The transplantable mouse tumour models included in this analysis were sarcomas EMT6, RIF, KHT and FsaN, Lewis lung carcinoma, SCCVII squamous cell carcinoma (SCC) and slowly growing moderately differentiated AT17 SCC. An example of spontaneous mouse adenocarcinoma was also examined. Staining with specific monoclonal antibodies was used to identify the various cell populations present in these tumours. The main characteristic of Photofrin cellular accumulation was a very high photosensitiser content found exclusively in a subpopulation of tumourassociated macrophages (TAMs). Photosensitiser levels similar to or lower than in malignant cells were observed in the remaining TAMs and other tumour-infiltrating host cells. Photofrin accumulation in malignant cells was not equal in all tumour models, but may have been affected by tumour blood perfusion/ vascularisation. Results consistent with the above findings were obtained with SCC of buccal mucosa induced by 9,10-dimethyl-1,2-benzanthracene in Syrian hamsters. The TAM subpopulation that accumulates by far the highest cellular Photofrin levels in tumours is suggested to be responsible for the tumour-localised photosensitiser fluorescence.

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Section: Materials and Methods Tumour Modelsmentioning

confidence: 99%

Photofrin accumulation in malignant and host cell populations of various tumours

Korbelik

Krosl²

1996

Br J Cancer

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“…Melanoma B16BL6 (Poste et al, 1980) and fibrosarcoma MCA205 (Barth et al, 1990) were grown in syngeneic C57BL/6 mice, and fibrosarcoma FsaR (Volpe et al, 1985) in syngeneic C3H/HeN mice using 6 -8-week-old females. The mice were kept in sterile cages housed in the animal facility of the British Columbia Cancer Research Centre.…”

Section: Tumour Modelsmentioning

confidence: 99%

Potentiation of photodynamic therapy of cancer by complement: the effect of γ-inulin

Korbelik

Cooper

2006

Br J Cancer

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Host response elicited by photodynamic therapy (PDT) of cancerous lesions is a critical contributor to the clinical outcome, and complement system has emerged as its important element. Amplification of complement action was shown to improve tumour PDT response. In search of a clinically relevant complement activator for use as a PDT adjuvant, this study focused on g-inulin and examined its effects on PDT response of mouse tumours. Intralesional g-inulin (0.1 mg mouse À1 ) delivered immediately after PDT rivaled zymosan (potent classical complement activator) in delaying the recurrence of B16BL6 melanomas. This effect of g-inulin was further enhanced by IFN-g pretreatment. Tumour C3 protein levels, already elevated after individual PDT or g-inulin treatments, increased much higher after their combination. With fibrosarcomas MCA205 and FsaR, adjuvant g-inulin proved highly effective in reducing recurrence rates following PDT using four different photosensitisers (BPD, ce6, Photofrin, and mTHPC). At 3 days after PDT plus g-inulin treatment, over 50% of cells found at the tumour site were CTLs engaged in killing specific targets via perforingranzyme pathway. This study demonstrates that g-inulin is highly effective PDT adjuvant and suggests that by amplifying the activation of complement system, this agent potentiates the development of CTL-mediated immunity against PDT-treated tumours.

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“…The syngeneic FSaII (mouse fibrosarcoma) 14 and LLc (mouse lung carcinoma) 15 tumor models were implanted in the thigh of C3H/He (Charles River Laboratories, Brussels, Belgium) and C57Bl/6J (Elevage Janvier, Le Genest-St.-Isle, France) (WT and eNOS Ϫ/Ϫ ) mice, respectively. C57BL/6J eNOS Ϫ/Ϫ mice were originally from the Jackson Laboratory (JAX GEMM Strain, Bar Harbor, ME) and were inbred at the FATH laboratory (UCL, Brussels, Belgium).…”

Section: Animal Tumor Modelsmentioning

confidence: 99%

Nitric oxide as a radiosensitizer: Evidence for an intrinsic role in addition to its effect on oxygen delivery and consumption

Jordan

Sonveaux

Feron

et al. 2004

Intl Journal of Cancer

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Different nitric oxide (NO)-mediated treatments (e.g., isosorbide dinitrate, insulin and electrical stimulation of the host tissue) have been investigated for their effects on tumor oxygenation and radiation sensitivity. We further address the issue of the role played by modulation of the NO-pathway in tumor radiosensitivity. For this purpose, the local concentration of NO was monitored after treatment in FSaII tumors and a comparison between the sensitivity of LLC tumors implanted both on eNOS ؊/؊ and wild-type (WT) mice was carried out. First, we demonstrate the central role played by eNOS in the radiosensitizing effect after application of insulin treatment and electrical stimulation: a significant increase in tumor NO content is induced by these treatments and the increase in tumor oxygenation, as well as the radiosensitizing effect are abolished in eNOS knock-out mice, in contrast to WT mice. Second, by comparing the level of oxygen and NO achieved in tumors after NO-mediated treatments and carbogen, we provide evidence that these NO-mediated treatments are not simply acting by a single oxygen effect. These treatments induced significant regrowth delays compared to carbogen, despite a smaller increase in tumor oxygenation. For the NO-mediated treatments, there was a direct correlation between the NO content and the radiosensitizing effect. These data strongly suggest that NO is a complementary factor additive to oxygen in determining the sensitivity to irradiation and we therefore propose that NO acts as an intrinsic radiosensitizer in vivo. © 2004 Wiley-Liss, Inc. Key words: tumor; radiation sensitivity; eNOS Ϫ/Ϫ ; nitric oxide; oxygenTumor oxygenation and blood flow are of fundamental importance to many forms of cancer therapy. The partial pressure of oxygen (pO 2 ) plays an important role in the response of tumors to cytotoxic treatments such as chemotherapy, radiotherapy and photodynamic therapy. Both oxygen diffusion and oxygen consumption by tumor cell metabolism contribute to the occurrence of hypoxia. Oxygen deficiency is caused by an insufficient oxygen supply as a result of inadequate tumor perfusion (diffusion limited hypoxia) and fluctuations in red cell flux (acute hypoxia). 1 A promising approach in cancer therapy consists of the manipulation of tumor blood oxygen delivery and oxygen consumption to improve either radio-or chemotherapeutic response. Vasoactive agents, 2 modifiers of tumor cell oxygen consumption 3 or carbogen breathing 4 that is already being tested in Phase III clinical studies, are currently being evaluated for their potential therapeutic interest.We documented recently that nitric oxide (NO)-dependent modifiers of tumor hemodynamics were able to radiosensitize experimental tumors in vivo. Three strategies were considered for that purpose: (i) administration of a NO donor (isosorbide dinitrate), 5,6 (ii) slow infusion of insulin, 7 and (iii) electrical stimulation of the host tissue. 8 The first treatment acted by a direct release of exogenous NO whereas the others were actua...

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Metastatic properties of murine sarcomas and carcinomas I. Positive correlation with lung colonization and lack of correlation with s.c. tumor take

Cited by 47 publications

References 15 publications

Photofrin accumulation in malignant and host cell populations of various tumours

Photofrin accumulation in malignant and host cell populations of various tumours

Potentiation of photodynamic therapy of cancer by complement: the effect of γ-inulin

Nitric oxide as a radiosensitizer: Evidence for an intrinsic role in addition to its effect on oxygen delivery and consumption

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