Platelet—tumor‐cell interactions in mice. The role of platelets in the spread of malignant disease

Gasic, Gabriel J.; Gasic, Tatiana B.; Galanti, Norbel; Johnson, Thomas G.; Murphy, Scott

doi:10.1002/ijc.2910110322

Cited by 412 publications

(229 citation statements)

References 17 publications

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“…There have been suggestions that coagulation in animal experimental models influences the extent and degree of tumour metastases (Wood, 1971;Chew and Wallace, 1976). Factors which reduce coagulation, such as heparin, coumarin and thrombocytopenia, have been reported to reduce the number of metastases (Wood, 1971;Hilgard et al, 1977;Gasic, Gasic and Stewart, 1968;Gasic et al, 1973) whereas protamine increases metastases (Wood, 1971). However, there is some evidence that these factors may not affect tumour dissemination (Hagmar, 1970).…”

Section: Discussionmentioning

confidence: 99%

Intravascular coagulation resulting from intravenous injection of C. parvum in mice

Lampert¹,

Jones²,

Sadler³

et al. 1977

Br J Cancer

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In mice, i.v. C. parvum induces intravascular coagulation. This is a prolonged reaction lasting up to 7 days. It results in thrombosis in hepatic vessels with consequent hepatic necrosis, and thrombosis in pulmonary and splenic vessels. This may be important in the assessment of the tumour-inhibitory activity of C. parvum. Images Fig. 1 Fig. 2 Fig. 3 Fig. 4

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Section: Discussionmentioning

confidence: 99%

Intravascular coagulation resulting from intravenous injection of C. parvum in mice

Lampert¹,

Jones²,

Sadler³

et al. 1977

Br J Cancer

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“…[11][12][13] Platelet adhesion and aggregation are two processes critical to hematogenous tumor cell metastasis. [16][17][18] The aggregation of tumor cells and platelets may assist in metastasis by producing a mixed platelet-tumor cell mass that supports adherence of tumor cells to the blood vessel wall and protects the tumor cells from destruction by the immune system. [16][17][18][19][20] In this study, we investigated the disposition of vWF in osteosarcoma through the analysis of messenger RNA (mRNA) and protein expression in tumor samples.…”

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confidence: 99%

von Willebrand factor expression in osteosarcoma metastasis

et al. 2005

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A number of genes are implicated in the initiation and progression of osteosarcoma; however, cytogenetic and comparative genomic hybridization studies indicate the involvement of additional unidentified genes. An examination of gene expression profiles in 22 high-grade osteosarcoma tumor specimens from 15 patients (including paired primary and metastatic samples from five patients) indicated that von Willebrand factor (vWF) mRNA expression may increase during tumor progression. vWF, a large glycoprotein previously considered to be expressed exclusively by endothelial cells and megakaryocytes, is involved in platelet aggregation and adhesion to the subendothelial matrix, processes critical to hematogenous tumor cell metastasis to the lung. Analysis of paired primary and metastatic osteosarcoma tumor samples from 10 patients revealed an increase in vWF gene expression in metastases (P ¼ 0.005). Immunohistochemistry showed that, in addition to the endothelial cells, vWF protein was also detected in osteosarcoma cells in vivo in 13 of 29 tumor specimens as well as in SAOS2, an osteosarcoma cell line. The tumor cell staining correlated positively with high vWF expression in the sample (P ¼ 0.006). Although vascular endothelial cells contribute to the vWF mRNA detected in the tumor samples, there was neither any correlation between vascular density (VD) and vWF mRNA expression nor between VD and clinical outcome. These findings suggest that vWF expression is deregulated in osteosarcoma tumors, potentially contributing to metastasis.

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“…Although the NC carcinoma is thought to have low immunogenicity (Hewitt et al, 1976) FLU tended to increase the lymphocyte content of tumours . With regard to tumour spread, aspirin is antimetastatic in mice, possibly due to inhibition of platelet aggregation (Gasic et al, 1973). Other speculations are that the drugs inhibited the formation or dilatation of tumour blood vessels, so reducing either tuimour metabolism or the escape of malignant cells into the bloodstream.…”

Section: Discussionmentioning

confidence: 99%

Increased survival of cancer-bearing mice treated with inhibitors of prostaglandin synthesis alone or with chemotherapy

Bennett¹,

Berstock²,

Carroll³

1982

Br J Cancer

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Summary.-In mice with a transplantable mammary carcinoma, treatment with the prostaglandin-synthesis inhibitors flurbiprofen or indomethacin produced various beneficial effects. Survival time after excision of the transplanted tumour was increased, particularly when the drugs were given with the chemotherapeutic agents methrotrexate and melphalan, and there were more disease-free survivors. The combined treatment with flurbiprofen also gave less tumour recurrence at the excision site. Flurbiprofen did not seem to alter the bioavailability of the chemotherapeutic agents.

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Platelet—tumor‐cell interactions in mice. The role of platelets in the spread of malignant disease

Cited by 412 publications

References 17 publications

Intravascular coagulation resulting from intravenous injection of C. parvum in mice

Intravascular coagulation resulting from intravenous injection of C. parvum in mice

von Willebrand factor expression in osteosarcoma metastasis

Increased survival of cancer-bearing mice treated with inhibitors of prostaglandin synthesis alone or with chemotherapy

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