The pattern of metastases in human breast cancer: Methodological aspects and influence of prognostic factors

Kamby, Claus

doi:10.1016/0305-7372(90)90075-q

Cited by 54 publications

(26 citation statements)

References 130 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition small micrometastases and single tumour cells are observed in the lungs of S5-R37 tumour-bearing rats, and these lesions can be recognized more easily by immunocytochemical staining for S100A4. Their occurrence in vascular spaces adjacent either to blood cells or to lymphocytes suggests that they may have spread to the lungs from the primary tumour via both blood vessels and lymphatics, perhaps similar, in this respect, to the pattern of spread of human breast cancer (Kamby, 1990). The decreased latent period for the formation of primary tumours produced by Rama cells transfected with foreign DNA, particularly after passage of the transfected cells in rats, has been noted previously (Davies et al, , 1994Jamieson et al, 1990a).…”

Section: Discussionmentioning

confidence: 98%

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

et al. 1998

View full text Add to dashboard Cite

The rodent S100-related calcium-binding protein, S100A4 induces metastasis in non-metastatic rat and mouse benign mammary cells and co-operates with benign-tumour-inducing changes in two transgenic mouse models, to yield metastatic mammary tumours. Cotransfection of the human gene for S100A4 with pSV2neo into the benign rat mammary cell line, Rama 37, yielded cells which expressed a low level of the endogenous S100A4 mRNA, and either high or undetectable levels of human S100A4 mRNA. The cells which expressed a high level of human S100A4 mRNA induced metastasis in the benign rat mammary cell line Rama 37 in an in vivo assay, whereas the cells which expressed an undetectable level of human S100A4 did not induce any detectable metastases. The primary tumours arising from the S100A4-expressing cells contained high levels of immunocytochemically-detected S100A4 and this high level of S100A4 and the metastatic potential were maintained when cells from a metastasis were re-injected into syngeneic rats. The results show that the human S100A4 possesses metastasis-inducing capabilities.

show abstract

Section: Discussionmentioning

confidence: 98%

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

et al. 1998

View full text Add to dashboard Cite

show abstract

“…[12] The increased use of hormonal treatment might cause the shift since ER-positive tumours tend to metastasize to bone, ER and PR negativity are commonly associated with visceral metastases, especially liver and CNS. [13][14][15][16][17][18] The increased proportion of CNS metastases might also reflect improvement in adjuvant systemic treatment;…”

Section: Discussionmentioning

confidence: 99%

Unfavourable pattern of metastases in M0 breast cancer patients during 1978-2008: a population-based analysis of the Munich Cancer Registry

Hurk

Eckel

Poll‐Franse

et al. 2011

Breast Cancer Res Treat

View full text Add to dashboard Cite

Key words: metastases pattern, time to metastases, survival, breast cancer 2 ABSTRACT PurposeLittle is known about time trends in metastases in patients treated in routine health care facilities without metastases at diagnosis (M0) and about survival after these metastases. Methods Data ConclusionsIn the period 1978-2008, unfavourable changes in the pattern of metastases were exhibited and no improvement was observed in survival of patients after occurrence of metastases. An explanation might be the increased use of adjuvant systemic treatment, which has less effect on the highly lethal liver and CNS metastases than on bone metastases. The increased use also appeared to contribute to the overall prevention of metastases in breast cancer and therefore to improvement of overall survival.3

show abstract

“…Metastasis is a complex process of genetic and phenotypic change that ultimately results in tumor cell dissemination and the formation of secondary tumors (1). The adhesive glycoprotein osteopontin (OPN) has been heavily implicated in exacerbating the processes of neoplastic transformation, cancer progression, and metastasis (2) and as such is of considerable oncologic interest.…”

Section: Introductionmentioning

confidence: 99%

Agelastatin A: a novel inhibitor of osteopontin-mediated adhesion, invasion, and colony formation

Mason

McFarlane

Johnston

et al. 2008

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

Effective inhibitors of osteopontin (OPN) -mediated neoplastic transformation and metastasis are still lacking. (-)-Agelastatin A is a naturally occurring oroidin alkaloid with powerful antitumor effects that, in many cases, are superior to cisplatin in vitro . In this regard, past comparative assaying of the two agents against a range of human tumor cell lines has revealed that typically (-)-agelastatin A is 1.5 to 16 times more potent than cisplatin at inhibiting cell growth, its effects being most pronounced against human bladder, skin, colon, and breast carcinomas. In this study, we have investigated the effects of (-)-agelastatin A on OPN-mediated malignant transformation using mammary epithelial cell lines. Treatment with (-)-agelastatin A inhibited OPN protein expression and enhanced expression of the cellular OPN inhibitor, Tcf-4. (-)-Agelastatin A treatment also reduced B-catenin protein expression and reduced anchorage-independent growth, adhesion, and invasion in R37 OPN pBK-CMV and C9 cell lines. Similar effects were observed in MDA-MB-231 and MDA-MB-435s human breast cancer cell lines exposed to (-)-agelastatin A. Suppression of Tcf-4 by RNA interference (short interfering RNA) induced malignant/invasive transformation in parental benign Rama 37 cells; significantly, these events were reversed by treatment with (-)-agelastatin A. Our study reveals, for the very first time, that (-)-agelastatin A down-regulates B-catenin expression while simultaneously up-regulating Tcf-4 and that these combined effects cause repression of OPN and inhibition of OPN-mediated malignant cell invasion, adhesion, and colony formation in vitro. We have also shown that (-)-agelastatin A inhibits cancer cell proliferation by causing cells to accumulate in the G 2 phase of cell cycle.

show abstract

The pattern of metastases in human breast cancer: Methodological aspects and influence of prognostic factors

Cited by 54 publications

References 130 publications

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

Unfavourable pattern of metastases in M0 breast cancer patients during 1978-2008: a population-based analysis of the Munich Cancer Registry

Agelastatin A: a novel inhibitor of osteopontin-mediated adhesion, invasion, and colony formation

Contact Info

Product

Resources

About