Comments on hematogenous metastatic patterns in humans as revealed by autopsy

Weiss, Leonard

doi:10.1007/bf00132751

Cited by 175 publications

(118 citation statements)

References 17 publications

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“…The extent of metastasis measured in spontaneous versus experimental metastasis assays can provide insights into mechanisms of host compartment-mediated influence on metastasis (15,(18)(19)(20)(21)(22)(23). For example, in models where primary tumor growth is unchanged between treatment groups, i.v.…”

Section: Discussionmentioning

confidence: 99%

Estrogen Induces Lung Metastasis through a Host Compartment–Specific Response

et al. 2006

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Direct proliferative effects of estrogen (E 2 ) on estrogen receptor-positive tumors are well documented; however, the potential for E 2 to mediate effects selective for the host (i.e., angiogenesis, vascular permeability, or stromal effects), which influence tumor growth and/or metastasis, has received less attention. In this study, we examine the capacity for E 2 to promote tumor growth and/or metastasis independent of direct effects on tumor cells. In these studies, we distinguish host versus tumor compartment components of E 2 action in tumor growth and metastasis by analysis of E 2 -nonresponsive tumor cells implanted in ovariectomized (OVX) mice that contain s.c. implants of placebo (OVX) or E 2 -containing slowrelease pellets (OVX + E 2 ). We show that the D121 lung carcinoma cell line is E 2 -nonresponsive, and following s.c. implantation in OVX versus OVX + E 2 mice, E 2 action on the host compartment leads to an increase in spontaneous metastasis but not primary tumor growth or neovascularization. Similarly, experimental lung metastasis of E 2 -nonresponsive 4T1 mammary carcinoma cells also leads to increased tumor burden in the lungs of OVX + E 2 mice. These results suggest that the E 2 status of the host compartment influences late steps in tumor cell metastasis that can provide important insights into the role of E 2 in the tumor versus host compartments. (Cancer Res 2006; 66(7): 3667-72)

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Section: Discussionmentioning

confidence: 99%

Estrogen Induces Lung Metastasis through a Host Compartment–Specific Response

et al. 2006

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“…Clinical and preclinical data have shown that primary tumors disseminate to selective secondary organs, which cannot solely be explained by the anatomic distribution of the blood flow to the various organs (22). Whereas breast cancer has a predilection for the skeleton, uveal melanoma and colon cancer preferentially spread to liver (reviewed in refs.…”

Section: Introductionmentioning

confidence: 99%

The Tumor Suppressor Smad4 Is Required for Transforming Growth Factor β–Induced Epithelial to Mesenchymal Transition and Bone Metastasis of Breast Cancer Cells

Deckers

Dinther²,

Buijs³

et al. 2006

Cancer Research

346

291

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Transforming growth factor B (TGF-B) can act as suppressor and promoter of cancer progression. Intracellular Smad proteins (i.e., receptor regulated Smads and common mediator Smad4) play a pivotal role in mediating antimitogenic and proapoptotic effects of TGF-B, but their function in TGF-B-induced invasion and metastasis is unclear. Here, we have investigated the role of Smad4 in a cellular and mouse model for TGF-B-induced breast cancer progression. Consistent with its tumor suppressor function, specific silencing of Smad4 in NMuMG mammary gland epithelial cells using small hairpin RNA (shRNA)-expressing RNAi vectors strongly mitigated TGF-B-induced growth inhibition and apoptosis. Smad4 knockdown also potently inhibited TGF-B-induced epithelial to mesenchymal transition of NMuMG cells as measured by morphologic transformation from epithelial to fibroblast-like cells, formation of stress fibers, inhibition of E-cadherin expression, and gain of expression of various mesenchymal markers. Furthermore, we show that knockdown of Smad4 in MDA-MB-231 breast cancer cells strongly inhibited the frequency of bone metastasis in nude mice by 75% and significantly increased metastasis-free survival. Communication of MDA-MB-231 cells with the bone microenvironment, which is needed for optimal tumor cell growth and metastasis, may be affected in Smad4 knockdown cells as TGF-B-induced expression of interleukin 11 was attenuated on Smad4 knockdown. Taken together, our results show that Smad4 plays an important role in both tumor suppression and progression of breast cancer cells.

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“…These have all been relatively small-scale studies (Abrams et al, 1950;Weiss et al, 1988;Weiss, 1992;Disibio and French, 2008). However, we may now study these patterns using computational methods on large data sets.…”

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confidence: 99%

Cancer metastasis networks and the prediction of progression patterns

et al. 2009

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BACKGROUND: Metastasis patterns in cancer vary both spatially and temporally. Network modelling may allow the incorporation of the temporal dimension in the analysis of these patterns. METHODS: We used Medicare claims of 2 265 167 elderly patients aged X65 years to study the large-scale clinical pattern of metastases. We introduce the concept of a cancer metastasis network, in which nodes represent the primary cancer site and the sites of subsequent metastases, connected by links that measure the strength of co-occurrence. RESULTS: These cancer metastasis networks capture both temporal and subtle relational information, the dynamics of which differ between cancer types. Using these networks as entities on which the metastatic disease of individual patients may evolve, we show that they may be used, for certain cancer types, to make retrograde predictions of a primary cancer type given a sequence of metastases, as well as anterograde predictions of future sites of metastasis. CONCLUSION: Improvements over traditional techniques show that such a network-based modelling approach may be suitable for studying metastasis patterns.

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Comments on hematogenous metastatic patterns in humans as revealed by autopsy

Cited by 175 publications

References 17 publications

Estrogen Induces Lung Metastasis through a Host Compartment–Specific Response

Estrogen Induces Lung Metastasis through a Host Compartment–Specific Response

The Tumor Suppressor Smad4 Is Required for Transforming Growth Factor β–Induced Epithelial to Mesenchymal Transition and Bone Metastasis of Breast Cancer Cells

Cancer metastasis networks and the prediction of progression patterns

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