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Host microenvironment in breast cancer development: inflammatory cells, cytokines and chemokines in breast cancer progression: reciprocal tumor-microenvironment interactions.

Ben-Baruch A - Breast Cancer Res. (2002)

Bottom Line: A comprehensive overview of breast cancer development and progression suggests that the process is influenced by intrinsic properties of the tumor cells, as well as by microenvironmental factors.Indeed, in breast carcinoma, an intensive interplay exists between the tumor cells on one hand, and inflammatory cells/cytokines/chemokines on the other.The purpose of the present review is to outline the reciprocal interactions that exist between these different elements, and to shed light on their potential involvement in breast cancer development and progression.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cell Research and Immunology, George S Wise Faculty of Life Sciences, Tel-Aviv University, Israel. aabb@post.tau.ac.il

ABSTRACT
A comprehensive overview of breast cancer development and progression suggests that the process is influenced by intrinsic properties of the tumor cells, as well as by microenvironmental factors. Indeed, in breast carcinoma, an intensive interplay exists between the tumor cells on one hand, and inflammatory cells/cytokines/chemokines on the other. The purpose of the present review is to outline the reciprocal interactions that exist between these different elements, and to shed light on their potential involvement in breast cancer development and progression.

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A proposed model for the potential role of the interactions between tumor cells and inflammatory elements in breast cancer progression. The expression of monocyte chemoattractants (CCL5 and CCL2) by breast tumor cells may induce monocyte infiltration to breast tumor sites. The resulting tumor-associated macrophages (TAM) may express promalignant mediators, such as tumor necrosis factor alpha (TNF-α). This inflammatory cytokine may further promote the expression of tumor-supporting factors by the tumor cells, including matrix metalloproteinases (MMP) and the monocyte chemoattractants CCL5 and CCL2. The elevated expression of these chemokines by the tumor cells may result in additional monocyte recruitment, and in the stimulation of TAM at the tumor site. TAM stimulation may give rise to promoted levels of expression of promalignant factors, such as MMP, angiogenic mediators and TNF-α. Some of these activities may be stimulated directly by the chemokines. TAM-derived TNF-α may in turn further increase the expression of monocyte chemoattractants (e.g. CCL5, CCL2) by the tumor cells, and so on. This process may be aided by other functions of inflammatory cells/cytokines/chemokines (vascularization, release of growth factors, etc.; see Table 1) that eventually support the growth of the primary tumor and distant metastasis formation (possibly assisted by other chemokines, such as CXCL12).
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Figure 1: A proposed model for the potential role of the interactions between tumor cells and inflammatory elements in breast cancer progression. The expression of monocyte chemoattractants (CCL5 and CCL2) by breast tumor cells may induce monocyte infiltration to breast tumor sites. The resulting tumor-associated macrophages (TAM) may express promalignant mediators, such as tumor necrosis factor alpha (TNF-α). This inflammatory cytokine may further promote the expression of tumor-supporting factors by the tumor cells, including matrix metalloproteinases (MMP) and the monocyte chemoattractants CCL5 and CCL2. The elevated expression of these chemokines by the tumor cells may result in additional monocyte recruitment, and in the stimulation of TAM at the tumor site. TAM stimulation may give rise to promoted levels of expression of promalignant factors, such as MMP, angiogenic mediators and TNF-α. Some of these activities may be stimulated directly by the chemokines. TAM-derived TNF-α may in turn further increase the expression of monocyte chemoattractants (e.g. CCL5, CCL2) by the tumor cells, and so on. This process may be aided by other functions of inflammatory cells/cytokines/chemokines (vascularization, release of growth factors, etc.; see Table 1) that eventually support the growth of the primary tumor and distant metastasis formation (possibly assisted by other chemokines, such as CXCL12).

Mentions: Reciprocal interactions that exist between the breast tumor cells and stroma/inflammatory cells are mediated by inflammatory cytokines and chemokines, and may affect tumor development and progression. Many inflammatory factors, including cells, cytokines and chemokines, may divergently regulate the progression process. However, major emphasis has recently been placed on the potential role of TAM in breast cancer progression, mediated by their ability to express promalignant factors. Monocyte migration to breast tumors was highly correlated with the expression of monocyte-attracting chemokines by the tumor cells and stroma cells. As suggested in Figure. 1, these chemokines may act in a cooperative manner to attract leukocytes, primarily monocytes, to tumor sites. This may be followed by chemokine-induced stimulation of monocyte-derived promalignant activities at the tumor site. The result of this process may be a further increased expression of protumorigenic properties by the infiltrating monocytes. Monocyte-derived cytokines, such as TNF-α, could intensify chemokine expression by the tumor or stroma cells, as well as other promalignant properties. The resulting positive feedback loop may act in conjunction with other promalignant activities of tumor-derived and inflammatory cell-derived factors, as well as with chemokine-induced site-specific metastasis formation (through CXCL12). The overall effect of these activities may play a key role in determining the metastatic spread of breast tumors, and therefore disease progression.


Host microenvironment in breast cancer development: inflammatory cells, cytokines and chemokines in breast cancer progression: reciprocal tumor-microenvironment interactions.

Ben-Baruch A - Breast Cancer Res. (2002)

A proposed model for the potential role of the interactions between tumor cells and inflammatory elements in breast cancer progression. The expression of monocyte chemoattractants (CCL5 and CCL2) by breast tumor cells may induce monocyte infiltration to breast tumor sites. The resulting tumor-associated macrophages (TAM) may express promalignant mediators, such as tumor necrosis factor alpha (TNF-α). This inflammatory cytokine may further promote the expression of tumor-supporting factors by the tumor cells, including matrix metalloproteinases (MMP) and the monocyte chemoattractants CCL5 and CCL2. The elevated expression of these chemokines by the tumor cells may result in additional monocyte recruitment, and in the stimulation of TAM at the tumor site. TAM stimulation may give rise to promoted levels of expression of promalignant factors, such as MMP, angiogenic mediators and TNF-α. Some of these activities may be stimulated directly by the chemokines. TAM-derived TNF-α may in turn further increase the expression of monocyte chemoattractants (e.g. CCL5, CCL2) by the tumor cells, and so on. This process may be aided by other functions of inflammatory cells/cytokines/chemokines (vascularization, release of growth factors, etc.; see Table 1) that eventually support the growth of the primary tumor and distant metastasis formation (possibly assisted by other chemokines, such as CXCL12).
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC154133&req=5

Figure 1: A proposed model for the potential role of the interactions between tumor cells and inflammatory elements in breast cancer progression. The expression of monocyte chemoattractants (CCL5 and CCL2) by breast tumor cells may induce monocyte infiltration to breast tumor sites. The resulting tumor-associated macrophages (TAM) may express promalignant mediators, such as tumor necrosis factor alpha (TNF-α). This inflammatory cytokine may further promote the expression of tumor-supporting factors by the tumor cells, including matrix metalloproteinases (MMP) and the monocyte chemoattractants CCL5 and CCL2. The elevated expression of these chemokines by the tumor cells may result in additional monocyte recruitment, and in the stimulation of TAM at the tumor site. TAM stimulation may give rise to promoted levels of expression of promalignant factors, such as MMP, angiogenic mediators and TNF-α. Some of these activities may be stimulated directly by the chemokines. TAM-derived TNF-α may in turn further increase the expression of monocyte chemoattractants (e.g. CCL5, CCL2) by the tumor cells, and so on. This process may be aided by other functions of inflammatory cells/cytokines/chemokines (vascularization, release of growth factors, etc.; see Table 1) that eventually support the growth of the primary tumor and distant metastasis formation (possibly assisted by other chemokines, such as CXCL12).
Mentions: Reciprocal interactions that exist between the breast tumor cells and stroma/inflammatory cells are mediated by inflammatory cytokines and chemokines, and may affect tumor development and progression. Many inflammatory factors, including cells, cytokines and chemokines, may divergently regulate the progression process. However, major emphasis has recently been placed on the potential role of TAM in breast cancer progression, mediated by their ability to express promalignant factors. Monocyte migration to breast tumors was highly correlated with the expression of monocyte-attracting chemokines by the tumor cells and stroma cells. As suggested in Figure. 1, these chemokines may act in a cooperative manner to attract leukocytes, primarily monocytes, to tumor sites. This may be followed by chemokine-induced stimulation of monocyte-derived promalignant activities at the tumor site. The result of this process may be a further increased expression of protumorigenic properties by the infiltrating monocytes. Monocyte-derived cytokines, such as TNF-α, could intensify chemokine expression by the tumor or stroma cells, as well as other promalignant properties. The resulting positive feedback loop may act in conjunction with other promalignant activities of tumor-derived and inflammatory cell-derived factors, as well as with chemokine-induced site-specific metastasis formation (through CXCL12). The overall effect of these activities may play a key role in determining the metastatic spread of breast tumors, and therefore disease progression.

Bottom Line: A comprehensive overview of breast cancer development and progression suggests that the process is influenced by intrinsic properties of the tumor cells, as well as by microenvironmental factors.Indeed, in breast carcinoma, an intensive interplay exists between the tumor cells on one hand, and inflammatory cells/cytokines/chemokines on the other.The purpose of the present review is to outline the reciprocal interactions that exist between these different elements, and to shed light on their potential involvement in breast cancer development and progression.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cell Research and Immunology, George S Wise Faculty of Life Sciences, Tel-Aviv University, Israel. aabb@post.tau.ac.il

ABSTRACT
A comprehensive overview of breast cancer development and progression suggests that the process is influenced by intrinsic properties of the tumor cells, as well as by microenvironmental factors. Indeed, in breast carcinoma, an intensive interplay exists between the tumor cells on one hand, and inflammatory cells/cytokines/chemokines on the other. The purpose of the present review is to outline the reciprocal interactions that exist between these different elements, and to shed light on their potential involvement in breast cancer development and progression.

Show MeSH
Related in: MedlinePlus