Vascular remodelling during the normal and malignant life cycle of the mammary gland

Djonov, Valentin; Andres, Anne‐Catherine; Ziemiecki, Andrew

doi:10.1002/1097-0029(20010115)52:2<182::aid-jemt1004>3.0.co;2-m

Cited by 165 publications

(88 citation statements)

References 41 publications

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“…Macrophages may also significantly affect other matrix molecules through expression of different proteases as well as molecules involved in matrix remodeling such as Lysyl oxidase and SPARC (Sangaletti et al 2008). For example, macrophages are rich sources of MMP9 that is involved in ECM remodeling (Djonov et al 2001;Egeblad and Werb 2002).…”

Section: Leukocytes In Mammary Development and Cancermentioning

confidence: 99%

Leukocytes in Mammary Development and Cancer

Coussens

Pollard

2010

Cold Spring Harbor Perspectives in Biology

165

135

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Section: Leukocytes In Mammary Development and Cancermentioning

confidence: 99%

Leukocytes in Mammary Development and Cancer

Coussens

Pollard

2010

Cold Spring Harbor Perspectives in Biology

165

135

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“…However, it is unknown whether the loss of Robo4, alone, will result in increased angiogenesis during normal developmental processes, in part because there are few examples of robust blood vessel growth in the adult animal. In the mammary gland, however, there is a normal developmental event, pregnancy, associated with exuberant sprouting angiogenesis (18) that is driven by VEGF-A (19, 20) (Fig. S3O).…”

Section: Combined Loss Of Robo1 and Robo4 Leads To Increased Vesselmentioning

confidence: 99%

“…The gland undergoes stereotyped cycles of cell growth and differentiation under the influence of estrus and pregnancy hormones. In the virgin, the estrus cycle does not cause expansion of the vasculature, but pregnancy is accompanied by robust capillary sprouting that provides increased blood supply to promote lobulo-alveolar expansion (17,18). Classic studies on vascular patterning of the gland demonstrated the importance of the epithelium because its absence resulted in only the major vessels and none of the duct-associated capillary plexuses (17).…”

mentioning

confidence: 99%

Vascular Robo4 restricts proangiogenic VEGF signaling in breast

Marlow

Binnewies

Sorensen

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Formation of the vascular system within organs requires the balanced action of numerous positive and negative factors secreted by stromal and epithelial cells. Here, we used a genetic approach to determine the role of SLITs in regulating the growth and organization of blood vessels in the mammary gland. We demonstrate that vascularization of the gland is not affected by loss of Slit expression in the epithelial compartment. Instead, we identify a stromal source of SLIT, mural cells encircling blood vessels, and show that loss of Slit in the stroma leads to elevated blood vessel density and complexity. We examine candidate SLIT receptors, Robo1 and Robo4, and find that increased vessel angiogenesis is phenocopied by loss of endothelial-specific Robo4, as long as it is combined with the presence of an angiogenic stimulus such as preneoplasia or pregnancy. In contrast, loss of Robo1 does not affect blood vessel growth. The enhanced growth of blood vessels in Robo4 −/− endothelium is due to activation of vascular endothelial growth factor (VEGF)-R2 signaling through the Src and FAK kinases. Thus, our studies present a genetic dissection of SLIT/ROBO signaling during organ development. We identify a stromal, rather than epithelial, source of SLITs that inhibits blood vessel growth by signaling through endothelial ROBO4 to down-regulate VEGF/ VEGFR2 signaling.angiogenesis | ROBO | SLIT | mammary gland | organogenesis

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“…Moreover, the microvascularization of the lobules and the ducts differ considerably. Lobules show a low number of microvessels with large diameter and sinusoidal shape, whereas ducts are surrounded by a high number of microvessels with the appearance of typical small capillaries [71]. It has been shown that cells of ductal carcinoma in situ require increased glucose uptake supplied by the vasculature for invasion, which contributes to the correlation of increased amounts of functional capillaries with a shortened survival of the breast cancer patients [72,73].…”

Section: The Wall: Structure Of Blood Vessels In Tumor Cell Disseminamentioning

confidence: 99%

The Interrelating Dynamics of Hypoxic Tumor Microenvironments and Cancer Cell Phenotypes in Cancer Metastasis

Bartkowiak

Pantel

2011

Cancer Microenvironment

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The interrelating dynamics of the primary tumor cells and their surrounding microenvironment might determine phenotypic characteristics of disseminated tumor cells and contribute to cancer metastasis. Cytoprotective mechanisms (e.g., energy metabolism control, DNA damage response, global translation control and unfolded protein response) exert selective pressure in the tumor microenvironment. In particular, adaptation to hypoxia is vital for survival of malignant cells in the tumor and at distant sites such as the bone marrow. In addition to the stress response, the ability of tumor cells to undergo certain cellular re-differentiation programmes like the epithelial-mesenchymal transition (EMT), which is linked to cancer stemness, appears to be important for successful cancer cell spread. Here we will discuss the selection pressures that eventually lead to the formation of overt metastases. We will focus the properties of the microenvironment including (i) metabolic and cytoprotective programs that ensure survival of disseminated tumor cells, (ii) blood vessel structure, and (iii) the hypoxianormoxia switch as well as intrinsic factors affecting the evolvement of novel tumor cell populations.

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Vascular remodelling during the normal and malignant life cycle of the mammary gland

Cited by 165 publications

References 41 publications

Leukocytes in Mammary Development and Cancer

Leukocytes in Mammary Development and Cancer

Vascular Robo4 restricts proangiogenic VEGF signaling in breast

The Interrelating Dynamics of Hypoxic Tumor Microenvironments and Cancer Cell Phenotypes in Cancer Metastasis

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