Interactions between cancer cells and the microvasculature: a rate-regulator for metastasis

Abstract

Hematogenous metastasis is a major consideration in the staging, treatment and prognosis of patients with cancer. Key events affecting hematogeneous metastasis occur in the microvasculature. This is a brief, selective review of some interactions involving cancer cells and the microvasculature in pathologic sequence, specifically: (1) intravasation of cancer cells; (2) the arrest of circulating cancer cells in the microvasculature; (3) cancer cell trauma associated with arrest; (4) microvascular trauma; (5) the inflammatory; and (6) the hemostatic coagulative responses associated with arrest, and finally (7) angiogenesis, leading to tumor vascularization. The evidence shows that through a series of complex interactions with cancer cells, the microvasculature acts as a rate-regulator for the metastatic process, in addition to providing routes for cancer cell dissemination and arrest sites for cancer cell emboli.

MTA1 overexpression correlates significantly with tumor grade and angiogenesis in human breast cancers

“…(8)(9)(10) Previous experimental studies highlight the role of angiogenesis in tumor progression, such as tumor growth and blood-borne metastasis. (11,12) In breast cancer, the overall results of reported studies suggest that human breast cancer is an angiogenic-dependent tumor, and anti-angiogenic therapy may be beneficial for breast cancer patients.…”

Dissection of tumour and host cells from target organs of metastasis for testing gene expression directly ex vivo

“…Also, in recent years the concept of 'dynamic heterogeneity' was introduced. It suggests that the metastatic phenotype, although it is a genetically controlled trait, is inherently dynamic or unstable (Weiss et al, 1980;Ling et al, 1985;Vaage, 1988). Because of this phenotypic instability, an adequate methodology has to be established for direct typing of tumour cells at distinct stages of the metastatic process without in vitro culture.…”

Role of parathyroid hormone-related peptide in hypercalcemia of malignancy and osteolytic bone disease

“…The initial step, namely shedding of tumor cells from the primary site, involves detachment of tumor cells from adjacent cells, followed by invasion of adjacent tissue in the primary organs. The cells then enter tumor capillaries (stimulated by specific angiogenesis factors produced by the tumor) and via these capillaries reach the general circulation (Weiss et al 1989). The steps involved in entering the tumor blood vessels at the primary site are similar to those which are involved in exit from the vasculature in the bone marrow cavity.…”