**Author details**

#### Serdar Altınay

new molecules named migfilin, mitogen‐inducible gene‐2 (Mig‐2), and Ras suppressor‐1 (RSU‐ 1) in the cell‐ECM adhesion fields. The authors reached the conclusion that cell‐ECM adhesion proteins are predisposed to function such as adaptor proteins in the form of multiple protein‐

Even though the different effects in various types of cancer cells were discussed, they added that cell adhesion, which is crucial in terms of cell metastasis in many cases, supported cell

Despite the "skill" they display in moving away from the site in which they were first formed, tumor cells are rather ineffective in terms of forming colonies in distant organs. Millions of cells drop off even from small tumors every single day; even though macroscopic metastases have not developed, it is possible to identify these cells in the blood circulation and in small foci in the bone marrow. The dormant state of micrometastases, which is defined as the capacity to preserve their existence for a long period without any progression, was observed in breast

In the studies demonstrating that ECM undertook a dynamic niche role in the progression of cancer in recent years [5–7], investigators indicated that the microenvironment or niche played a major role in the development of cancer. Abnormal ECM directly promotes cellular trans‐

A successful metastasis does not require local niche supporting only cancer cell development in the primary focus, but also necessitates the survival, colonization of the cancer cells invading

The molecular mechanisms of colonization have just begun to be enlightened in mice models, but the view claiming that tumor cells impact normal stroma cells and secrete cytokines, growth factors and proteases, which transform the site of metastasis into an environment

As metastatic mechanisms are better understood at a molecular level, it will be significantly easier for physicians to use these mechanisms as a treatment goal [90]. The identification of tissue‐specific signals involved in metastatic progression will open the way to new therapeutic strategies. For this purpose, the authors [91] reviewed recent progress in the field, with particular emphasis on the mechanisms of organ‐specific dissemination and colonization of breast cancer (**Figure 5**). Despite what has been described so far, it may not be possible to estimate exactly which cancer type may metastasize. But a noteworthy area of forthcoming cancer research will be to determine whether abnormal ECM could be an effective cancer therapeutic target. So we should understand how ECM composition and organization are

formation and metastasis and impacted the progression of cancer [84].

the metastatic niches and their achievement of macrometastasis [85–87].

where cancer cells may live, appears to be suitable [88, 89].

protein interaction in the cell‐ECM adhesion fields.

**2.11. Is ECM the main constituent of niches?**

invasion and apoptosis.

34 Tumor Metastasis

and prostate cancer [29, 30, 44].

**3. Concluding remarks**

Address all correspondence to: drserdara@yahoo.com

Department of Pathology, Medical Faculty, Selcuk University , Konya, Turkey
