We are analyzing https://link.springer.com/article/10.1007/s10555-007-9103-x.

Title:
A “class action” against the microenvironment: do cancer cells cooperate in metastasis? | Cancer and Metastasis Reviews
Description:
The authors review how cancer cells may cooperate in metastasis by means of microenvironmental changes. The main mechanisms underlying this cooperation are clustered migration of cancer cells, extracellular matrix degradation, paracrine loops of released signaling factors and/or induction of adhesion molecules on stromal cells. Another critical factor could be temporal cooperation: successive waves of cancer cells may induce progressive conditioning of the microenvironment. The “class action” of cancer cells against the microenvironment involves successive steps of the metastatic process: invasion of the primary tumor microenvironment, collective migration through the extracellular matrix, blood vessel disruption, vascular or lymphatic tumor emboli, establishment of a premetastatic niche by secreted factors and endothelial precursor recruitment, induction of cell adhesion molecule expression in endothelial cells, extravasation, micrometastasis dormancy and establishment of a new growth in distant sites. As a result, after completion of the metastatic process, the series of microenvironmental changes from the primary tumor to the metastatic site may promote colonization of metastases by nonmetastatic cancer cells of the primary tumor.
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Keywords {🔍}

cancer, google, scholar, article, pubmed, cas, metastasis, cells, tumor, cell, journal, metastatic, breast, research, reviews, microenvironment, migration, nature, bone, invasion, clinical, bidard, marrow, primary, oncology, biology, progression, pathology, privacy, cookies, content, mechanisms, matrix, international, interactions, liver, analysis, data, publish, search, françoisclément, vincentsalomon, cooperation, adhesion, collective, premetastatic, niche, micrometastasis, access, endothelium,

Topics {✒️}

month download article/chapter françois-clément bidard dynamic hetero-cellular communications jean-yves pierga collective cell movement stromal-derived matrix metalloproteinases tumour-mediated upregulation lung-metastatic cancer cells full article pdf cell–cell interaction e-selectin expression privacy choices/manage cookies collective migration minimal residual disease article bidard premetastatic niche therapeutic aid multicellular resistance carcinoma invasion host proinflammatory response pre-metastatic niche �pre-metastatic niche living mouse liver cell–matrix adhesion related subjects tumor cell motility specific colonization clinical breast cancer cell adhesive interactions tumour metastasis cancer cell interactions primary melanoma explants independent prognostic factor powerful prognostic factor iii breast cancer nature cell biology latent disseminated cells nature clinical practice primary tumor microenvironment metastatic breast cancer clinical cancer research induce progressive conditioning blood vessel disruption real-time observation aacr annual meeting breast cancer cells main mechanisms underlying bone marrow cells molecular cell biology local matrix reorganization

Questions {❓}

A “class action” against the microenvironment: do cancer cells cooperate in metastasis?
A “class action” against the microenvironment: do cancer cells cooperate in metastasis?
Active versus passive mechanisms in metastasis: Do cancer cells crawl into vessels, or are they pushed?
Can detection of circulating tumor cells in peripheral blood provide prognostic data in breast cancer?
Tumour metastasis: Is tissue an issue?

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      description:The authors review how cancer cells may cooperate in metastasis by means of microenvironmental changes. The main mechanisms underlying this cooperation are clustered migration of cancer cells, extracellular matrix degradation, paracrine loops of released signaling factors and/or induction of adhesion molecules on stromal cells. Another critical factor could be temporal cooperation: successive waves of cancer cells may induce progressive conditioning of the microenvironment. The “class action” of cancer cells against the microenvironment involves successive steps of the metastatic process: invasion of the primary tumor microenvironment, collective migration through the extracellular matrix, blood vessel disruption, vascular or lymphatic tumor emboli, establishment of a premetastatic niche by secreted factors and endothelial precursor recruitment, induction of cell adhesion molecule expression in endothelial cells, extravasation, micrometastasis dormancy and establishment of a new growth in distant sites. As a result, after completion of the metastatic process, the series of microenvironmental changes from the primary tumor to the metastatic site may promote colonization of metastases by nonmetastatic cancer cells of the primary tumor.
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