The process of metastasisation for breast cancer

Engel, Jutta; Eckel, Renate; Kerr, Jacqueline; Schmidt, Marjanka K.; Fürstenberger, G.; Richter, Rudolf; Sauer, H.; Senn, Hans; Hölzel, Dieter

doi:10.1016/s0959-8049(03)00422-2

Cited by 148 publications

(108 citation statements)

References 76 publications

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“…In addition, patients recorded by the MCR showed advantageous stage distribution over the periods, which also contributed to improved prognosis. Time from initial diagnosis to metastasis is prolonged for pT1 versus pT2 [8], but changes in adjuvant systemic treatment will also have lengthened the time. [10,11] The adjuvant treatment prevents the development of metastases or at least postpones it.…”

Section: Discussionmentioning

confidence: 99%

“…The MCR has in the last period a catchment area of 2.5 million residents (since 2002 3.9 million residents) and records data on all patients newly diagnosed with cancer. [8,9] The unequal subdivision into time periods of initial diagnosis marks steps in the changes from a hospital-based (up to 1984) to a populationbased registry of Munich and surrounding area's. The MCR is for breast cancer population-based since 1994, when the pathologists of the region started structural cooperation with the MCR.…”

Section: Study Population and Data Collectionmentioning

confidence: 99%

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Unfavourable pattern of metastases in M0 breast cancer patients during 1978-2008: a population-based analysis of the Munich Cancer Registry

Hurk

Eckel

Poll‐Franse

et al. 2011

Breast Cancer Res Treat

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Key words: metastases pattern, time to metastases, survival, breast cancer 2 ABSTRACT PurposeLittle is known about time trends in metastases in patients treated in routine health care facilities without metastases at diagnosis (M0) and about survival after these metastases. Methods Data ConclusionsIn the period 1978-2008, unfavourable changes in the pattern of metastases were exhibited and no improvement was observed in survival of patients after occurrence of metastases. An explanation might be the increased use of adjuvant systemic treatment, which has less effect on the highly lethal liver and CNS metastases than on bone metastases. The increased use also appeared to contribute to the overall prevention of metastases in breast cancer and therefore to improvement of overall survival.3

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Section: Discussionmentioning

confidence: 99%

Section: Study Population and Data Collectionmentioning

confidence: 99%

Unfavourable pattern of metastases in M0 breast cancer patients during 1978-2008: a population-based analysis of the Munich Cancer Registry

Hurk

Eckel

Poll‐Franse

et al. 2011

Breast Cancer Res Treat

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“…Seeding can occur to multiple organs, but metastatic tumours may grow in only one or a few 5 . There is also increasing evidence that in some cases cancer cells can lie dormant for many years, and that seeding may occur several years before diagnosis of the primary tumour [6][7][8][9][10] . In another phenomenon, termed angiogenic dormancy, there is a balance of proliferation and apoptosis that results in micrometastases that do not progress further 11,12 .…”

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Microenvironmental regulation of metastasis

2008

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Metastasis is a multistage process that requires cancer cells to escape from the primary tumour, survive in the circulation, seed at distant sites and grow. Each of these processes involves ratelimiting steps that are influenced by non-malignant cells of the tumour microenvironment. Many of these cells are derived from the bone marrow, particularly the myeloid lineage, and are recruited by cancer cells to enhance their survival, growth, invasion and dissemination. This Review describes experimental data demonstrating the role of the microenvironment in metastasis, identifies areas for future research and suggests possible new therapeutic avenues.A variety of stromal cells in the surrounding environment are recruited to tumours, and these not only enhance growth of the primary cancer but also facilitate its metastatic dissemination to distant organs. Cancer cells in an aggressive primary mass are adept at exploiting that particular tissue microenvironment; however, once they leave these favourable surroundings, they must possess traits that will allow them to survive in new environments. In order for a metastasis to occur, the intravasated cancer cell must survive in the circulation, arrive at the target organ (seeding), extravasate into the parenchyma and show persistent growth 1 . Each of these stages is inefficient and some are rate limiting 1,2 . For example, senescence or apoptosis of cancer cells at the stage of entry into the metastatic site prevents the spread of the majority of circulating cells [2][3][4] . Seeding can occur to multiple organs, but metastatic tumours may grow in only one or a few 5 . There is also increasing evidence that in some cases cancer cells can lie dormant for many years, and that seeding may occur several years before diagnosis of the primary tumour [6][7][8][9][10] . In another phenomenon, termed angiogenic dormancy, there is a balance of proliferation and apoptosis that results in micrometastases that do not progress further 11,12 . The microenvironment clearly suppresses NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript the malignancy of these potentially metastatic cells 10 , and their re-activation to form a clinically relevant metastasis probably occurs through perturbations in the microenvironment. Nevertheless, despite this evidence for early seeding and dormancy, tumour size and grade are the main predictors of metastasis, and this has been reinforced in recent studies in mouse models 13 and by gene expression analysis that linked large tumour size with metastasis-enhancing gene signatures 14 . It has been hypothesized that this may be due to metastatic re-seeding to primary tumours 15 . If this is the case, nothing is currently known about the underlying mechanisms. Successful metastatic outgrowth thus depends on the cumulative ability of cancer cells to appropriate distinct microenvironments at each step in the metastatic cascade: the primary tumour, systemic circulation and the final metastatic site. In this Review we discuss instruct...

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“…Une tumeur d'un cm de diamètre compte environ 10 9 cellules. Il y a une corrélation directe entre les dimensions de la tumeur primitive et le risque de maladie métastatique [3]. Enfin, l'apparition de métastases macroscopiques est souvent un 1 Alors que la plupart des cancers détectés à un stade précoce peuvent être guéris, un patient qui développe des métastases est souvent incurable.…”

Section: Le Modèle De La Sélection Clonaleunclassified

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Les étapes précoces du processus métastatique

Hubert

Abastado

2014

Med Sci (Paris)

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> Le développement de métastases est la cause principale des décès par cancer. Bien que les métastases ne deviennent cliniquement détectables que tardivement, un certain nombre d'études récentes, dans des modèles animaux et chez les patients, montrent que la dissémination des cellules cancéreuse à partir de la tumeur primitive est parfois un événement précoce. Toutefois, les cellules cancéreuses disséminées peuvent demeurer dormantes pendant des mois, voire des années. Mais alors, comment les cellules cancéreuses acquièrent-elles cette capacité à disséminer si rapidement ? Quelles sont les pressions sélectives qui favorisent leur dissémination ? Quels sont les signaux qui contrôlent leur dormance, et pourquoi certaines cellules échappent-elles finalement à ces contrôles et se développent-elles en métastases macroscopiques ? Nous présentons dans cet article les conceptions les plus récentes de ces questions et discutons leurs possibles implications cliniques. < sortir de ces vaisseaux (extravasation) et coloniser un nouvel organe où elles se multiplient et, à terme, se développent en tumeurs secondaires (métastases). Chacune de ces étapes nécessite l'acquisition de caractéristiques particulières : capacité à dégrader la matrice extracellulaire, motilité, résistance aux forces de cisaillement rencontrées dans la circulation sanguine, échappement au système immunitaire, capacité de survivre et, surtout, acquisition de la capacité à proliférer dans un nouvel environnement [43, 44] ( §). L'acquisition d'un nombre si important de caractères est mal comprise. Dans cette revue, nous discuterons une série de résultats obtenus récemment qui décrivent la cinétique d'acquisition du phénotype métastatique, les mécanismes permettant cette acquisition et les conditions permettant leur sélection. Le modèle de la sélection clonaleLe paradigme traditionnel, appelé modèle linéaire de la sélection clonale (Figure 2A), considère que toutes les caractéristiques nécessaires à l'acquisition du phénotype métastatique dépendent de l'accumulation de mutations indépendantes dans la cellule cancéreuse [2]. On sait que la probabilité d'apparition d'une mutation dans une population (de cellules) donnée dépend du taux de mutation à chaque génération, de la taille de la population et de la durée. Les cellules cancéreuses sont, de fait, caractérisées par une instabilité génétique, compatible avec un taux de mutation élevé. La taille de la tumeur primitive contribue éga-lement à l'émergence de métastases. Une tumeur d'un cm de diamètre compte environ 10 9 cellules. Il y a une corrélation directe entre les dimensions de la tumeur primitive et le risque de maladie métastatique [3]. Enfin, l'apparition de métastases macroscopiques est souvent un

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The process of metastasisation for breast cancer

Cited by 148 publications

References 76 publications

Unfavourable pattern of metastases in M0 breast cancer patients during 1978-2008: a population-based analysis of the Munich Cancer Registry

Unfavourable pattern of metastases in M0 breast cancer patients during 1978-2008: a population-based analysis of the Munich Cancer Registry

Microenvironmental regulation of metastasis

Les étapes précoces du processus métastatique

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