Abstract
Metastasis, also called secondary neoplastic disease, is a tumour newly formed in a site different from that of origin, as a consequence of cancer progression and dissemination largely through blood and lymphatic vessels. The ability to form metastases is the main property that distinguishes malignant from benign tumours. Treatments for metastatic cancer are similar in practice to those for primary tumours, but such treatments are mostly palliative; indeed, almost all deaths caused by solid tumours occur in the metastatic phase. Increasing evidence supports the concept that therapies for primary tumours are inadequate to treat metastasis and can even promote formation of metastases, while exerting local growth control. Furthermore, recurrent tumours, which are denoted by increased aggressiveness and therapy resistance in comparison with the primary tumour, have an increased metastatic potential. Genetic modifications occurring during tumour progression lead to substantial differences between the primary and metastatic tumours. This emphasises the importance of designing novel therapies for metastasis. In the last decade, a number of studies have contributed to the understanding of the genetic rearrangements underlying the conversion of cancer cells into the metastasis founder cells. The present article aims at reviewing recent advances in metastasis research and attempts to discuss the reasons for which the therapeutic strategies against primary tumours may not satisfactorily address their metastatic counterparts.
Keywords: Cancer therapy, CSC, EMT, genetic and epigenetic modifications, metastasis, tumour heterogeneity, Tumour progression.
Current Medicinal Chemistry
Title:Cellular and Molecular Background Underlying the Diversity in Therapeutic Responses Between Primary Tumours and Metastases
Volume: 21 Issue: 14
Author(s): Simona Romano, Anna D'Angelillo, Alfredo Romano, Giovanna Nappo and Maria Fiammetta Romano
Affiliation:
Keywords: Cancer therapy, CSC, EMT, genetic and epigenetic modifications, metastasis, tumour heterogeneity, Tumour progression.
Abstract: Metastasis, also called secondary neoplastic disease, is a tumour newly formed in a site different from that of origin, as a consequence of cancer progression and dissemination largely through blood and lymphatic vessels. The ability to form metastases is the main property that distinguishes malignant from benign tumours. Treatments for metastatic cancer are similar in practice to those for primary tumours, but such treatments are mostly palliative; indeed, almost all deaths caused by solid tumours occur in the metastatic phase. Increasing evidence supports the concept that therapies for primary tumours are inadequate to treat metastasis and can even promote formation of metastases, while exerting local growth control. Furthermore, recurrent tumours, which are denoted by increased aggressiveness and therapy resistance in comparison with the primary tumour, have an increased metastatic potential. Genetic modifications occurring during tumour progression lead to substantial differences between the primary and metastatic tumours. This emphasises the importance of designing novel therapies for metastasis. In the last decade, a number of studies have contributed to the understanding of the genetic rearrangements underlying the conversion of cancer cells into the metastasis founder cells. The present article aims at reviewing recent advances in metastasis research and attempts to discuss the reasons for which the therapeutic strategies against primary tumours may not satisfactorily address their metastatic counterparts.
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Romano Simona, D'Angelillo Anna, Romano Alfredo, Nappo Giovanna and Romano Fiammetta Maria, Cellular and Molecular Background Underlying the Diversity in Therapeutic Responses Between Primary Tumours and Metastases, Current Medicinal Chemistry 2014; 21 (14) . https://dx.doi.org/10.2174/09298673113209990225
DOI https://dx.doi.org/10.2174/09298673113209990225 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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