Metastatic progression is the main cause of mortality in cancer patients. Despite advances in therapies that target oncogenic drivers of cancer, not all patients with metastasis benefit from such treatments. Even in the presence of targetable oncogenic alterations, the site of disease can influence response to therapy. A notable example is brain metastasis, a devastating outcome of cancer progression. Brain metastases are refractory to currently available therapeutic strategies, including drugs that otherwise control disease in extracranial sites. Therefore, a better understanding of how the brain microenvironment impacts tumor growth is needed to develop new treatments for this patient population.
Accumulating evidence suggests that the tumor microenvironment (TME) contributes to this clinical challenge, but the mechanisms underlying how the TME influences the biology of cancer cells that colonize the brain as opposed to the primary site are incompletely understood. Brain metastases remain refractory to targeted therapies for two reasons: i) the blood-brain/blood-tumor barrier (BBB/BTB) hinders the delivery of drugs to brain metastases and ii) the brain TME reduces the efficacy of these therapies even when they accrue in brain metastases. In this special issue, we aim to explore the biology of brain metastasis through a multidisciplinary lens in order to provide a clear and compelling landscape of recent advances in the field.
To metastasize, cancer cells must adapt to the unique nutrient microenvironment of different organs. To proliferate, cells must acquire materials necessary to replicate their biomass, while providing sufficient energy reserves. Both available nutrients and the cell’s metabolic capacity dictate this ability to duplicate mass. The presence of the blood brain/tumor barrier (BBB/BTB) and local CNS stroma define the biology of metastatic cells and impact therapeutic outcomes. A better understanding of the brain metastatic cascade holds promise for improving treatment of brain metastasis.
Topics to cover (with an emphasis on oncogenic and metabolic adaptations) include but are not limited to:
1) Eetastatic cascade
2) Therapy resistance
3) Druggable vulnerabilities
4) Spatial quantification and imaging
5) BBB and BTB
6) CNS tumor-immune landscape
7) Physical properties of brain metastases
8) Prevention vs treatment
9) Preclinical models and translational research & drug screens
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Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Metastatic progression is the main cause of mortality in cancer patients. Despite advances in therapies that target oncogenic drivers of cancer, not all patients with metastasis benefit from such treatments. Even in the presence of targetable oncogenic alterations, the site of disease can influence response to therapy. A notable example is brain metastasis, a devastating outcome of cancer progression. Brain metastases are refractory to currently available therapeutic strategies, including drugs that otherwise control disease in extracranial sites. Therefore, a better understanding of how the brain microenvironment impacts tumor growth is needed to develop new treatments for this patient population.
Accumulating evidence suggests that the tumor microenvironment (TME) contributes to this clinical challenge, but the mechanisms underlying how the TME influences the biology of cancer cells that colonize the brain as opposed to the primary site are incompletely understood. Brain metastases remain refractory to targeted therapies for two reasons: i) the blood-brain/blood-tumor barrier (BBB/BTB) hinders the delivery of drugs to brain metastases and ii) the brain TME reduces the efficacy of these therapies even when they accrue in brain metastases. In this special issue, we aim to explore the biology of brain metastasis through a multidisciplinary lens in order to provide a clear and compelling landscape of recent advances in the field.
To metastasize, cancer cells must adapt to the unique nutrient microenvironment of different organs. To proliferate, cells must acquire materials necessary to replicate their biomass, while providing sufficient energy reserves. Both available nutrients and the cell’s metabolic capacity dictate this ability to duplicate mass. The presence of the blood brain/tumor barrier (BBB/BTB) and local CNS stroma define the biology of metastatic cells and impact therapeutic outcomes. A better understanding of the brain metastatic cascade holds promise for improving treatment of brain metastasis.
Topics to cover (with an emphasis on oncogenic and metabolic adaptations) include but are not limited to:
1) Eetastatic cascade
2) Therapy resistance
3) Druggable vulnerabilities
4) Spatial quantification and imaging
5) BBB and BTB
6) CNS tumor-immune landscape
7) Physical properties of brain metastases
8) Prevention vs treatment
9) Preclinical models and translational research & drug screens
--
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.