Living in their specific microenvironment cells execute a continuous counterbalance between proliferation, differentiation, and cell death to preserve a normal and healthy structure and function. These tasks involve an unceasing choreography, evidenced by cellular architecture and coordinated by paracrine interactions. The loss of these homeostatic dynamics can be triggered by cell damage or stress, causing aberrant proliferation, an essential step to trigger tumor development. Although most cellular damage can be rapidly fixed by several intrinsic mechanisms, cells coursing an unregulated cellular growth struggle for restricted oxygen, critical nutrients and growth factors; hence, many die. Therefore, for rendering tumor development possible, cells must acquire abilities such as unconstrained growth, cell death evasion, milieu acidification, angiogenesis stimulation, and eventually invasion. All these alterations could transform a unified cell group into a small tumor ecosystem, in which different cell phenotypes compete and eventually collaborate for available space and resources with the aim to survive and proliferate.
A major strategy for tumor suppression could consist of a fine balance between apoptosis and necrosis; however, they are not concluding fates per se. Furthermore, cellular senescence includes the loss of mitotic activity, yet it also generates harmful molecules and could favor tumorigenesis, which afterwards can be cleared by autophagy, the removal of damaged or unnecessary cellular by-products. In addition, tumor cells are able to stimulate autophagy to survive somehow. Still, abundant autophagy could result in destruction and ultimately induce apoptosis. Since no single feature conveys a net growth-suppressive advantage, outlining the prior cell phenotypes during tumor development and the interaction between them is particularly important for an optimal tumor settlement.
Concerning therapeutic approaches, the combination of these mechanisms compels tumor course, affecting therapy reaction by endorsing drug resistance or, to the contrary, raising the possibility for drug effectiveness. It was long assumed that chemotherapeutic agents harm was directly responsible for the antitumor result. However, injury induced by these drugs is not steadily lethal but instead intensely triggers damage responses, which will determine the fate of the cell.
The tumor ecosystem will dynamically rearrange to a novel state leading to chemo-tolerant sub-clones that might have susceptibility towards different cellular programs, even intercepting existing tumor-suppressor networks. By understanding these relationships, current tumor suppressive therapies could be employed more effectively.
Endocrine tissue usually presents diverse cell subtypes responsive to a plethora of cell signaling and capable of a fine-tuning adjustment for physiological homeostasis maintenance. Endocrine tumors, defined as neoplasia of hormone-secreting cells of classic endocrine glands, occur less frequently compared with other types of neoplasia, in part because many of them remain undiagnosed. These lesions undergo nodular hyperplasia or adenoma formation and usually present complex phenotypes and paradoxical behavior patterns, whose management still depends on the classic histopathological criteria. In these tissues, appropriate interpretation of different phenotypes or cellular outcomes during tumor growth is potentially useful because the pathogenesis of many endocrine adenomas is unclear and the histological characteristics used for prognosis are of limited value.
Decisions between surviving or dying, to proliferate or be arrested are made in the face of many divergent influences. To compensate disturbances, biological networks are settled through intricate dialogues entailing growth factors, cytokines, hormones, and proteases, components of the extracellular matrix, and cell-cell interactions. Understanding how a single component of such a complex and multifaceted network collaborates toward the outcome of each process is a key aspect to understanding the larger picture of system dynamics.
This Research Topic focuses on the nature of the heterogenic features of growth-inhibitory programs during tumor growth, and its implications in the evolution and treatment of endocrine tumors. We seek contributions in the form of reviews, mini reviews, original research, and perspectives from investigators addressing these questions across diverse fields, including but not limited to:
• Contribution of apoptosis, necrosis, autophagy, cellular senescence, and other cellular programs involved in endocrine tumor development, shaping the dynamic of cellular growth or as response to chemotherapeutic treatment.
• Central signalling pathways implicated in cellular abilities to shift and lead to choice decision during endocrine tumorigenesis.
• Participation of cellular or molecular immune regulation of cellular fate choices within the tumor mass or in the microenvironment.
• Involvement of cellular differentiation, transformation, de-differentiation, and stem cell niche shaping the dynamic of cellular growth or as response to chemotherapeutic treatment.
Living in their specific microenvironment cells execute a continuous counterbalance between proliferation, differentiation, and cell death to preserve a normal and healthy structure and function. These tasks involve an unceasing choreography, evidenced by cellular architecture and coordinated by paracrine interactions. The loss of these homeostatic dynamics can be triggered by cell damage or stress, causing aberrant proliferation, an essential step to trigger tumor development. Although most cellular damage can be rapidly fixed by several intrinsic mechanisms, cells coursing an unregulated cellular growth struggle for restricted oxygen, critical nutrients and growth factors; hence, many die. Therefore, for rendering tumor development possible, cells must acquire abilities such as unconstrained growth, cell death evasion, milieu acidification, angiogenesis stimulation, and eventually invasion. All these alterations could transform a unified cell group into a small tumor ecosystem, in which different cell phenotypes compete and eventually collaborate for available space and resources with the aim to survive and proliferate.
A major strategy for tumor suppression could consist of a fine balance between apoptosis and necrosis; however, they are not concluding fates per se. Furthermore, cellular senescence includes the loss of mitotic activity, yet it also generates harmful molecules and could favor tumorigenesis, which afterwards can be cleared by autophagy, the removal of damaged or unnecessary cellular by-products. In addition, tumor cells are able to stimulate autophagy to survive somehow. Still, abundant autophagy could result in destruction and ultimately induce apoptosis. Since no single feature conveys a net growth-suppressive advantage, outlining the prior cell phenotypes during tumor development and the interaction between them is particularly important for an optimal tumor settlement.
Concerning therapeutic approaches, the combination of these mechanisms compels tumor course, affecting therapy reaction by endorsing drug resistance or, to the contrary, raising the possibility for drug effectiveness. It was long assumed that chemotherapeutic agents harm was directly responsible for the antitumor result. However, injury induced by these drugs is not steadily lethal but instead intensely triggers damage responses, which will determine the fate of the cell.
The tumor ecosystem will dynamically rearrange to a novel state leading to chemo-tolerant sub-clones that might have susceptibility towards different cellular programs, even intercepting existing tumor-suppressor networks. By understanding these relationships, current tumor suppressive therapies could be employed more effectively.
Endocrine tissue usually presents diverse cell subtypes responsive to a plethora of cell signaling and capable of a fine-tuning adjustment for physiological homeostasis maintenance. Endocrine tumors, defined as neoplasia of hormone-secreting cells of classic endocrine glands, occur less frequently compared with other types of neoplasia, in part because many of them remain undiagnosed. These lesions undergo nodular hyperplasia or adenoma formation and usually present complex phenotypes and paradoxical behavior patterns, whose management still depends on the classic histopathological criteria. In these tissues, appropriate interpretation of different phenotypes or cellular outcomes during tumor growth is potentially useful because the pathogenesis of many endocrine adenomas is unclear and the histological characteristics used for prognosis are of limited value.
Decisions between surviving or dying, to proliferate or be arrested are made in the face of many divergent influences. To compensate disturbances, biological networks are settled through intricate dialogues entailing growth factors, cytokines, hormones, and proteases, components of the extracellular matrix, and cell-cell interactions. Understanding how a single component of such a complex and multifaceted network collaborates toward the outcome of each process is a key aspect to understanding the larger picture of system dynamics.
This Research Topic focuses on the nature of the heterogenic features of growth-inhibitory programs during tumor growth, and its implications in the evolution and treatment of endocrine tumors. We seek contributions in the form of reviews, mini reviews, original research, and perspectives from investigators addressing these questions across diverse fields, including but not limited to:
• Contribution of apoptosis, necrosis, autophagy, cellular senescence, and other cellular programs involved in endocrine tumor development, shaping the dynamic of cellular growth or as response to chemotherapeutic treatment.
• Central signalling pathways implicated in cellular abilities to shift and lead to choice decision during endocrine tumorigenesis.
• Participation of cellular or molecular immune regulation of cellular fate choices within the tumor mass or in the microenvironment.
• Involvement of cellular differentiation, transformation, de-differentiation, and stem cell niche shaping the dynamic of cellular growth or as response to chemotherapeutic treatment.
