About this Research Topic
One of the milestones in 1970 was the discovery of the Cytotoxicity of T lymphocytes. T lymphocytes are able to kill virus-infected and tumour cells in vitro. However, it is not clear whether cytotoxicity is the main mechanism by which T lymphocytes control tumours in vivo. Due to the antigenic heterogeneity of tumours, it is unlikely that T lymphocytes will kill 100 per cent of the tumour cells. Unfortunately, even if a very small fraction of these tumour cells remain after a T lymphocyte attack, this is likely to give rise to the development of new tumours.
Both normal tissues and tumours are composed of dividing and resting cells. The percentage of proliferative cells contributing to tumour growth is called the cellular growth fraction. The remaining non-proliferating cells are in the so-called led G0 phase. These cells are most likely the cancer stem cells that have the ability to reconstitute tumours. Disseminated non-dividing (dormant) cancer cells are regarded as the major challenge for the successful treatment of cancer. However, prolonged maintenance of the steady state of the disseminated cancer cell population in the G0 state by immunosurveillance mechanisms can be regarded as a cure.
Accumulating evidence indicates apart from cytotoxicity, cytostatic mechanisms of T lymphocytes may be important in tumour control. Rejection of allogeneic tumours by CD8+ T-lymphocytes that were not lytic for the tumour has been described more than 30 years ago. Decreased cytotoxic T-cell activity in vitro was associated with augmented antitumor immunity in a mouse model. The most direct and solid evidence, indicating the cytostatic effect of T lymphocytes on tumour cells was obtained using newly developed FUCCI technology: it has been demonstrated that T lymphocytes drive proliferating tumour cells into quiescent G1 or G0 phase. Recent evidence indicates that cancer cells that survive upon adoptive T cell therapy do not proliferate.
This Research Topic aims to address the following topical issues:
1. New technologies or strategies to evaluate the proportion of cycling cells (growth fraction) within tumours and normal tissues
2. New mechanisms regulating the transit of cells between the G0 and G1 phases of the cell cycle
3. Characterisation of the proliferative state of cancer stem cells
4. Signalling between T lymphocytes and tumour cells, which influences the proliferative state of tumour cells
5. New mechanisms of interaction between the immune system and cancer stem cells
6. New mechanisms of the immune system that maintain tumour cells in a dormant state
We welcome Original Research, Review/Mini-Review, Hypothesis and Theory, Systematic Review, Clinical Trial articles, Opinions, and Perspective articles.
Please Note: Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
Both normal tissues and tumours are composed of dividing and resting cells. The percentage of proliferative cells contributing to tumour growth is called the cellular growth fraction. The remaining non-proliferating cells are in the so-called led G0 phase. These cells are most likely the cancer stem cells that have the ability to reconstitute tumours. Disseminated non-dividing (dormant) cancer cells are regarded as the major challenge for the successful treatment of cancer. However, prolonged maintenance of the steady state of the disseminated cancer cell population in the G0 state by immunosurveillance mechanisms can be regarded as a cure.
Accumulating evidence indicates apart from cytotoxicity, cytostatic mechanisms of T lymphocytes may be important in tumour control. Rejection of allogeneic tumours by CD8+ T-lymphocytes that were not lytic for the tumour has been described more than 30 years ago. Decreased cytotoxic T-cell activity in vitro was associated with augmented antitumor immunity in a mouse model. The most direct and solid evidence, indicating the cytostatic effect of T lymphocytes on tumour cells was obtained using newly developed FUCCI technology: it has been demonstrated that T lymphocytes drive proliferating tumour cells into quiescent G1 or G0 phase. Recent evidence indicates that cancer cells that survive upon adoptive T cell therapy do not proliferate.
This Research Topic aims to address the following topical issues:
1. New technologies or strategies to evaluate the proportion of cycling cells (growth fraction) within tumours and normal tissues
2. New mechanisms regulating the transit of cells between the G0 and G1 phases of the cell cycle
3. Characterisation of the proliferative state of cancer stem cells
4. Signalling between T lymphocytes and tumour cells, which influences the proliferative state of tumour cells
5. New mechanisms of interaction between the immune system and cancer stem cells
6. New mechanisms of the immune system that maintain tumour cells in a dormant state
We welcome Original Research, Review/Mini-Review, Hypothesis and Theory, Systematic Review, Clinical Trial articles, Opinions, and Perspective articles.
Please Note: Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
Keywords: Immunosurveillance, Cytostatic T-Lymphocytes, Cancer
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
