Anti-angiogenic therapy in combination with immunotherapy hold more promise than either alone.
Make the argument for and against.
Angiogenesis refers to the growth of new vasculature driven by the hypoxia that tumour cells face.
Immunotherapy can help the body fight cancer cells as they can evade the immune system.
Examples of anti-angiogenic drugs include VEGF inhibitors (e.g. Bevacizumab) and Avastin.
Immunotherapy often involves. Angiogenesis can interfere with the Tumour Microenvironment and
result in one that is immune-suppressive and not supportive. While immunotherapy on its own can
significantly improve treatment for a multitude for patients, it is estimated 87% patients do not
attain any long-term benefit. ^1 This raises the question as to whether combining it with another
form of therapy may increase its efficacy. Multiple studies can confirm that angiogenesis and
immunotherapy combined can result in more effective treatments for patients.
A high CD8 positive T cell number in the Tumour Micro environment is correlated with a good
prognosis amongst patients. What is yet to be confirmed is whether anti-angiogenic therapy in
combination with immunotherapy holds any promise for those cancers in which a high CD8* positive
T cell does not correlate with better prognostic outcomes. So called ‘vascular- normalization’ can
help revert an immune-suppressive tumour microenvironment.
Studies conducted at University Hospital of Basel, EPFL and the Roche Innovation Centre Zurich Anti-
CD40 antibodies help scavenge Natural Killer Cells but they can only be detected in peripheral areas
of the tumour and not in the interior of the tumour. This can also be explained by the
immunosuppressive environment caused by the irregular vasculature. Delivering an anti-angiogenic
(Avastin) adjuvant to the CD-40 antibody was shown to improve response amongst ‘cold’ tumours
(i.e. tumours that showed little to no response to traditional monotherapy)
The tumour microenvironment ability to allow tumour cells to evade the immune system is
increased by angiogenesis. The binding of VEGF to VEGFR results in several events which allow a
tumour to evade the immune system. VEGF is one of these negative factors which upon secretion
mediates the conversion of to dendritic cells (the first messengers of the adaptive immune system)
as they present antigens to T cells.
The binding of VEGF to VEGFR helps recruit immuno-suppressive members of the immune system
such as myeloid-derived suppressor cells, M2 like TAMs through the activation of the STAT3
Make the argument for and against.
Angiogenesis refers to the growth of new vasculature driven by the hypoxia that tumour cells face.
Immunotherapy can help the body fight cancer cells as they can evade the immune system.
Examples of anti-angiogenic drugs include VEGF inhibitors (e.g. Bevacizumab) and Avastin.
Immunotherapy often involves. Angiogenesis can interfere with the Tumour Microenvironment and
result in one that is immune-suppressive and not supportive. While immunotherapy on its own can
significantly improve treatment for a multitude for patients, it is estimated 87% patients do not
attain any long-term benefit. ^1 This raises the question as to whether combining it with another
form of therapy may increase its efficacy. Multiple studies can confirm that angiogenesis and
immunotherapy combined can result in more effective treatments for patients.
A high CD8 positive T cell number in the Tumour Micro environment is correlated with a good
prognosis amongst patients. What is yet to be confirmed is whether anti-angiogenic therapy in
combination with immunotherapy holds any promise for those cancers in which a high CD8* positive
T cell does not correlate with better prognostic outcomes. So called ‘vascular- normalization’ can
help revert an immune-suppressive tumour microenvironment.
Studies conducted at University Hospital of Basel, EPFL and the Roche Innovation Centre Zurich Anti-
CD40 antibodies help scavenge Natural Killer Cells but they can only be detected in peripheral areas
of the tumour and not in the interior of the tumour. This can also be explained by the
immunosuppressive environment caused by the irregular vasculature. Delivering an anti-angiogenic
(Avastin) adjuvant to the CD-40 antibody was shown to improve response amongst ‘cold’ tumours
(i.e. tumours that showed little to no response to traditional monotherapy)
The tumour microenvironment ability to allow tumour cells to evade the immune system is
increased by angiogenesis. The binding of VEGF to VEGFR results in several events which allow a
tumour to evade the immune system. VEGF is one of these negative factors which upon secretion
mediates the conversion of to dendritic cells (the first messengers of the adaptive immune system)
as they present antigens to T cells.
The binding of VEGF to VEGFR helps recruit immuno-suppressive members of the immune system
such as myeloid-derived suppressor cells, M2 like TAMs through the activation of the STAT3
