Emens, L.A., Butterfield, L.H., Hodi, F.S.Jr., Marincola, F.M., Kaufman, H.L. (2016) Cancer immunotherapy trials: leading a paradigm shift in drug development, Journal of ImmunoTherapy of Cancer, 4:42
Khalil (2016) The future of cancer treatment: immunomodulation, CARs and combination immunotherapy, Nature Reviews Clinical Oncology, 13.5 (May): 273 -
Orgose et al., (2017) Frequent expression of HLA-I and the status of intratumoral immune cells in alveolar soft part sarcoma, Oncology Letters, 13(4): 2169-
- Patients with a better prognosis had CD8+ T-cell infiltrate in tumors that expressed HLA-I, the target of T-cell receptors. Suggested, but not shown, that these patients had cytotoxic T-cell responses to their tumors.
- Patients with a better prognosis had CD8+ T-cell infiltrate in tumors that expressed HLA-I, the target of T-cell receptors. Suggested, but not shown, that these patients had cytotoxic T-cell responses to their tumors.
Orentas (2012) Identification of cell surface proteins as potential immunotherapy targets in 12 pediatric cancers, Frontiers in Oncology, 2: 194
Wilky et al. (2014) Immunotherapy in sarcoma: a new frontier, Discovery Medicine, 14 April 2014
Jagodzinska-Mucha et al., (2017) Long-term results of therapy with sunitinib in metastatic alveolar soft part sarcoma, Tumori, 103(3): 231-
- Over half of patients with metastatic disease responded to the receptor tyrosine kinase inhibitor, sunitinib, and tolerated long-term treatment.
- Over half of patients with metastatic disease responded to the receptor tyrosine kinase inhibitor, sunitinib, and tolerated long-term treatment.
Read & WIlliams (2016) Metastatic alveolar soft part sarcoma responsive to pazopanib after progression through suntinib and bevacizumab: two cases, Case Report Oncology, 9(3): 639-643.
- Two patients had over one year response to the tyrosine kinase / VEGF and angiogenesis inhibitor suntinib but eventually progressed through it and bevacizumab (aka Avastin, a humanized mAb to VEGF-A). Both patients responded to, and were stabilized by treatment with pazopanib, another tyrosine kinase / angiogenesis inhibitor.
- Two patients had over one year response to the tyrosine kinase / VEGF and angiogenesis inhibitor suntinib but eventually progressed through it and bevacizumab (aka Avastin, a humanized mAb to VEGF-A). Both patients responded to, and were stabilized by treatment with pazopanib, another tyrosine kinase / angiogenesis inhibitor.
Tanaka et al. (2016) Modeling alveolar soft part sarcoma reveals novel mechanism of metastasis, Cancer Research, 77(4): 897-
- The ASPSCR1-TFE3 fusion protein increases expression of a number of genes including GPNMB, which codes for a surface glycoprotein seen at sites where the tumor leaves blood vessels, facilitating metastasis.
- Note that GPNMB is the target of a humanized monoclonal antibody-drug fusion now in clinical trials for melanoma & breast cancer. Once internalized by the cell, the drug (monomethyl auristatin E) is released to kill the cancer cell. Tumor regression is seen in preclinical mouse models.
- The ASPSCR1-TFE3 fusion protein increases expression of a number of genes including GPNMB, which codes for a surface glycoprotein seen at sites where the tumor leaves blood vessels, facilitating metastasis.
- Note that GPNMB is the target of a humanized monoclonal antibody-drug fusion now in clinical trials for melanoma & breast cancer. Once internalized by the cell, the drug (monomethyl auristatin E) is released to kill the cancer cell. Tumor regression is seen in preclinical mouse models.