Photodynamic therapy (PDT) utilizes a sensitizer agent and light to produce selective cell death. Dermatologists are familiar with PDT for the treatment of actinic keratoses and early nonmelanoma skin cancers, and recent studies have elucidated that PDT has resulted in improved morbidity and secondary outcomes for the treatment of various cancerous and precancerous solid tumors. Light source and dosimetry may be modified to selectively target tissue, and novel techniques such as fractionation, metronomic pulsation, continuous light delivery, and chemophototherapy are under investigation for further optimization of therapy. This article aims to review the expanding indications for PDT and demonstrate the potential of this modality to decrease morbidity and increase quality of life for patients. To illustrate these new indications, we provide a focused review of the latest literature on PDT for dermatologic and other solid tumors including gastrointestinal, peritoneal, lung, genitourinary, brain, breast, and head and neck. Data on efficacy, survival, and side effects vary across tumor types but support PDT for the treatment of numerous solid tumors. With new advances in PDT, indications for this therapeutic modality may expand.

Pancreatic neuroendocrine tumors (PanNETs) are a type of pancreatic cancer with limited therapeutic options. Consequently, most patients with advanced disease die from tumor progression. Current evidence indicates that a subset of cancer cells is responsible for tumor development, metastasis, and recurrence, and targeting these tumor-initiating cells is necessary to eradicate tumors. However, tumor-initiating cells and the biological processes that promote pathogenesis remain largely uncharacterized in PanNETs. Here we profile primary and metastatic tumors from an index patient and demonstrate that MET proto-oncogene activation is important for tumor growth in PanNET xenograft models. We identify a highly tumorigenic cell population within several independent surgically acquired PanNETs characterized by increased cell-surface protein CD90 expression and aldehyde dehydrogenase A1 (ALDHA1) activity, and provide in vitro and in vivo evidence for their stem-like properties. We performed proteomic profiling of 332 antigens in two cell lines and four primary tumors, and showed that CD47, a cell-surface protein that acts as a “don’t eat me” signal co-opted by cancers to evade innate immune surveillance, is ubiquitously expressed. Moreover, CD47 coexpresses with MET and is enriched in CD90hi cells. Furthermore, blocking CD47 signaling promotes engulfment of tumor cells by macrophages in vitro and inhibits xenograft tumor growth, prevents metastases, and prolongs survival in vivo.

No abstract

No abstract

No abstract