What We're Reading
Cancer Immunol Res March 1 2017 5 (3) 181-181;
Nab-paclitaxel (Abraxane) is used to treat pancreatic ductal adenocarcinoma. Nab-paclitaxel is internalized by tumor-associated macrophages via macropinocytosis and activates them toward an immunostimulatory, M1 state. This mechanism of action may be applicable to other cancers exhibiting macrophage infiltration.
Treating cancers by combining approaches is thought to hold great promise. This study demonstrates that caution will be necessary in the selection of antibody therapies that target T cells when trying to enhance antitumor efficacy in B-cell lymphoma.
Immune therapies are usually successful in a fraction of patients. Squamous cell carcinomas originate in a stratified epithelium, and distinctly different immune responses were found to be driven by the state of differentiation of the tumor-initiating cell.
Antitumor vaccines are still inefficient. However, when tumor cells were infected ex vivo with an IL12-expressing oncolytic virus and used as a vaccine, peritoneal carcinomatosis mouse models showed a 90% cure rate and protective immunity from rechallenge.
Effective antitumor vaccines have been elusive. Two tumor models were used to test vaccines comprising liposome-encapsulated synthetic long peptides and TLR-activating adjuvants. These could cure 75–100% of the mice of large established HPV-expressing tumors and showed immunological memory.
Resistance to anti-estrogen therapy is common among metastatic breast cancer patients. Estradiol increased secretion of TGFβ1 from cancer cells and LFA-1 on neutrophils, which led to increased cancer cell dissemination. Targeting these pathways may enhance treatment efficacy.
Patients with gastric cancer had few NK cells infiltrating their tumors, a condition associated with tumor progression and poor survival. These intratumoral NK cells were functionally impaired, due to the presence of TGFβ1 derived from tumor-associated monocytes/macrophages.
Lung cancer initially prompts an antitumor immune response, which devolves into a powerfully immunosuppressive environment. Myeloid STAT3 was found to be the culprit responsible for transforming tumor immunosurveillance into the tumor-promoting inflammation that nurtures tumorigenesis.