Curcumin is a polyphenol extracted from the rhizomes of the turmeric plant, Curcuma longa which has anti-inflammatory, and anticancer properties. Chronic inflammation is associated with the development of cancer. Curcumin acts on the regulation of various immune modulators, including cytokines, cyclooxygenase-2 (COX-2), and reactive oxygen species (ROS), which partly explains its anticancer effects. It also takes part in the downregulation of growth factors, protein kinases, oncogenic molecules and various signaling pathways, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), c-Jun N-terminal kinase (JNK) and signal transducer and activator of transcription 3 (STAT3) signaling. Clinical trials of curcumin have been completed or are ongoing for various types of cancer. This review presents the molecular mechanisms of curcumin in different types of cancer and the evidence from the most recent clinical trials.

Cancer is a life-threatening disease and one of the leading causes of death worldwide. Despite significant advancements in therapeutic options, most available anti-cancer agents have limited efficacy. In this context, natural compounds with diverse chemical structures have been investigated for their multimodal anti-cancer properties. Curcumin is a polyphenol isolated from the rhizomes of Curcuma longa and has been widely studied for its anti-inflammatory, anti-oxidant, and anti-cancer effects. Curcumin acts on the regulation of different aspects of cancer development, including initiation, metastasis, angiogenesis, and progression. The phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) pathway is a key target in cancer therapy, since it is implicated in initiation, proliferation, and cancer cell survival. Curcumin has been found to inhibit the PI3K/Akt pathway in tumor cells, primarily via the regulation of different key mediators, including growth factors, protein kinases, and cytokines. This review presents the therapeutic potential of curcumin in different malignancies, such as glioblastoma, prostate and breast cancer, and head and neck cancers, through the targeting of the PI3K/Akt signaling pathway.

Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants for the treatment of depression in patients with Parkinson's Disease (PD) but data on their efficacy are controversial.

Central nervous system (CNS) germ cell tumors (GCT) have not been epidemiologically well described. Our study describes 2 population-based series of nonpineal CNS GCT. Data on all primary (malignant and nonmalignant) CNS (ICD-O-3 sites: C70.0–C72.9, C75.1–C75.3) GCT diagnosed between 2000 and 2004 from the Central Brain Tumor Registry of the United States (CBTRUS) and on all malignant GCT diagnosed between 1992 and 2005 from the Surveillance, Epidemiology, and End Results (SEER) were analyzed. Of 234 nonpineal GCT in CBTRUS, the most common site was brain, NOS (31.6%). Males had a greater frequency (59.7%) than females (40.3%). However, by age group, the male-to-female incidence rate ratio (IRR) differed: children (0–14 years) had an IRR of 1.1, young adults (15–29 years) an IRR of 2.3, and adults (aged 30+) an IRR of 1.0. For children and young adults, most tumors were malignant (86.8% and 89.0%, respectively), whereas for adults, more than half were nonmalignant (56.8%). Germinoma was the most frequent diagnosis (61.5%). In SEER, the frequency of malignant GCT in the CNS (2.5%) was greater than that in the mediastinum (2.1%). Of 408 malignant CNS GCT, 216 (52.9%) were nonpineal. The male-to-female IRR was 1.5. Overall relative survival for nonpineal CNS malignant GCT was 85.3% at 2 years, 77.3% at 5 years, and 67.6% at 10 years. Previous studies of GCT that have not stratified by site have suggested greater gender disparity. Nonpineal CNS GCT show no significant gender preference, yet have outcomes similar to pineal GCT.