Scavenger receptors typically bind to multiple ligands on a cell surface, including endogenous and modified host-derived molecules and microbial pathogens. They promote the elimination of degraded or harmful substances such as non-self or altered-self targets through endocytosis, phagocytosis, and adhesion. Currently, scavenger receptors are subdivided into eight classes based on several variations in their sequences due to alternative splicing. Since recent studies indicate targeting scavenger receptors has been involved in cancer prognosis and carcinogenesis, we will focus on the current knowledge about the emerging role of scavenger receptor classes A to E in cancer progression.

Over recent years, several new molecular and immunogenic therapeutic approaches to melanoma treatment have been approved and implemented in clinical practice. Mechanisms of resistance to these new therapies have become a major problem. Mutation-specific pharmacotherapy can result in simultaneous emergence of resistant clones at many separate body sites despite an initially positive therapeutic response. Additionally, treatments aimed at inducing apoptosis are subject to resistance due to escape through other known mechanisms of regulated cell death (RCD). In this review, we discuss the complexity in pharmacological manipulation of melanoma with c-Kit, BRAF, MEK, and/or mTOR mutant cell lines. This study also addresses melanoma evasion of cell death through modalities of RCD such as apoptosis, autophagy, and necroptosis. This study also examines new combination therapies which have been approved to target both cell cycle dysregulation and cell death pathways. Lastly, we recognize the importance of immunomodulation though manipulation of the body's natural killing mechanisms with CTLA4, PD1, and CSF1 inhibition. As we begin to recognize tumor cell activation of alternate pathways, evasion of programmed cell death, and manipulation of the tumor microenvironment, it is increasingly important to grasp the complexity of personalized therapy in melanoma treatment.
Apoptosis ; Autophagy ; Cell Cycle ; Cell Death* ; Cell Line ; Clone Cells ; Drug Therapy ; Hand Strength ; Homicide ; Humans ; Immunomodulation ; Melanoma* ; TOR Serine-Threonine Kinases ; Tumor Microenvironment ; United Nations

Melanoma is one of the most aggressive cancers in the world and is responsible for the majority of skin cancer deaths. Recent advances in the field of immunotherapy using active, adoptive, and antigen-specific therapeutic approaches, have generated the expectation that these technologies have the potential to improve the treatment of advanced malignancies, including melanoma. Treatment options for metastatic melanoma patients have been dramatically improved by the FDA approval of new therapeutic agents including vemurafenib, dabrafenib, and sorafenib. These kinase inhibitors have the potential to work in tandem with MEK, PI3K/AKT, and mTOR to inhibit the activity of melanoma inducing BRAF mutations. This review summarizes the effects of the new therapeutic agents against melanoma and the underlying biology of these BRAF inhibitors.
Biology ; Humans ; Immunotherapy ; Melanoma ; Mitogen-Activated Protein Kinase Kinases ; Phosphotransferases ; Skin Neoplasms

Genitourinary syndrome of menopause significantly affects the quality of life in postmenopausal women with few evidence-based alternatives to vaginal estrogen for women with contraindications. This systematic review evaluates the evidence for vaginal vitamin E efficacy in reducing patient-reported genitourinary symptoms in healthy postmenopausal women compared to placebo or vaginal control therapy. This systematic review evaluated randomized controlled trials before October 2020 that assessed the efficacy of vitamin E vaginal suppositories in reducing genitourinary symptoms in postmenopausal women compared with a control group of healthy postmenopausal women. Outcomes included patient-perceived genitourinary symptoms. Of the 31 studies, four met the inclusion criteria. One 8-week trial (n = 42) found a significant reduction in vaginal symptoms in the 1 mg vitamin E group than the placebo group (difference in means, 5.3; 95% confidence interval [CI], 4.4 to 6.2). Another 8-week trial (n = 40) found 5 mg vaginal hyaluronic acid superior to 1 mg vitamin E (difference in means –0.50, 95% CI, –0.95 to –0.05). Two 12-week trials (n = 52 in each) found no difference between 0.5 g vaginal estrogen and 100 IU vaginal vitamin E in healthy postmenopausal women (difference in means: –0.19, 95% CI, –4.4 to 4.0, and −3.47, 95% CI, −13.8 to 6.8). Evidence from small, limited studies suggests that vaginal vitamin E may be effective in alleviating symptoms of genitourinary syndrome of menopause; however, additional high-quality studies are needed to determine efficacy, ideal dosing, and long-term safety.