ABSTRACT
Blisters and subsequent desquamation of the skin in the presence of acute edema is a well-known clinical phenomenon. In this case report, we describe a new variant that we have termed anasarca-induced desquamation in a 50-year-old man with molting of the entire cutaneous surface after acute edema, in a setting of 40-lb weight gain over 5 days. Laboratory workup for infectious causes and punch biopsies of skin lesions ruled out Stevens-Johnson syndrome and staphylococcal scalded skin syndrome, which have a similar clinical presentation to anasarca-induced desquamation. In patients with diffuse superficial desquamation in the setting of acute edema, anasarca-induced desquamation is worth investigating to avoid the use of corticosteroids and intravenous antibiotics in this inherently benign condition.
Subject(s)
Staphylococcal Scalded Skin Syndrome , Stevens-Johnson Syndrome , Edema/diagnosis , Edema/etiology , Humans , Male , Middle Aged , Molting , Skin/pathology , Stevens-Johnson Syndrome/etiologyABSTRACT
BACKGROUND: Melanoma is the deadliest variant of skin cancer and its incidence continues to increase. There are limited treatment options for advanced and metastatic cases of melanoma, despite advances in immunotherapy and chemotherapy. Melanoma is notorious as a radioresistant tumor. Previous studies found that phytochemicals, such as resveratrol and those found in green tea and blueberry, can sensitize various cancer cells, including melanoma, to radiotherapy. Our previous study also revealed that kiwifruit extract (KE) has antitumor activity to melanoma cells. This study was designed to expand upon our previous investigation and determine KE's potential as a radiosensitizer on CRL-11147 melanoma cancer cells and elucidate the possible mechanisms behind its potential. MATERIALS AND METHODS: Proliferation and apoptosis of CRL-11147 melanoma cells under radiation therapy (RT) plus KE versus RT alone were investigated using Proliferative cell nuclear antigen (PCNA) staining, quick cell proliferation assay, clonogenic assay, and caspase-3 activity assay. Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) were then used to investigate the mechanisms behind the observed results. RESULTS: The percentage of CRL-11147 colonies, PCNA staining intensity, and the optic density value of CRL-11147 cells decreased with RT/KE vs. RT alone. Relative caspase-3 activity was increased with RT/KE vs. RT alone. Increased expression of the anti-proliferative molecule p27 and pro-apoptotic molecule TRAILR1 correlated with the anti-tumor effect seen in the RT/KE group versus the RT alone group. CONCLUSION: KE augments radiosensitivity of CRL-11147 by up-regulating both p27 and TRAILR1 to inhibit proliferation and increase apoptosis, respectively.
Subject(s)
Actinidia/chemistry , Fruit/chemistry , Plant Extracts/pharmacology , Radiation-Sensitizing Agents/pharmacology , Apoptosis/drug effects , Cell Line, Tumor , Cell Proliferation/drug effects , Gene Expression Regulation, Neoplastic/drug effects , Humans , Immunohistochemistry , Melanoma/genetics , Melanoma/metabolism , Plant Extracts/chemistry , Radiation-Sensitizing Agents/chemistryABSTRACT
BACKGROUND: Cervical cancer (CC) is one of the leading causes of mortality worldwide. Previously, we reported that blueberry extract constrains the growth of CC. Raspberry is a widely consumed fruit that exhibits antitumor properties against several cancer types but little is known about its direct effect on CC. This study was designed to investigate the potential antitumor effect of raspberry extract (RE) on CC cells and to elucidate the possible mechanisms behind it. MATERIALS AND METHODS: Clonogenic survival assay and caspase-3 activity kits were used to evaluate the effects of RE on cell survival, proliferation, and apoptosis of a widely used CC cell line, HeLa. Possible molecular mechanisms were investigated using reverse transcription-polymerase chain reaction. RESULTS: The percentage of colonies and optic density value of HeLa cells decreased in the presence of RE in comparison to controls. Relative caspase-3 activity in cancer cells increased in the presence of RE in comparison to controls. The antitumor effect displayed on HeLa cells by RE was associated with the increased expression of antiproliferative molecule P53 and the increased expression of pro-apoptotic molecule tumor necrosis factor receptor superfamily member 6 (FAS). CONCLUSION: RE displays anticancer activity against CC HeLa cells. The mechanism behind this is by up-regulation of anti-proliferative molecule P53 and pro-apoptotic molecule FAS.
Subject(s)
Antineoplastic Agents/pharmacology , Plant Extracts/pharmacology , Rubus/chemistry , Uterine Cervical Neoplasms/drug therapy , Apoptosis/drug effects , Caspase 3/metabolism , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Survival/drug effects , Female , HeLa Cells , Humans , Up-Regulation/drug effects , Uterine Cervical Neoplasms/metabolism , fas Receptor/metabolismABSTRACT
Skin cancers are the most common cancers in the world and among the different types of skin cancers, melanoma is the deadliest and incidence is rising. Previous studies have shown promising in vitro and human evidence of kiwifruit exhibiting anti-cancer effects. This study was designed to investigate if kiwifruit extract (KE) has any effect on CRL-11147 melanoma cancer cells and to investigate the possible mechanisms behind the results. The effects of KE on CRL-11147 melanoma cell survival, proliferation, and apoptosis was investigated using clonogenic survival assay, cell proliferation, and caspase-3 activity kits. Potential anti-tumor molecular mechanisms were elucidated using RT-PCR and IHC. Addition of KE decreased CRL-11147 cell colonies percentages indicated by a decreased optical density value of cancer cells when compared to control. Furthermore, treatment with KE increased relative caspase-3 activity in cancer cells, which indicated increased apoptosis of cancer cells. The anti-proliferative effect of KE on cancer cells corresponded with decreased expression of the pro-proliferative molecule Cyclin E and CDK4, while increased expression of the pro-apoptotic molecule TRAILR1 corresponded with the pro-apoptotic effect. KE decreases CRL-11147 melanoma cell growth via downregulation of Cyclin E and CDK4 and upregulation in TRAILR1. Our study suggests a potential use for KE in treatment of melanoma.
Subject(s)
Actinidia/chemistry , Cyclin E/metabolism , Fruit/chemistry , Melanoma/drug therapy , Oncogene Proteins/metabolism , Plant Extracts/pharmacology , Receptors, TNF-Related Apoptosis-Inducing Ligand/metabolism , Skin Neoplasms/drug therapy , Apoptosis , Cell Line, Tumor , Cell Proliferation , Cyclin-Dependent Kinase 4/metabolism , Humans , Melanoma/metabolism , Melanoma/pathology , Skin Neoplasms/metabolism , Skin Neoplasms/pathologyABSTRACT
Programmed cell death receptor 1 (PD-1) inhibitors are promising and effective treatments for various cancers. Cutaneous adverse events, such as lichenoid drug eruptions, are well-known common side effects associated with PD-1 inhibitors. Lichenoid drug eruptions associated with PD-1 inhibitors show rapid improvement with high potency topical steroids and do not require cessation of the offending drug. We present the case of an 84-year-old female with progressive pembrolizumab therapy-associated lichenoid eruption that was resistant to several treatments and ultimately required discontinuation of pembrolizumab and treatment with methotrexate to resolve. This report includes histological findings of the pembrolizumab-associated lichenoid eruption.