Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
1.
Rev. Hosp. Ital. B. Aires (2004) ; 39(4): 146-148, dic. 2019. ilus
Article in Spanish | LILACS | ID: biblio-1099838

ABSTRACT

Los anticuerpos monoclonales que inhiben los puntos de control PD-1 y CTLA-4 se usan actualmente en el tratamiento del melanoma y cáncer metastásico de pulmón de células no pequeñas, entre otros. Se refiere el caso de una paciente con cáncer de pulmón en tratamiento con pembrolizumab. La paciente se presentó con edema facial y parálisis facial periférica. En el laboratorio se observó la hormona tirotrofina (TSH) elevada y se llegó al diagnóstico de hipotiroidismo por pembrolizumab. Inició tratamiento con levotiroxina con mejoría clínica. Se presenta este caso por el importante papel del dermatólogo en el manejo multidisciplinario del paciente oncológico. (AU)


Monoclonal antibodies that inhibit PD-1 and CTLA-4 control points are currently used in the treatment of melanoma and metastatic non-small cell lung cancer, among others. The case of a patient, with lung cancer being treated with Pembrolizumab. The patient was presented with facial edema and peripheral facial paralysis and in the laboratory the elevated hormone Tyrotrophin (TSH) was observed, the diagnosis of pembrolizumab hypothyroidism was reached. She started treatment with levothyroxine with clinical improvement. This case is presented by the important role of the dermatologist in the multidisciplinary management of the cancer patient. (AU)


Subject(s)
Humans , Female , Middle Aged , M Phase Cell Cycle Checkpoints/drug effects , Immunotherapy/adverse effects , Antibodies, Monoclonal/adverse effects , Thyroxine/therapeutic use , Brain Neoplasms/complications , Brain Neoplasms/drug therapy , Thyrotropin/analysis , Carboplatin/administration & dosage , Carcinoma, Non-Small-Cell Lung/complications , Carcinoma, Non-Small-Cell Lung/drug therapy , Tumor Suppressor Proteins/drug effects , Dermatology , Facial Injuries , Facial Paralysis , CTLA-4 Antigen/drug effects , CTLA-4 Antigen/physiology , Programmed Cell Death 1 Receptor/drug effects , Programmed Cell Death 1 Receptor/physiology , Pemetrexed/administration & dosage , Melanoma/complications , Melanoma/drug therapy , Antibodies, Monoclonal/administration & dosage , Antibodies, Monoclonal/therapeutic use , Neoplasm Metastasis/drug therapy
2.
Article in English | WPRIM | ID: wpr-174930

ABSTRACT

Mcl-1 and Bcl-xL, key anti-apoptotic proteins of the Bcl-2 family, have attracted attention as important molecules in the cell survival and drug resistance. In this study, we investigated whether inhibition of Bcl-xL influences cell growth and apoptosis against simultaneous treatment of resveratrol and clofarabine in the human malignant mesothelioma H-2452 cells. Resveratrol and clofarabine decreased Mcl-1 protein levels but had little effect on Bcl-xL levels. In the presence of two compounds, any detectable change in the Mcl-1 mRNA levels was not observed in RT-PCR analysis, whereas pretreatment with the proteasome inhibitor MG132 led to its accumulation to levels far above basal levels. The knockdown of Bcl-xL inhibited cell proliferation with cell accumulation at G2/M phase and the appearance of sub-G0/G1 peak in DNA flow cytometric assay. The suppression of cell growth was accompanied by an increase in the caspase-3/7 activity with the resultant cleavages of procaspase-3 and its substrate poly (ADP-ribose) polymerase, and increased percentage of apoptotic propensities in annexin V binding assay. Collectively, our data represent that the efficacy of resveratrol and clofarabine for apoptosis induction was substantially enhanced by Bcl-xL-lowering strategy in which the simultaneous targeting of Mcl-1 and Bcl-xL could be a more effective strategy for treating malignant mesothelioma.


Subject(s)
Adenine Nucleotides/pharmacology , Antimetabolites, Antineoplastic/pharmacology , Apoptosis/drug effects , Arabinonucleosides/pharmacology , Caspase 3/metabolism , Caspase 7/metabolism , Cell Line, Tumor , Cell Proliferation/drug effects , G2 Phase Cell Cycle Checkpoints/drug effects , Gene Knockdown Techniques , Humans , Leupeptins/pharmacology , Lung Neoplasms/metabolism , M Phase Cell Cycle Checkpoints/drug effects , Mesothelioma/metabolism , Myeloid Cell Leukemia Sequence 1 Protein/antagonists & inhibitors , RNA Interference , RNA, Messenger/metabolism , RNA, Small Interfering/metabolism , Stilbenes/pharmacology , bcl-X Protein/antagonists & inhibitors
3.
Indian J Biochem Biophys ; 2013 Dec; 50(6): 485-491
Article in English | IMSEAR | ID: sea-150261

ABSTRACT

Triptolide, a diterpene derived from Tripterygium wilfordii Hook f., a Chinese medicinal herb, has been reported to inhibit cell proliferation and induce apoptosis in various human cancer cells, but its anticancer effects on human osteosarcoma cells have not yet been elucidated. In this study, we investigated whether triptolide induces apoptosis in human osteosarcoma cells and the underlying molecular mechanisms. We firstly demonstrated that triptolide inhibited cell growth and induced apoptosis in U2OS cells. Western blot analysis showed that the levels of procaspase-8, -9, Bcl-2, Bid and mitochondrial cytochrome c were downregulated in triptolide-treated U2OS cells, whereas the levels of Fas, FasL, Bax, cytosolic cytochrome c, cleaved caspase-3 and cleaved PARP were upregulated. These results suggest that triptolide induces apoptosis in U2OS cells by activating both death receptor and mitochondrial apoptotic pathways.


Subject(s)
Antineoplastic Agents/pharmacology , Apoptosis/drug effects , Caspase 3/metabolism , Cell Line, Tumor , Cell Proliferation/drug effects , Diterpenes/pharmacology , Enzyme Activation/drug effects , Epoxy Compounds/pharmacology , G2 Phase Cell Cycle Checkpoints/drug effects , Humans , M Phase Cell Cycle Checkpoints/drug effects , Mitochondria/drug effects , Mitochondria/metabolism , Osteosarcoma/pathology , Phenanthrenes/pharmacology , Poly(ADP-ribose) Polymerases/metabolism , Proteolysis/drug effects
SELECTION OF CITATIONS
SEARCH DETAIL