ABSTRACT
Toxic epidermal necrolysis (TEN) is a severe mucocutaneous syndrome that can be occasionally caused by anticonvulsant drugs. In some cases, cranial irradiation may act as a precipitating factor. Thus, in cancer patients who suffer from brain metastases and are administered antiepileptic drugs for seizure prophylaxis, the risk of developing TEN after receiving palliative brain radiotherapy cannot be ignored. We is reported. The case of a young patient with non-small cell lung cancer (NSCLC) treated with prophylactic phenobarbital who developed TEN within a few days of completing cranial radiotherapy for brain metastases is reported. To minimize the risk of TEN in patients undergoing brain radiotherapy, prophylactic anticonvulsant therapy is recommended only after an accurate measurement of the true benefits. Alternatively, discontinuation of antiepileptic treatment before the initiation of brain radiotherapy, or the use of anticonvulsants associated with a lower risk of developing cutaneous reactions might be considered.
Subject(s)
Anticonvulsants/adverse effects , Brain Neoplasms/radiotherapy , Radiation Injuries/etiology , Stevens-Johnson Syndrome/etiology , Adult , Brain Neoplasms/secondary , Carcinoma, Non-Small-Cell Lung/pathology , Humans , Lung Neoplasms/pathology , MaleABSTRACT
Despite advances in our understanding of the molecular and genetic basis of pancreatic cancer, the disease remains a clinical challenge. Gemcitabine, the standard chemotherapy for pancreatic cancer, offers modest improvement of tumor-related symptoms and marginal advantage of survival. New approaches, alone and in combination with gemcitabine, are being developed to combat this cancer. In this article we review the current status of investigations into several classes of agents: matrix metalloproteinase inhibitors; farnesyl transferase inhibitors; epidermal growth factor receptor inhibitors, including monoclonal antibodies and tyrosine kinase inhibitors; cyclooxygenase-2 inhibitors, and others. The scientific rationale, mechanism of action, and clinical trial data for these novel agents are discussed.
Subject(s)
Adenocarcinoma/drug therapy , Deoxycytidine/analogs & derivatives , Pancreatic Neoplasms/drug therapy , Adenocarcinoma/blood supply , Adenocarcinoma/genetics , Adenocarcinoma/therapy , Angiogenesis Inhibitors/therapeutic use , Antimetabolites, Antineoplastic , Antineoplastic Combined Chemotherapy Protocols/administration & dosage , Cysteine Endopeptidases , Deoxycytidine/therapeutic use , Epidermal Growth Factor/antagonists & inhibitors , Humans , Hydroxamic Acids/therapeutic use , Matrix Metalloproteinase Inhibitors , Metalloendopeptidases/antagonists & inhibitors , Multienzyme Complexes/antagonists & inhibitors , Pancreatic Neoplasms/blood supply , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/therapy , Proteasome Endopeptidase Complex , Protein-Tyrosine Kinases/antagonists & inhibitors , RNA, Antisense , GemcitabineABSTRACT
Despite advances in our understanding of the molecular and genetic basis of pancreatic cancer, the disease remains a clinical challenge. Gemcitabine, the standard chemotherapy for pancreatic cancer, offers modest improvement of tumor-related symptoms and marginal advantage of survival. New approaches, alone and in combination with gemcitabine, are being developed to combat this cancer. In this article we review the current status of investigations into several classes of agents: matrix metalloproteinase inhibitors; farnesyl transferase inhibitors; epidermal growth factor receptor inhibitors, including monoclonal antibodies and tyrosine kinase inhibitors; cyclooxygenase-2 inhibitors, and others. The scientific rationale, mechanism of action, and clinical trial data for these novel agents are discussed.
