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The interrelationship between cerebral ischemic stroke and glioma: a comprehensive study of recent reports.
Ghosh, Mrinal K; Chakraborty, Dipankar; Sarkar, Sibani; Bhowmik, Arijit; Basu, Malini.
Afiliación
  • Ghosh MK; 1Signal Transduction in Cancer and Stem Cells Laboratory, Division of Cancer Biology and Inflammatory Disorder, Council of Scientific and Industrial Research-Indian Institute of Chemical Biology (CSIR-IICB), 4 Raja S.C. Mullick Road, Kolkata 700032 and CN-06, Sector-V, Salt Lake, Kolkata, 700091 Ind
  • Chakraborty D; 1Signal Transduction in Cancer and Stem Cells Laboratory, Division of Cancer Biology and Inflammatory Disorder, Council of Scientific and Industrial Research-Indian Institute of Chemical Biology (CSIR-IICB), 4 Raja S.C. Mullick Road, Kolkata 700032 and CN-06, Sector-V, Salt Lake, Kolkata, 700091 Ind
  • Sarkar S; 1Signal Transduction in Cancer and Stem Cells Laboratory, Division of Cancer Biology and Inflammatory Disorder, Council of Scientific and Industrial Research-Indian Institute of Chemical Biology (CSIR-IICB), 4 Raja S.C. Mullick Road, Kolkata 700032 and CN-06, Sector-V, Salt Lake, Kolkata, 700091 Ind
  • Bhowmik A; 2Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37 S. P. Mukherjee Road, Kolkata, 700 026 India.
  • Basu M; Department of Microbiology, Dhruba Chand Halder College, Dakshin Barasat, South 24, Paraganas, 743372 India.
Article en En | MEDLINE | ID: mdl-31637020
Glioma and cerebral ischemic stroke are two major events that lead to patient death worldwide. Although these conditions have different physiological incidences, ~10% of ischemic stroke patients develop cerebral cancer, especially glioma, in the postischemic stages. Additionally, the high proliferation, venous thrombosis and hypercoagulability of the glioma mass increase the significant risk of thromboembolism, including ischemic stroke. Surprisingly, these events share several common pathways, viz. hypoxia, cerebral inflammation, angiogenesis, etc., but the proper mechanism behind this co-occurrence has yet to be discovered. The hypercoagulability and presence of the D-dimer level in stroke are different in cancer patients than in the noncancerous population. Other factors such as atherosclerosis and coagulopathy involved in the pathogenesis of stroke are partially responsible for cancer, and the reverse is also partially true. Based on clinical and neurosurgical experience, the neuronal structures and functions in the brain and spine are observed to change after a progressive attack of ischemia that leads to hypoxia and atrophy. The major population of cancer cells cannot survive in an adverse ischemic environment that excludes cancer stem cells (CSCs). Cancer cells in stroke patients have already metastasized, but early-stage cancer patients also suffer stroke for multiple reasons. Therefore, stroke is an early manifestation of cancer. Stroke and cancer share many factors that result in an increased risk of stroke in cancer patients, and vice-versa. The intricate mechanisms for stroke with and without cancer are different. This review summarizes the current clinical reports, pathophysiology, probable causes of co-occurrence, prognoses, and treatment possibilities.
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Texto completo: 1 Bases de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Signal Transduct Target Ther Año: 2019 Tipo del documento: Article

Texto completo: 1 Bases de datos: MEDLINE Tipo de estudio: Prognostic_studies Idioma: En Revista: Signal Transduct Target Ther Año: 2019 Tipo del documento: Article