Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0677930 (primary tumor)
 20,210 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral edema and fluid-filled cysts are common accompaniments of brain tumors. They contribute to the mass effect imposed by the primary tumor and are often responsible for a patient's signs and symptoms. Cerebral edema significantly increases the morbidity associated with tumor biopsy, excision, radiation therapy, and chemotherapy. Both edema and cyst formation are thought to result from a deficiency in the blood-brain barrier, with consequent extravasation of water, electrolytes, and plasma proteins from altered tumor microvessels. The resultant expansion of the cerebral interstitial space contributes to the elevated intracranial pressure observed with brain tumors. Departure from the typical blood-brain barrier microvascular architecture may only partially explain the occurrence of edema and tumor cyst formation. Biochemical mediators have also been implicated in vascular extravasation. Vascular permeability factor or vascular endothelial growth factor (VPF/VEGF) is a protein that has recently been isolated from a variety of tumors including human brain tumors. VPFb is an extraordinarily potent inducer of both microvascular extravasation (edemagenesis) and the formation of new blood vessels (angiogenesis). Its role in tumor growth and progression would therefore appear pivotal. Herein, the author presents an updated account of the investigation of VPF. Historical and clinical perspectives of the study and treatment of tumor associated edema are provided. The efficacy of high-dose dexamethasone in the treatment of neoplastic brain edema is discussed. A hypothetical role for VPF in edemagenesis is presented and discussed. It is hoped that an expanded understanding of the mechanisms responsible for the genesis of edema will ultimately facilitate therapeutic intervention.
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PMID:The genesis of peritumoral vasogenic brain edema and tumor cysts: a hypothetical role for tumor-derived vascular permeability factor. 751 4

We herein report a case of symptomatic brain metastases (BM) from lung adenocarcinoma in a 73-year-old female patient, which developed during salvage cytotoxic chemotherapy following failure of osimertinib treatment. The patient was proven to have a T790M mutation prior to osimertinib therapy, and achieved a clinical benefit from osimertinib for 3 years until the primary tumor progressed. Although active BM were not detected prior to initiating salvage cytotoxic chemotherapy, the patient developed numbness of the left hand, severe dizziness, and disturbance of behavior and thought after the 3-month course of the salvage cytotoxic chemotherapy. Brain magnetic resonance imaging revealed multiple BM with severe peritumoral brain edema. To avoid radiation-induced cognitive impairment, osimertinib re-challenge was undertaken. At 2 weeks after osimertinib initiation, the patient's neurological symptoms drastically improved. One month later, radiological evaluation revealed apparent shrinkage of the BM and subsiding brain edema, although the primary lung tumor remained stable. Therefore, osimertinib re-challenge may be a viable treatment option for BM developing during salvage cytotoxic chemotherapy.
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PMID:Rapid effect of osimertinib re-challenge on brain metastases developing during salvage cytotoxic chemotherapy after osimertinib treatment failure: A case report. 3093 Nov 16

Meningiomas, as the most common primary tumor of the central nervous system, are known to harbor genomic aberrations that associate with clinical phenotypes. Here we performed genome-wide genotyping for cranial meningiomas in 383 Chinese patients and identified 9,821 copy-number variations (CNVs). Particularly, patients with diverse clinical features had distinct tumor CNV profiles. CNV burdens were greater in high-grade (WHO grade II and III) samples, recurrent lesions, large tumors (diameter >4.3 cm), and those collected from male patients. Nevertheless, the level of CNV burden did not relate to tumor locations, peritumoral brain edema, bone invasion, or multiple lesions. Overall, the most common tumor CNVs were the copy-number gain (CNG) at 22q11.1 and the copy-number losses (CNLs) at 22q13.2, 14q11.2, 1p34.3, and 1p31.3. Recurrent lesions were featured by the CNLs at 1p31.3, 6q22.31, 9p21.3, and 11p12, and high-grade samples had more CNVs at 4q13.3 and 6q22.31. Meanwhile, large tumors were more likely to have the CNVs at 1p31.3 and 1p34.3. Additionally, recurrence prediction indicated the CNLs at 4p16.3 (p = 0.009, hazard ratio = 5.69) and 10p11.22 (p = 0.037, hazard ratio = 4.53) were candidate independent risk factors.
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PMID:High Copy-Number Variation Burdens in Cranial Meningiomas From Patients With Diverse Clinical Phenotypes Characterized by Hot Genomic Structure Changes. 3292 90