Incidence and risk of thromboembolism during treatment of high-grade gliomas: a prospective study

Brandes, Alba A.; Scelzi, E.; Salmistraro, G; Ermani, Mario; Carollo, C.; Berti, Franco; Zampieri, Paolo; Baiocchi, Claudia; Fiorentino, Mario V.

doi:10.1016/s0959-8049(97)00167-6

Cited by 200 publications

(135 citation statements)

References 21 publications

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“…In a study of 77 postoperative high-grade glioma patients receiving low-dose heparin and mechanical prophylaxis, symptomatic VTE occurred in 21% of patients by 12 months and in 32% of patients by 24 months. 12 Our results differ considerably from earlier studies. Differences in VTE prevention and detection likely account for these discrepant results.…”

Section: Discussioncontrasting

confidence: 99%

Venous thromboembolism occurs infrequently in meningioma patients receiving combined modality prophylaxis

Gerber

Segal

Salhotra

et al. 2007

Cancer

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The long‐term disease‐free survival in patients with metastatic transitional cell carcinoma (TCC) is still considerably low. Novel chemotherapeutic agents are needed to decrease the morbidity and mortality of TCC. In this study, we have evaluated several epigenetic modifiers for their therapeutic application in bladder cancer. Both histone deacetylase inhibitors (FK228, TSA) and DNA hypomethylating agent (5‐Azacytidine) were tested using in vitro assays such as cell viability, cell cycle analysis and western blot to determine their mechanisms of action. Drug combination experiments were also designed to study any additive or synergistic effects of these agents. In addition, two bladder cancer xenograft models (one subcutaneous and one orthotopic) were employed to assess the therapeutic efficacy of these agents in vivo. Three agents exhibited various growth inhibitory effects on 5 different TCC cell lines in a dose‐ and time‐dependent manner. In addition to G2/M cell cycle arrest, FK228 is more potent in inducting apoptosis than the two other single agents, and combination of both FK228 and 5‐Aza further enhances this effect. p21 induction is closely associated with FK228 or TSA but not 5‐Aza, which is mediated via p53‐independent pathway. Consistent with in vitro results, FK228 exhibited a significant in vivo growth inhibition of TCC tumor in both subcutaneous and orthotopic xenograft models. FK228 is a potent chemotherapeutic agent for TCC in vivo with minimal undesirable side effects. The elevated p21 level mediated via p53 independent pathway is a hallmark of FK228 mechanism of action. © 2007 Wiley‐Liss, Inc.

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Section: Discussioncontrasting

confidence: 99%

Venous thromboembolism occurs infrequently in meningioma patients receiving combined modality prophylaxis

Gerber

Segal

Salhotra

et al. 2007

Cancer

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“…The high incidence of deep vein thrombosis and pulmonary embolism in patients with HGG confounds separation as an independent toxicity of antiangiogenic therapies, although antiangiogenic therapy may aggravate this thrombogenic predisposition. [51][52][53][54] A retrospective review of bevacizumab plus therapy in patients with recurrent HGG suggests that concurrent use of anticoagulation appears safe without an apparent increased risk of hemorrhage. 33 In conclusion, bevacizumab as a single agent used at this dose and schedule in patients with previously treated alkylator chemotherapy-refractory recurrent 1p19q codeleted AO appears of benefit (as determined by response rate and PFS-6) for recurrent alkylator-refractory AO/ AOA.…”

Section: Original Articlementioning

confidence: 99%

Bevacizumab for recurrent alkylator‐refractory anaplastic oligodendroglioma

Chamberlain

Johnston

2009

Cancer

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BACKGROUND:A retrospective evaluation of single agent bevacizumab was carried out in adults with recurrent alkylator‐refractory 1p19q codeleted anaplastic oligodendrogliomas (AO) with an objective of determining progression‐free survival (PFS). There is no standard therapy for alkylator‐resistant AO, and hence a need exists for new therapies.METHODS:Twenty‐two patients aged 24 to 60 years with recurrent AO were treated. All patients had previously been treated with surgery, radiotherapy, adjuvant chemotherapy (temozolomide, 17; carmustine wafers, 4; carmustine, 1), and 1 salvage regimen (procarbazine, lomustine, and vincristine, 15; temozolomide, 6; carmustine wafers, 1). Eleven patients underwent repeat surgery. Patients were treated at second recurrence with bevacizumab, once every 2 weeks, defined as a single cycle. Neurological evaluation was performed every 2 weeks, and neuroradiographic assessment was made after the initial 2 cycles of bevacizumab and subsequently after every 4 cycles of bevacizumab.RESULTS:A total of 391 cycles of bevacizumab (median, 14.5 cycles; range, 2‐39 cycles) were administered. Bevacizumab‐related toxicity included fatigue (14 patients; 4 grade 3), leukopenia (9; 1 grade 3), anemia (5; 0 grade 3), hypertension (5; 1 grade 3), deep vein thrombosis (4; 1 grade 3), and wound dehiscence (2; 1 grade 3). Fifteen (68%) patients demonstrated a partial radiographic response, 1 (5.0%) demonstrated stable disease, and 6 (27%) demonstrated progressive disease after 2 cycles of bevacizumab. Time to tumor progression ranged from 1 to 18 months (median, 6.75 months). Survival ranged from 3 to 19 months (median, 8.5 months). Six‐month and 12‐month PFS were 68% and 23%, respectively.CONCLUSIONS:Bevacizumab demonstrated efficacy and acceptable toxicity in this cohort of adults with recurrent 1p19q codeleted alkylator‐refractory AO. Cancer 2009. © 2009 American Cancer Society.

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“…Se consi dera, que en general, el cáncer incrementa el riesgo de TEV unas 4.1 veces, y la qui mioterapia lo hace en 6,5 veces 100,101 . El TEV es una complicación frecuente y una de las principales causas de muerte en el paciente con tumor cerebral 102,103 . Cerca del 34% de estos pacientes desarrolla TEV en el curso de su enfermedad 104,105 ; a pesar de ello la terapia anticoagulante se asocia con temor por el riesgo de sangrado, especial mente de hemorragia intracraneal 106,107 .…”

Section: Manejo De Tromboembolismo Venoso (Tev)unclassified

Manejo perioperatorio de tumores intracraneales: rol del neurocirujano

Polo-Torres¹,

Alvis-Miranda²,

Villa-Delgado³

et al. 2013

Anales Sis San Navarra

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revisiones0 Manejo perioperatorio de tumores intracraneales: rol del neurocirujanoPerioperative management of intracranial tumours: the neurosurgeon's role C. Polo-Torres, H.r. Alvis-Miranda, r. villa-Delgado, L.r. Moscote-salazar resUMen El manejo perioperatorio de los pacientes con tu mores cerebrales es un reto para el neurocirujano y todo el equipo quirúrgico. El médico debe considerar factores como el tipo de tumor, la extensión de la enfer medad, el tratamiento recibido, la presencia de comor bilidades y el pronóstico de la patología. La ejecución correcta de todos los aspectos implicados en el manejo perioperatorio en pacientes con tumores intracranea les contribuirá a prolongar la vida y a mejorar la calidad de vida de los pacientes.Palabras clave. Tumores cerebrales. Evaluación pre ope ratoria. Neurocirugía. ABsTrACTThe perioperative management of patients with brain tumours is a challenge for the neurosurgeon and the entire surgical team. The treating physician should consider factors such as the type of tumour, extent of disease, treatment received, the presence of comorbidities and prognosis of the disease itself. The successful execution of all aspects involved in perio perative management in patients with brain tumours will help prolong the life and improve the quality of life of patients.

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Incidence and risk of thromboembolism during treatment of high-grade gliomas: a prospective study

Cited by 200 publications

References 21 publications

Venous thromboembolism occurs infrequently in meningioma patients receiving combined modality prophylaxis

Venous thromboembolism occurs infrequently in meningioma patients receiving combined modality prophylaxis

Bevacizumab for recurrent alkylator‐refractory anaplastic oligodendroglioma

Manejo perioperatorio de tumores intracraneales: rol del neurocirujano

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