The impact of specific treatment patterns on survival for children with low and high grade gliomas: analysis of the 1973–2002 SEER data

2008 ◽  
Vol 26 (15_suppl) ◽  
pp. 10016-10016
Author(s):  
W. Woods-Swafford ◽  
J. F. Kuttesch Jr. ◽  
J. Barnholtz-Sloan
2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 11528-11528
Author(s):  
P. Costa ◽  
F. Braga ◽  
C. Sottomayor ◽  
M. Honavar ◽  
M. Resende ◽  
...  

11528 Background: The authors analyse retrospectively the impact on tumour control and toxicity of concomitant radiotherapy (RT) and Temozolomide (TMZ) in high grade gliomas (HGG) of the CNS, in patients treated in the Clínica de Radioterapia do Porto - Portugal. Methods: This cohort represents all patients with HGG treated between January 2002 and January 2006, with concomitant RT a median total dose of 60 Gy, 2 Gy per treatment given once daily 5-days/week and TMZ 75mg/m2 for 42 days, followed by adjuvant treatment with TMZ 5-days schedule every 28 days (150 mg/m2 for the first cycle increased to 200mg/m2). The cohort was retrospectively analyzed for gender distribution, age, extent of surgical resection, initial KPS, median overall survival (OS) and haematological toxicity. Results: 23 with HGG (6 females, 17 males) were treated with concomitant RT (44–72 Gy) and TMZ followed by adjuvant TMZ; median age was 58 (ranging from 17–72); median KPS was 80 (ranging from 40–90); 3 patients had complete resection, 17 partial resection and 3 biopsy. All patients except one, who had treatment interruption for thrombocytopenia, completed the concomitant phase of treatment; 19 patients continued to received adjuvant treatment with TMZ (median number of cycles was 5 (ranging from 1–20). Median OS (measured from the date of diagnosis to the date of death) was 20.4 month and 1 yr OS was 54%. During concomitant phase, one patient had grade 3–4 thrombocytopenia. During the adjuvant TMZ therapy 4 patients had grade 3–4 haematological toxicity (anaemia: 1; thrombocytopenia: 1; leucopoenia and thrombocytopenia: 2). Conclusions: The results of concomitant RT+TMZ followed by TMZ in these patients with HGG showed values in accordance with the latest data published on literature for this association. Differences observed might be due to the small sample size.RT+TMZ followed by adjuvant TMZ is a well tolerated treatment with better results in median OS comparatively with previous results of RT only treatment in HGG. Treatment related toxicity was within acceptable levels, and this approach became routine practice in this set of patients. No significant financial relationships to disclose.


2016 ◽  
Vol 32 ◽  
pp. 346-347
Author(s):  
I. Chabert ◽  
E. Barat ◽  
F. Dhermain ◽  
F. Poisson ◽  
S. Ammari ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (22) ◽  
pp. 5678
Author(s):  
Lia Pinto ◽  
Hanane Baidarjad ◽  
Natacha Entz-Werlé ◽  
Eric Van Dyck

Despite their low incidence, pediatric high-grade gliomas (pHGGs), including diffuse intrinsic pontine gliomas (DIPGs), are the leading cause of mortality in pediatric neuro-oncology. Recurrent, mutually exclusive mutations affecting K27 (K27M) and G34 (G34R/V) in the N-terminal tail of histones H3.3 and H3.1 act as key biological drivers of pHGGs. Notably, mutations in H3.3 are frequently associated with mutations affecting ATRX and DAXX, which encode a chaperone complex that deposits H3.3 into heterochromatic regions, including telomeres. The K27M and G34R/V mutations lead to distinct epigenetic reprogramming, telomere maintenance mechanisms, and oncogenesis scenarios, resulting in distinct subgroups of patients characterized by differences in tumor localization, clinical outcome, as well as concurrent epigenetic and genetic alterations. Contrasting with our understanding of the molecular biology of pHGGs, there has been little improvement in the treatment of pHGGs, with the current mainstays of therapy—genotoxic chemotherapy and ionizing radiation (IR)—facing the development of tumor resistance driven by complex DNA repair pathways. Chromatin and nucleosome dynamics constitute important modulators of the DNA damage response (DDR). Here, we summarize the major DNA repair pathways that contribute to resistance to current DNA damaging agent-based therapeutic strategies and describe the telomere maintenance mechanisms encountered in pHGGs. We then review the functions of H3.3 and its chaperones in chromatin dynamics and DNA repair, as well as examining the impact of their mutation/alteration on these processes. Finally, we discuss potential strategies targeting DNA repair and epigenetic mechanisms as well as telomere maintenance mechanisms, to improve the treatment of pHGGs.


2014 ◽  
Vol 90 (4) ◽  
pp. 894-902 ◽  
Author(s):  
Chad G. Rusthoven ◽  
Julie A. Carlson ◽  
Timothy V. Waxweiler ◽  
Miranda J. Dally ◽  
Anna E. Barón ◽  
...  

2015 ◽  
Vol 29 (3) ◽  
pp. 295-308
Author(s):  
Adriana Baritchii ◽  
A. Gubian ◽  
St.I. Florian

Abstract Malignant gliomas are aggressive brain cancers. After many decades of intensive research they represent a major cause of cancer related mortality and morbidity. Management of malignant gliomas is very difficult. None of the current treatments are curative. High grade gliomas are optimally treated with surgery followed by radiotherapy and chemotherapy. The impact of surgery on progression free survival and overall survival was a constant preoccupation and debate for decades among neurosurgeons. Different studies published in the last 25 years have provided evidence that the extent of resection of high grade gliomas can influence time to progression and median survival, although so far there is no class I prospective randomized trial to fully answer this question. Some of the most important studies are reviewed here. The modern neurosurgery relay on some tools that proved to be very helpful in guiding the surgeon to achieve the maximal tumoral cytoreduction with minimum impact on the brain’s eloquent areas. iMRI has been proved to be safe and became an important tool during tumor surgery, used alone or in conjuction with other important techniques: intraoperative neurophysiology, awake cortical mapping, 5-ALA fluorescence etc. Although so far the prognostic of high grade gliomas is still disappointing, further understanding of the biology of these tumors and a patient-tailored treatment could be the keys of finding a cure in the future.


2012 ◽  
Vol 42 (4) ◽  
pp. 270-277 ◽  
Author(s):  
S. Yamaguchi ◽  
H. Kobayashi ◽  
S. Terasaka ◽  
N. Ishii ◽  
J. Ikeda ◽  
...  

2010 ◽  
Vol 100 (3) ◽  
pp. 417-426 ◽  
Author(s):  
Andrea Talacchi ◽  
Sergio Turazzi ◽  
Francesca Locatelli ◽  
Francesco Sala ◽  
Alberto Beltramello ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Daniela Rizzo ◽  
Antonio Ruggiero ◽  
Maurizio Martini ◽  
Valentina Rizzo ◽  
Palma Maurizi ◽  
...  

High-grade gliomas are the main cause of death in children with brain tumours. Despite recent advances in cancer therapy, their prognosis remains poor and the treatment is still challenging. To date, surgery followed by radiotherapy and temozolomide is the standard therapy. However, increasing knowledge of glioma biology is starting to impact drug development towards targeted therapies. The identification of agents directed against molecular targets aims at going beyond the traditional therapeutic approach in order to develop a personalized therapy and improve the outcome of pediatric high-grade gliomas. In this paper, we critically review the literature regarding the genetic abnormalities implicated in the pathogenesis of pediatric malignant gliomas and the current development of molecularly targeted therapies. In particular, we analyse the impact of molecular biology on the prognosis and treatment of pediatric high-grade glioma, comparing it to that of adult gliomas.


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