Glioblastoma in long‐term survivors of acute lymphoblastic leukemia: Report of two cases

Zi, Wenjie; Terakawa, Yuzo; Goto, Hiroyuki; Tsuyuguchi, Naohiro; Sato, Hidetoshi; Abe, Junya; Ohata, Kenji

doi:10.1111/ped.12843

Cited by 3 publications

(2 citation statements)

References 12 publications

(36 reference statements)

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“…Among them, gliomas at WHO I and WHO II grades grow at a low rate with favorable prognosis, while those at WHO III and WHO IV grades are highly invasive with poor prognosis 2,3. Research indicates that the median survival for glioma patients is about 14–16 months after combined surgery, chemotherapy and radiotherapy 4,5. Therefore, it is urgent to search for a new sally port for the early diagnosis and targeted treatment of glioma.…”

Section: Introductionmentioning

confidence: 99%

<p>ANO6 promotes cell proliferation and invasion in glioma through regulating the ERK signaling pathway</p>

Xuan¹,

Wang²,

Xie³

2019

OTT

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Anoctamin6 (ANO6) plays a crucial role in several cancers, whereas the specific role of ANO6 in glioblastoma is unclear. Methods: Kaplan-Meier survival analysis was used to analysis the correlation between ANO6 and survival rate of patients with glioblastoma. Univariate Cox regression analysis was used to analysis the correlation among ANO6 expression level,and age, gender, WHO and overall survival rate. Immunohistocemical technique, RT-PCR and western blot were used to dected the ANO6 expression. CCK8, colony formation and transwell were used to detected cell viability, cell proliferation and cell invasion in glioblastoma cells transfected with sh-ANO6 and ANO6 overexpression. In addition, after SHG-44 cells trasfected with ANO6 overexpression were ERK inhibitor (PD98059), CCK8, colony formation and transwell were used to detected cell viability, cell proliferation and cell invasion. Western blot was used to detected ERK protein level and the phosphorylation level of ERK in T89G and U87MG cells tranfected wih sh-ANO6. Results: The results indicated that the ANO6 expression level was significantly associated with patients' age and tumor stage. Univariate Cox regression analysis showed that the ANO6 expression level, age, gender and tumor stage were not related to the overall survival rate. ANO6 inhibition significantly suppressed the viability, invasion and the ability of colony formation in glioma cells, while ANO6 overexpression led to the opposite results in SHG-44 cells. ANO6 knockdown strongly inhibits the phosphorylation level and nuclear translocation of extracellular signal-regulated kinase (ERK) protein to inhibit ERK signaling. ERK inhibitor significantly decreased the cell proliferation and invasion in SHG-44 cells transfected with sh-ANO6. Conclusion: This study revealed that ANO6 activited ERK signaling pathway through promoting the nuclear translocation of ERK to increase the proliferation and invasion of glioblastoma cells.

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Section: Introductionmentioning

confidence: 99%

<p>ANO6 promotes cell proliferation and invasion in glioma through regulating the ERK signaling pathway</p>

Xuan¹,

Wang²,

Xie³

2019

OTT

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“…The incidence is relatively similar world-wide with a marginally higher rate of diagnosis in men (3). Reported risk factors for the development of glioma are pre-natal X-rays and prior radiotherapy for acute lymphoblastic leukemia, but are both rare occurrences and have been contested (4; 5). Peak disease incidence increases with age, but pediatric forms are commonly diagnosed as well.…”

Section: Gliomamentioning

confidence: 99%

Advances in immunotherapeutic research for glioma therapy

Miyauchi

Tsirka

2017

J Neurol

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Gliomas are primary malignancies of the brain. Tumors are staged based on malignancy, nuclear atypia, and infiltration of the surrounding brain parenchyma. Tumors are often diagnosed once patients become symptomatic, at which time the lesion is sizable. Glioblastoma (grade IV glioma) is highly aggressive and difficult to treat. Most tumors are diagnosed de novo. The gold standard of therapy, implemented over a decade ago, consists of fractionated radiotherapy and temozolomide, but unfortunately, chemotherapeutic resistance arises. Recurrence is common after initial therapy. The tumor microenvironment plays a large role in cancer progression and its manipulation can repress progression. The advent and implementation of immunotherapy, via manipulation and activation of cytotoxic T cells, have had an outstanding impact on reducing morbidity and mortality associated with peripheral cancers under certain clinical circumstances. An arsenal of immunotherapeutics is currently under clinical investigation for safety and efficacy in the treatment of newly diagnosed and recurrent high grade gliomas. These immunotherapeutics encompass antibody-drug conjugates, autologous infusions of modified chimeric antigen receptor expressing T cells, peptide vaccines, autologous dendritic cell vaccines, immunostimulatory viruses, oncolytic viruses, checkpoint blockade inhibitors, and drugs which alter the behavior of innate immune cells. Effort is focusing on determining which patient populations will benefit the most from these treatments and why. Research addressing synergism between treatment options is gaining attention. While advances in the treatment of glioma stagnated in the past, we may see a considerable evolution in the management of the disease in the upcoming years.

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Three case reports of radiation-induced glioblastoma after complete remission of acute lymphoblastic leukemia

et al. 2018

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Radiation therapy is sometimes performed to control intracranial acute lymphoblastic leukemia (ALL), but may lead to radiation-induced malignant glioma. The clinical, radiological, histological, and molecular findings are described of three cases of radiation-induced glioblastoma after the treatment for ALL. They received radiation therapy at age 6-8 years. The latency from radiation therapy to the onset of radiation-induced glioblastoma was 5-10 years. Magnetic resonance imaging demonstrated diffuse lesions with multiple small enhanced lesions in all cases. Histological examination showed that the tumors consisted of mainly small round astrocytic atypical cells in one case, and astrocytic atypical cells with elongated cytoplasm and nuclear pleomorphism with small cell component in two cases. Microvascular proliferation was present in all cases. Immunohistochemical analysis for B-Raf V600E, and mutational analysis for the isocitrate dehydrogenase (IDH) 1, IDH2, and H3F3A gene revealed the wild-type alleles in all three cases. The integrated diagnoses were IDH wild-type glioblastoma, and local irradiation and concomitant temozolomide were performed. After the initial treatment, significant shrinkage of the diffuse lesion and enhanced lesion was found in all cases. Radiation-induced glioblastoma occurring after the treatment for ALL had unique clinical, radiological, histological, and molecular characteristics in our three cases.

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Glioblastoma in long‐term survivors of acute lymphoblastic leukemia: Report of two cases

Cited by 3 publications

References 12 publications

<p>ANO6 promotes cell proliferation and invasion in glioma through regulating the ERK signaling pathway</p>

<p>ANO6 promotes cell proliferation and invasion in glioma through regulating the ERK signaling pathway</p>

Advances in immunotherapeutic research for glioma therapy

Three case reports of radiation-induced glioblastoma after complete remission of acute lymphoblastic leukemia

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