Early dural metastasis from a case of glioblastoma with primitive neuroectodermal differentiation: A case report and literature review

Konar, Subhas; Bir, Shyamal C.; Maiti, Tanmoy; Patra, Devi Prasad; Brahmbhatt, Angela C. DiPoto; Jacobsohn, Jamie A.; Nanda, Anil

doi:10.1016/j.jocn.2016.10.003

Cited by 13 publications

(10 citation statements)

References 12 publications

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“…Glioblastoma, also known as glioblastoma multiforme (GBM), is the most aggressive primary tumor of the brain ( 1 – 3 ). Despite advances in surgical technology and adjuvant treatment for glioblastoma, this tumor remains the most lethal disease worldwide ( 2 , 3 ). The molecular mechanisms underlying the invasion and metastasis of glioblastoma are still unknown.…”

Section: Introductionmentioning

confidence: 99%

Daam1 activates RhoA to regulate Wnt5a‑induced glioblastoma cell invasion

Liu

Yan

et al. 2017

Oncol Rep

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The signaling pathway of dishevelled-associated activator of morphogenesis 1 (Daam1) triggered by Wnt5a drives cell movement and migration during breast cancer metastasis. However, Wnt5a signaling in glioblastoma progression remains poorly defined. Wnt5a expression and activations of RhoA, Cdc42, and Rac1 were detected in human glioblastoma tissues by using ELISA assays and small G-protein activation assays, respectively. The cell invasion rate and Daam1 activation of glioblastoma U251 and T98MG cells were determined by cell invasion assays and pull-down assays, respectively. According to our experiments, Wnt5a expression and RhoA activation were upregulated in invasive glioblastoma tissues, with a significant positive correlation between them. Wnt5a activated Daam1 and RhoA, and subsequently promoted the invasion of glioblastoma U251 and T98MG cells. This process was abolished by secreted frizzled-related protein 2 (sFRP2), an antagonist that directly binds to Wnt5a. Specific small interfering RNA (siRNA) targeting Daam1 markedly inhibited Wnt5a-induced RhoA activation, stress fiber formation and glioblastoma cell invasion. CCG-1423, a RhoA inhibitor, decreased Wnt5a-induced stress fiber formation and glioblastoma cell invasion. Finally, siRNA targeting Daam1 or CCG-1423 treatment did not alter the cell proliferation of glioblastoma U251 and T98MG cells. We thus concluded that Wnt5a promoted glioblastoma cell invasion via Daam1/RhoA signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Daam1 activates RhoA to regulate Wnt5a‑induced glioblastoma cell invasion

Liu

Yan

et al. 2017

Oncol Rep

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“…For recurrent GBM different therapeutic approaches are provided such as resurgery, reirradiation and systemic chemotherapy based on alkylating agents, bevacizumab, carboplatin, etoposide and their combination (21). On the other hand PNETs of the brain show a high tendency of leptomeningeal dissemination and extracranial metastasization (22), so the standard therapy consists of surgery followed by CSI combined with concurrent platinum-based chemotherapy, particularly carboplatin, or other concomitant chemotherapeutic agents, such as etoposide and TMZ (11).…”

Section: Discussionmentioning

confidence: 99%

“…In 2017 Konar et al (22) reported a case of GBM/PNET which developed extraparenchymal metastasis (dural metastasis) of pure PNET component after surgery and chemoradiotherapy as Stupp protocol. According to the authors early CSI in GBM/PNET patients should be performed, even after completion of adjuvant radio-chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic approach in glioblastoma multiforme with primitive neuroectodermal tumor components: Case report and review of the literature

et al. 2018

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Abstract. Glioblastoma multiforme (GBM) is the most common and aggressive malignant glioma that is treated with first-line therapy, using surgical resection followed by local radiotherapy and concomitant/adjuvant temozolomide (TMZ) treatment. GBM is characterised by a high local recurrence rate and a low response to therapy. Primitive neuroectodermal tumour (PNET) of the brain revealed a low local recurrence rate; however, it also exhibited a high risk of cerebrospinal fluid (CSF) dissemination. PNET is treated with surgery followed by craniospinal irradiation (CSI) and platinum-based chemotherapy in order to prevent CSF dissemination. GBM with PNET-like components (GBM/PNET) is an emerging variant of GBM, characterised by a PNET-like clinical behaviour with an increased risk of CSF dissemination; it also may benefit from platinum-based chemotherapy upfront or following failure of GBM therapy. The results presented regarding the management of GBM/PNET are based on case reports or case series, so a standard therapeutic approach for GBM/PNET is not defined, constituing a challenging diagnostic and therapeutic dilemma. In this report, a case of a recurrent GBM/PNET treated with surgical resection and radiochemotherapy as Stupp protocol, and successive platinum-based chemotherapy due to the development of leptomeningeal dissemintation and an extracranial metastasis, is discussed. A review of the main papers regarding this rare GBM variant and its therapeutic approach are also reported. In conclusion, GBM/PNET should be treated with a multimodal approach including surgery, chemoradiotherapy, and/or the early introduction of CSI and platinum-based chemotherapy upfront or at recurrence.

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“…The prognosis of the disease is related to the craniospinal metastasis or recurrence of the tumor. 5 Early detection of the tumor can improve the prognosis of the disease. The physician's awareness of this tumor can lead to the early diagnosis, management, and decreasing the morbidity and mortality rate.…”

Section: Introductionmentioning

confidence: 99%