Cancer stem cells are thought to be closely related to tumor p rogression and recurrence, making them attractive therapeutic targets. Stem cells of various tissu es exist within n ich es main taining their stemness. Glioblastoma stem cells (GSCs) a re located to tu mo r cap illaries, perivascular niche, which are cons idered to have important ro le in maintaining GSCs . There were some extracellu lar matrixes (ECM) on th e perivascular connective tissu e, includin g type1 co llagen. We here evalu ated wheth er type1 collagen has a potential of niche fo r GSCs. Imu nohistochemical staining of type1 collagen and CD133 , one o f the GSCs markers , on gliob lasto ma (GBM) tissues showed CD133-positive cells were located in immed iate proximity to typ e1 collagen aro und tu mor vessels. We cultured human GBM cell lines, U87MG and GBM cells obtained from fresh surgical tissu es, T472 and T555, with serum-containin g med ium (SCM) or serum -free medium with some growth facto rs (SFM) and in non-coated (No n-coat) or type1 collag en-coated cell line cultu red in the Col/SFM had Capabilities of sp here formation and tumo rigenesis. Type1 co llagen was fou nd in the perivascular area and showed a p ossibility to maintain GSCs. These fin dings su ggest th at type1 collagen could be one impo rtant co mponent of niche fo r CD133 p ositive GSCs and main tain GSCs in adheren t cultu re.

The 10-year survival rate of CNS germinoma is approximately 90%. Most patients with CNS GCTs are children and young adults. Therefore, with the improving life prognosis of young patients, secondary neoplasms, secondary cerebral vasculopathy, neurocognitive deficits, and many other adverse effects induced by the initial treatments are problems to be solved in the next decade.

The purpose of this study was to distinguish pseudoprogression (PP) from early true progression in patients with glioblastoma (GBM) based on the presence of a mutation in isocitrate dehydrogenase 1 (IDH1). We retrospectively surveyed 32 patients with GBM or GBM with oligodendroglioma component (GBMO) who underwent biopsy or maximal tumor resection followed by concurrent radiotherapy and temozolomide (TMZ). We then selected patients with early radiological progression in magnetic resonance imaging within 6 months after concurrent radiotherapy and TMZ treatment. DNA was extracted from their tumor blocks. The IDH1 mutation was analyzed in the genomic region by direct sequencing as a biomarker for PP. Twenty-eight patients were diagnosed with GBM and four with GBMO. Eleven patients were discovered to have early radiological progression. PP was detected in two patients (6.3%) diagnosed with GBMO and one patient with GBM. Both of the GBMO patients with PP had the IDH1 mutation, the one GBM patient with PP and the other eight patients with early true progression with wild type. The sensitivity and specificity of the IDH1 mutation for detecting PP were 66.7 and 100%, respectively. This study suggests the IDH1 mutation may become a novel molecular biomarker for PP. Analyzing the IDH1 mutation, in the case of recognizing early radiological progression, may enable distinction of PP from early true progression, and we could determine the need for second-look surgery.

Optic pathway/hypothalamic pilocytic astrocytomas in children are usually treated with chemotherapy following a surgical biopsy. In this report, we retrospectively considered the role of surgical intervention. In a series of 25 patients without neurofibromatosis type 1, the median age at initial treatment was 3.1 years (range, 0-15 years). Twenty cases were verified by histology, and five cases were diagnosed by MRI findings. Twenty-three patients received chemotherapy. All patients were alive at median follow-up of 66 months. Aims of surgery at the initiation of treatment were biopsy in 12 cases (1 stereotactic and 11 craniotomies) and debulking in 7 cases. The 11 open biopsies revealed pilocytic astrocytoma; however, noticeable complications occurred in five children after the biopsies. Review of preoperative MRIs showed that all had typical findings indicating pilocytic astrocytoma. The open biopsy offered no noteworthy benefit for the patients despite surgical risk and delay of chemotherapy. The extent of the seven resection surgeries was 70% or less removal, and postoperative adjuvant therapy was needed for six of the seven patients. The remaining six children who did not undergo surgery obtained remission with chemotherapy alone. After relapse in nine patients, 15 bulk-reduction surgeries were performed. Surgical resection was not curative in any patient. In five patients, mostly older children, cystic expansion of tumor was partially resected, resulting in additional remission. In conclusion, considering the risk of open surgery and the effectiveness of chemotherapy, the role of surgical intervention is restricted to bulk-reduction surgery only when it is inevitable, especially at relapse after chemotherapy.