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  • Author or Editor: Jun-ichi Kuratsu x
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Hideo Nakamura, Keishi Makino, Masato Kochi, Yukitaka Ushio and Jun-ichi Kuratsu

Object

The authors evaluated the effectiveness of a neoadjuvant therapy (NAT) consisting of combined chemoand radiotherapy followed by complete resection of the residual tumor in patients with nongerminomatous malignant germ cell tumors (NGMGCTs).

Methods

The authors treated 14 consecutive patients in whom NGMGCTs were diagnosed based on elevated levels of the tumor markers α-fetoprotein, human chorionic gonadotropin, and the β-subunit of human chorionic gonadotropin (β-HCG). Chemotherapy and radiotherapy were performed, and after the serum tumor markers level was in the normal or near-normal range, the residual tumors were completely resected.

Results

Residual tumors were confirmed in 11 of the 14 patients after NAT, and total removal was successful in 10 of the 11 patients. In the other patient the residual tumor could not be completely excised because it was attached to a deep vein. The follow-up duration ranged from 1.2 to 22.2 years. The 5-year event-free and total survival rates were 86% and 93%, respectively. Although 3 patients died, 2 of tumor recurrence and 1 of a radiation-induced secondary tumor (glioblastoma), the other 11 are alive and without evidence of tumor recurrence.

Conclusions

The authors consider their NAT protocol for NGMGCT to be highly effective in relation to survival for the patients with NGMGCT, but there are several quality of life issues that need to be resolved.

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Tadashi Hamasaki, Keishi Makino, Motohiro Morioka, Shu Hasegawa, Masahito Kurino and Jun-Ichi Kuratsu

✓ The authors present a histological study of resected tissue obtained from an 18-month-old girl with split cord malformation Type II whose right foot was smaller than her left. Magnetic resonance imaging revealed duplication of the spinal cord below the level of L-1. On laminectomy it was discovered that the cord was tethered in the lumbosacral region. The resected tissue contained the cluster of paramedian dorsal root ganglia unique to this congenital anomaly. On histological examination, the ganglion cells expressed not only neuronal markers but also a marker for muscle cells indicative of pathological development of the midline structure. Further histological study is necessary to gain a deeper insight into this congenital disease and to obtain additional information for use in surgical planning.

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Naoki Shinojima, Masato Kochi, Jun-Ichiro Hamada, Hideo Nakamura, Shigetoshi Yano, Keishi Makino, Hiromasa Tsuiki, Kenji Tada, Jun-Ichi Kuratsu, Yasuji Ishimaru and Yukitaka Ushio

Object. Glioblastoma multiforme (GBM) remains incurable by conventional treatments, although some patients experience long-term survival. A younger age, a higher Karnofsky Performance Scale (KPS) score, more aggressive treatment, and long progression-free intervals have been reported to be positively associated with long-term postoperative patient survival. The aim of this retrospective study was the identification of additional favorable prognostic factors affecting long-term survival in surgically treated adult patients with supratentorial GBM.

Methods. Of 113 adult patients newly diagnosed with histologically verified supratentorial GBM who were enrolled in Phase III trials during the period between 1987 and 1998, six (5.3%) who survived for longer than 5 years were defined as long-term survivors, whereas the remaining 107 patients served as controls. All six were women and were compared with the controls; they were younger (mean age 44.2 years, range 31–60 years), and their preoperative KPS scores were higher (mean 85, range 60–100). Four of the six patients underwent gross-total resection. In five patients (83.3%) the progression-free interval was longer than 5 years and in three a histopathological diagnosis of giant cell GBM was made. This diagnosis was not made in the other 107 patients.

Conclusions. Among adult patients with supratentorial GBM, female sex and histopathological characteristics consistent with giant cell GBM may be predictive of a better survival rate, as may traditional factors (that is, younger age, good KPS score, more aggressive resection, and a long progression-free interval).

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Mareina Kudo, Hirofumi Jono, Satoru Shinriki, Shigetoshi Yano, Hideo Nakamura, Keishi Makino, Takuichiro Hide, Daisuke Muta, Mitsuharu Ueda, Kazutoshi Ota, Yukio Ando and Jun-ichi Kuratsu

Object

Interleukin-6 (IL-6) is a pleiotropic cytokine that regulates diverse physiological functions, including cell proliferation and survival. Recent studies have shown that IL-6 expression is often elevated in response to several types of glioma. Although IL-6 is said to play an important role in glioma, the involvement of IL-6 signaling has been quite controversial. The aim of this study was to evaluate the involvement of IL-6 signaling in glioma and the inhibitory effect of IL-6 signaling on glioma tumor proliferation.

Methods

The expression of IL-6 receptors (IL-6Rs) was evaluated in glioma tissues by means of immunohistochemical analysis, and the involvement of IL-6 signaling in glioblastoma multiforme (GBM) U87MG cell proliferation was also determined. In addition, to examine the inhibitory effect of IL-6 signaling on glioma cell proliferation, the authors investigated the effects of tocilizumab, the humanized anti–human IL-6R antibody in U87MG cells.

Results

Increased immunoreactivity for IL-6R was predominantly found in the cytoplasm of endothelial cells in all GBM samples. Inhibition of IL-6 signaling by both IL-6– and IL-6R–specific small interfering RNA and AG490, a specific inhibitor of JAK2 phosphorylation, suppressed glioma cell proliferation. Furthermore, tocilizumab, a clinically developed humanized anti–human IL-6R antibody, exerted an antiproliferative effect on cells from the GBM cell line U87MG via the IL-6R–dependent JAK-STAT3 pathway.

Conclusions

The IL-6 signaling pathway plays an important role in glioma cell proliferation, and tocilizumab exerts an antitumor effect in U87MG glioma cells. These results may bring new insight into the molecular pathogenesis of glioma and may lead to a new therapeutic intervention.