The cytoskeleton, consisting of actin filaments, intermediate filaments, and microtubules, plays an important role in cell motility during invasion of carcinomas or sarcomas into neighboring tissues. In malignant gliomas, migration of the tumor cells into the brain parenchyma promotes local and/or distant metastasis. In this article, the mechanism of cell motility is reviewed, focusing on actin, alpha cardiac muscle 1 (ACTC1) which is one of the six isoforms of actin.

Actin is present in two different forms in the cytoplasm, a globular monomer, called G-actin, and a linear polymer, called F-actin or actin filament. Actin filaments form networks through cross linkers. They are important for migration of malignant tumor cells, both through mesenchymal and amoeboid modes. The mesenchymal migration involves polymerization of actin filament at the leading edge of the lamellipodia, and by depolymerization of actin filament at the trailing edge, leading to contraction. On the contrary, the amoeboid migration is induced by the formation of a bleb, formed by contraction of actin-myosin complex in the cytoplasm, close to the cell membrane. The protruded bleb leads to migration through the extracellular matrix.

In malignant gliomas, the expression of ACTC1 is upregulated. In clinical situation, patients of ACTC1-positive glioblastoma demonstrated invasion of the contralateral cerebral hemisphere at the time of diagnosis, and distant metastasis in the remote areas of the brain at the time of recurrence. Time-lapse study demonstrated that the in vitro motility of glioblastoma cells was significantly inhibited by knockdown of ACTC1.

Actin filament-dependent cell motility is also important in migration of gliomas. Among the various isoforms of actin, ACTC1 may serve as a marker for migration in these malignant cells.

Ion channels have been suggested as hallmarks for cancer. This review provides an overview of transient receptor potential

(TRP) channels with respect to their identification and function in glioma. We conclude by discussing some outstanding questions and future directions in the study of TRP channels for the treatment of malignant glioma.

Metachronous germ cell tumor (GCT) is defined as multiple histologically different tumors occurring at different sites with a long interval between occurrences. In the central nervous system, metachronous GCTs are extremely rare. The authors report a rare case of yolk sac tumor with repeated metachronous recurrences. A 37-year-old male presented with general malaise at our hospital. Seven years ago, he underwent partial resection of a pineal yolk sac tumor followed by gamma knife surgery (GKS) at another hospital. Imaging study showed a new lesion in the left basal ganglia and recurrence of the pineal lesion. Because serum alpha-fetoprotein (AFP) was elevated, we diagnosed these lesions as recurrence of the yolk sac tumor and performed GKS followed by chemotherapy (ICE and BEP). However, six years later, new lesions appeared in the neurohypophysis and right basal ganglia. Serum AFP was not elevated, but serum beta-human chorionic gonadotropin was slightly elevated. The pathological diagnosis of the biopsy specimen of the neurohypophyseal lesion was pure germinoma. We performed chemotherapy (CARE), followed by whole ventricular irradiation and local irradiation.

Two years later, a new large lesion appeared in the right parietal lobe and serum AFP was markedly elevated. We performed total resection of the tumor followed by local irradiation. The pathological diagnosis was mixed germ cell tumor (yolk sac tumor and embryonal carcinoma). Six months later, the tumor showed direct invasion into the scalp and multiple metastases to the lungs and spinal cord. Based on this case and previously reported cases, it is assumed that metachronous GCT tends to occur outside the previous radiation field; therefore, radiation therapy involving extended fields, such as craniospinal irradiation, could be effective in preventing metachronous GCT.