Bone morphogenetic protein receptor inhibitors suppress the growth of glioblastoma cells.

Glioblastomas (GBMs) are aggressive brain tumors that are resistant to chemotherapy and radiation. Bone morphogenetic protein (BMP) ligand BMP4 is being examined as a potential therapeutic for GBMs because it induces differentiation of cancer stem cells (CSCs) to an astrocyte phenotype. ID1 is reported to promote self-renewal and inhibit CSC differentiation.

Single-cell mechanical analysis and tension quantification via electrodeformation relaxation.

The mechanical behavior and cortical tension of single cells are analyzed using electrodeformation relaxation. Four types of cells, namely, MCF-10A, MCF-7, MDA-MB-231, and GBM, are studied, with pulse durations ranging from 0.01 to 10 s.

Plexin-B2 facilitates glioblastoma infiltration by modulating cell biomechanics.

Infiltrative growth is a major cause of high lethality of malignant brain tumors such as glioblastoma (GBM). We show here that GBM cells upregulate guidance receptor Plexin-B2 to gain invasiveness. Deletion of Plexin-B2 in GBM stem cells limited tumor spread and shifted invasion paths from axon fiber tracts to perivascular routes.

Assessment of Needs in Children Suffering From Refractory Non-neurogenic Urinary and Fecal Incontinence and Their Caregivers' Needs and Attitudes Toward Alternative Therapies (SNM, TENS).

Non-neurogenic urinary and fecal incontinence (UI, FI) affects approximately 6% of North American children with 1% of cases becoming refractory (nonresponsive to standard therapies). Incontinence has major potential long-term physiological and psychological implications for patients and their families. While Sacral Neuromodulation (SNM) and Transcutaneous Nerve Stimulation (TENS) are alternative therapies available for the treatment of refractory UI/FI, these are not approved for use in children in Canada.

Teaching an Old Drug New Tricks: Dexamethasone as an In Vivo Inhibitor of Glioblastoma Dispersal.

Identifying drugs that can mitigate dispersal of glioblastoma cells, particularly after patients undergo radiotherapy and concomitant chemotherapy, may increase the length of time to recurrence and improve overall survival. Previous studies have shown that dexamethasone (Dex), a drug currently used to treat brain tumor-related edema, which is tapered immediately after the edema has resolved, induces fibronectin matrix assembly (FNMA) and reduces dispersal of primary human glioblastoma multiforme (GBM) cells in vitro and ex vivo. Here, we utilized an in vivo mouse retina dispersal assay to demonstrate that Dex also inhibits dispersal in vivo.