David S. Baskin
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View article: Case Report: A new noninvasive device-based treatment of a mesencephalic H3 K27M glioma
Case Report: A new noninvasive device-based treatment of a mesencephalic H3 K27M glioma Open
Brainstem gliomas have a poor prognosis and ineffective therapeutic options. We have developed a noninvasive device called an Oncomagnetic device that produces selective oncolysis of gliomas in vitro and marked reduction of contrast-enhanc…
View article: EXTH-13. Inhibition of mitochondrial electron transport, induction of oxidative stress, and DNA damage by oncomagnetic device in GBM cancer cells
EXTH-13. Inhibition of mitochondrial electron transport, induction of oxidative stress, and DNA damage by oncomagnetic device in GBM cancer cells Open
A new noninvasive cancer therapeutic device developed in our laboratory, called the Oncomagnetic device, involves repeated stimulation with oscillating magnetic fields (sOMF) produced by spinning permanent magnets. It is technologically an…
View article: EXTH-12. Oncomagnetic Monotherapy Mediated Anti-Tumor Immune Response in Glioblastoma
EXTH-12. Oncomagnetic Monotherapy Mediated Anti-Tumor Immune Response in Glioblastoma Open
BACKGROUND Glioblastoma (GBM) is the most lethal primary malignant brain tumor with a median survival of 15–20 months. Concurrent temozolomide (TMZ) chemotherapy and radiation (XRT) remain the current standard of care (SOC) treatment for n…
View article: INNV-63. Temporal optimization of the Stupp Protocol- Proper Use of Salvage Therapy including Bevacizumab significantly enhances survival and quality of life
INNV-63. Temporal optimization of the Stupp Protocol- Proper Use of Salvage Therapy including Bevacizumab significantly enhances survival and quality of life Open
We examined therapies that extend life after use of the Stupp protocol and their patient selection biases. There is a focus on the use of Bevacizumab to aid completion of the Stupp protocol, and the optimization of salvage strategies, re-r…
View article: TMET-63. Biochemical Characterization of Rhabdoid Meningioma by Proton Magnetic Resonance Spectroscopy
TMET-63. Biochemical Characterization of Rhabdoid Meningioma by Proton Magnetic Resonance Spectroscopy Open
Rhabdoid meningioma is a rare meningeal tumor, considered to be an aggressive meningioma subtype (WHO Grade-III) if the tumor is associated with highly elevated mitotic activity (≥20 mitoses/10 HPFs) and formation of pseudopapillary growth…
View article: CTNI-12. OSCILLATING MAGNETIC FIELDS TO TREAT GLIOBLASTOMA AND DIFFUSE MIDLINE GLIOMA-A POWERFUL TECHNOLOGY WITH STUDIES FROM THE PETRI DISH TO CLINICAL TRIALS
CTNI-12. OSCILLATING MAGNETIC FIELDS TO TREAT GLIOBLASTOMA AND DIFFUSE MIDLINE GLIOMA-A POWERFUL TECHNOLOGY WITH STUDIES FROM THE PETRI DISH TO CLINICAL TRIALS Open
We treated end-stage recurrent glioblastoma (GBM) and diffuse midline glioma (DMG) patients with oscillating magnetic fields with a wearable noninvasive Oncomagnetic device (OMD). OMD selectively kills and prevents proliferation of cancer …
View article: INNV-64. Doubling of survival in glioblastoma with modifications to the Stupp protocol: marked enhancement of survival with elimination of age bias, attention to timing of treatment intervals and dexamethasone dosages, and addition of a stereotactic radiosurgical boost
INNV-64. Doubling of survival in glioblastoma with modifications to the Stupp protocol: marked enhancement of survival with elimination of age bias, attention to timing of treatment intervals and dexamethasone dosages, and addition of a stereotactic radiosurgical boost Open
The Stupp protocol is the standard of care for treatment of glioblastoma (GBM). We explore age dependent treatment bias, the impact of a radiosurgical boost during chemoradiotherapy, proper adjustment of dexamethasone dosage, and optimal t…
View article: Case Report: Metabolic alterations and cholesterol esterification in a low-grade diffuse astrocytoma patient who progressed to glioblastoma at recurrence
Case Report: Metabolic alterations and cholesterol esterification in a low-grade diffuse astrocytoma patient who progressed to glioblastoma at recurrence Open
Background Metabolic alterations during transformation of low-grade gliomas (LGGs) into high-grade glioblastomas (GBMs) remain incompletely understood. Particularly, IDH wildtype (IDHwt) diffuse astrocytomas harboring TERT promoter (TERTp)…
View article: Radiosurgery for Intracranial Meningiomas: A Review of Anatomical Challenges and an Update on the Evidence
Radiosurgery for Intracranial Meningiomas: A Review of Anatomical Challenges and an Update on the Evidence Open
Radiation has been used to treat meningiomas since the mid-1970s. Traditionally, radiation was reserved for patients unfit for major surgery or those with surgically inaccessible tumors. With an increased quantity and quality of imaging, a…
View article: Radiosurgery for Intracranial Meningiomas: A Review of Anatomical Challenges and an Update on The Evidence
Radiosurgery for Intracranial Meningiomas: A Review of Anatomical Challenges and an Update on The Evidence Open
Radiation has been used to treat meningiomas since the mid-1970s. Traditionally, radiation was reserved for patients unfit for major surgery or those with surgically inaccessible tumors. With an increased quantity and quality of imaging an…
View article: SURG-54. RECURRENT BRAIN METASTASES (RBM) TREATED WITH SURGICALLY TARGETED RADIATION THERAPY (START): PRELIMINARY SAFETY EVALUATION FROM A MULTI-INSTITUTIONAL PROSPECTIVE REGISTRY
SURG-54. RECURRENT BRAIN METASTASES (RBM) TREATED WITH SURGICALLY TARGETED RADIATION THERAPY (START): PRELIMINARY SAFETY EVALUATION FROM A MULTI-INSTITUTIONAL PROSPECTIVE REGISTRY Open
BACKGROUND Resection and intraoperative brachytherapy for operable recurrent brain metastasis allows for pathologic confirmation of recurrent disease, mass effect relief, and immediate initiation of radiotherapy (RT). In this analysis, we …
View article: CSIG-04. ANTI-TUMOR RESPONSE OF ONCOMAGNETIC MONOTHERAPY IN GLIOBLASTOMA
CSIG-04. ANTI-TUMOR RESPONSE OF ONCOMAGNETIC MONOTHERAPY IN GLIOBLASTOMA Open
BACKGROUND Glioblastoma (GBM) is the most lethal primary malignant brain tumor with a median survival of 15–20 months. Concurrent temozolomide (TMZ) chemotherapy and radiation (XRT) remain the current standard of care (SOC) treatment for n…
View article: DNAR-03. ONCOMAGNETIC TREATMENT KILLS GLIOMA CELLS BY INHIBITING MITOCHONDRIAL ELECTRON TRANSPORT AND BY INDUCING OXIDATIVE STRESS AND DNA DAMAGE
DNAR-03. ONCOMAGNETIC TREATMENT KILLS GLIOMA CELLS BY INHIBITING MITOCHONDRIAL ELECTRON TRANSPORT AND BY INDUCING OXIDATIVE STRESS AND DNA DAMAGE Open
A new noninvasive cancer therapeutic device developed in our laboratory called the Oncomagnetic device involves repeated stimulation with oscillating magnetic fields (sOMF) produced by spinning permanent magnets. It is technologically and …
View article: CTNI-75. TRIALS IN PROGRESS: REGISTRY OF SAFETY & EFFICACY IN ADULTS WITH PRIMARY & METASTATIC INTRACRANIAL TUMORS TREATED WITH START (GAMMATILES (CS-131 SOURCE BRACHY-THERAPY)): NCT04427384
CTNI-75. TRIALS IN PROGRESS: REGISTRY OF SAFETY & EFFICACY IN ADULTS WITH PRIMARY & METASTATIC INTRACRANIAL TUMORS TREATED WITH START (GAMMATILES (CS-131 SOURCE BRACHY-THERAPY)): NCT04427384 Open
INTRO This is the first observational registry study of R+STaRT, delivered by Cs-131 sources in permanently implanted resorbable collagen tile carriers, for patients with intracranial tumors. METHODS Since October 2020, 37 sites to-date ha…
View article: TMET-38. BIOCHEMICAL CHARACTERIZATION OF PSAMMOMATOUS MENINGIOMA USING MAGNETIC RESONANCE SPECTROSCOPY
TMET-38. BIOCHEMICAL CHARACTERIZATION OF PSAMMOMATOUS MENINGIOMA USING MAGNETIC RESONANCE SPECTROSCOPY Open
Psammomatous meningioma is a histologic subtype of meningioma and is presented as a highly calcified intracranial or spinal lesion. Although computed tomography (CT) and short/zero echo-time MRI techniques can detect calcification in tumor…
View article: Targeting the Leloir Pathway with Galactose-Based Antimetabolites in Glioblastoma
Targeting the Leloir Pathway with Galactose-Based Antimetabolites in Glioblastoma Open
Background: Glioblastoma (GBM) uses Glut3 and/or Glut14 and the Leloir pathway to catabolize D-Galactose (Gal). UDP-4-deoxy-4-fluorogalactose (UDP-4DFG) is a potent inhibitor of the two key enzymes, UDP-galactose-4-epimerase (GALE) and UDP…
View article: EXTH-05. ANTI-TUMOR IMMUNE RESPONSE OF ONCOMAGNETIC MONOTHERAPY IN GLIOBLASTOMA
EXTH-05. ANTI-TUMOR IMMUNE RESPONSE OF ONCOMAGNETIC MONOTHERAPY IN GLIOBLASTOMA Open
BACKGROUND Glioblastoma (GBM) is the most lethal primary malignant brain tumor with a median survival of 15–20 months. Concurrent temozolomide (TMZ) chemotherapy and radiation (XRT) remain the current standard of care (SOC) treatment for n…
View article: TMET-14. PROBING TCA CYCLE ACTIVITY IN H3WT AND H3K27M-ALTERED DIFFUSE MIDLINE GLIOMAS
TMET-14. PROBING TCA CYCLE ACTIVITY IN H3WT AND H3K27M-ALTERED DIFFUSE MIDLINE GLIOMAS Open
DMG has high levels of α-ketoglutarate (α-KG), causing histone hypomethylation and promoting tumor growth. Therefore, targeting α-KG production in DMG tumors may be of therapeutic value. α-KG is synthesized in the tricarboxylic acid cycle …
View article: TMET-21. PROTON MAGNETIC RESONANCE SPECTROSCOPY (1H MRS) FOR THE DIAGNOSIS OF AGGRESSIVE MENINGIOMAS WITH RECURRENCE POTENTIAL
TMET-21. PROTON MAGNETIC RESONANCE SPECTROSCOPY (1H MRS) FOR THE DIAGNOSIS OF AGGRESSIVE MENINGIOMAS WITH RECURRENCE POTENTIAL Open
In our previous study, we have observed elevated steady state levels of both alanine and glutamine in surgically resected tissue specimens from atypical meningioma (grade-II) patients compared to the benign (grade-I) meningioma patients. W…
View article: Recurrent petit mal seizures in Erdheim-Chester disease mimicking an intra-axial brain tumor: illustrative case
Recurrent petit mal seizures in Erdheim-Chester disease mimicking an intra-axial brain tumor: illustrative case Open
BACKGROUND Erdheim-Chester disease (ECD) is a rare non–Langerhans cell histiocytosis characterized histologically by foamy histiocytes and Touton giant cells in a background of fibrosis. Bone pain with long bone osteosclerosis is highly sp…
View article: Data from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors
Data from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors Open
The emergence of treatment resistance significantly reduces the clinical utility of many effective targeted therapies. Although both genetic and epigenetic mechanisms of drug resistance have been reported, whether these mechanisms are stoc…
View article: Supplementary Table 7 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors
Supplementary Table 7 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors Open
Supplementary Table 7: DEG in LDE vs. control treated SI-CSC Ptch;p53 tumors
View article: Supplementary Table 5 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors
Supplementary Table 5 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors Open
Supplementary Table 5: mutational profiles for Fsmo;GFAP-cre SD-CSC tumors
View article: Supplementary Table 9 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors
Supplementary Table 9 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors Open
Supplementary Table 9: Differentially expressed proteins in LDE vs. control treated Ptch;p53 SI-CSC and SD-CSC tumors
View article: Supplementary Table 9 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors
Supplementary Table 9 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors Open
Supplementary Table 9: Differentially expressed proteins in LDE vs. control treated Ptch;p53 SI-CSC and SD-CSC tumors
View article: Supplementary Table 7 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors
Supplementary Table 7 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors Open
Supplementary Table 7: DEG in LDE vs. control treated SI-CSC Ptch;p53 tumors
View article: Supplementary Figures and Tables 1-2 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors
Supplementary Figures and Tables 1-2 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors Open
Supplementary figures and Tables 1 & 2
View article: Supplementary Table 5 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors
Supplementary Table 5 from Cancer Stem Cells, not Bulk Tumor Cells, Determine Mechanisms of Resistance to SMO Inhibitors Open
Supplementary Table 5: mutational profiles for Fsmo;GFAP-cre SD-CSC tumors