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Biomedical subjects

Martin Begemann

Publications and source records attributed to Martin Begemann.

7 recordsLinked to original sources

Systemic high-dose intravenous methotrexate for central nervous system metastases.

BACKGROUND: Treatment options for patients with recurrent central nervous system (CNS) metastases are limited. Rapid infusion of high-dose intravenous methotrexate (HD IV MTX) penetrates the blood-brain barrier (BBB) and has reported activity in leptomeningeal metastases. METHODS: Medical records were reviewed for all patients treated with HD IV MTX (3.5 g/m2) for CNS parenchymal or leptomeningeal metastases. Radiographic response rate, survival, and toxicity were determined. RESULTS: Thirty-one women and one man with a median age of 52 years (range 33-76) were treated with a total of 141 cycles (median 4, range 1-13). Twenty-nine patients had breast cancer, and one each had cancer of unknown primary (CUP), squamous cell carcinoma of the head and neck, and non-small cell lung cancer (NSCLC). An objective radiographic response and stable disease were each observed in nine patients (28%), and 13 (44%) patients progressed. Prior treatment with low-dose MTX for systemic disease did not affect response (P = 0.8). The median overall survival (n = 32) was 19.9 weeks (range 2.9-135.4+) with one patient alive at 135.4 weeks. Myelosuppression and elevated serum hepatic transaminases were the most common acute toxicities (21% and 9% of HD IV MTX cycles, respectively). CONCLUSIONS: HD IV MTX is effective in the treatment of CNS metastases with disease control (response or stable) as a best response in 56% of assessable patients. Further study is warranted.

Adult↗

Necrotizing vasculopathy of the CNS: case report.

A 62-year-old man with progressive cerebellar and brainstem dysfunction had gadolinium-enhancing lesions in basal ganglia and occipital lobe on MRI suggestive of primary CNS lymphoma (PCNSL). The patient, who had been treated with high-dose steroid hormones for several months, developed respiratory failure and expired before a histological diagnosis could be obtained. The postmortem examination showed Pneumocystis cariniiwas the cause of death. Pathology of the brain showed a necrotizing vasculopathy affecting the white matter of the cerebrum and cerebellum with involvement of the basal ganglia and the periventricular gray matter. Other organs such as liver, lung, and kidneys were spared. Necrotizing vasculopathy is a novel entity that should be considered in the differential diagnosis of PCNSL.

Brain Neoplasms↗

Brain metastases in hepatoblastoma.

Brain metastases from hepatoblastomas are rare. We report a 2-year-old male who developed multiple hemorrhagic intracranial metastases. Previous reports indicate that brain metastases are an almost uniformly fatal complication of hepatoblastoma, although one long-term survivor has been described. In a child with known hepatoblastoma, the development of neurologic signs or symptoms should lead to the performance of a brain imaging study to exclude the possibility of intracranial extension of the disease.

Biopsy↗

Primary leptomeningeal primitive neuroectodermal tumor.

Leptomeningeal metastases are a common complication of medulloblastomas and other primitive neuroectodermal tumors (PNETs). Much rarer are PNETs apparently arising in the leptomeninges. An 8-year-old boy presented with headache and vomiting, due to neoplastic meningitis from primary neuroectodermal tumor without an identifying mass. After craniospinal irradiation and chemotherapy (carboplatin, vincristine, cyclophosphamide and lomustine) the boy was in remission for 14 months, then suffered several relapses despite various chemotherapy regimens. After the initial presentation of 3.5 years the boy began to suffer from prolonged refractory non-convulsive status epilepticus and later expired from progression of primary leptomeningeal PNET.

Antineoplastic Combined Chemotherapy Protocols↗

Leptomeningeal metastases from recurrent squamous cell cancer of the skin.

We report two patients with leptomeningeal metastases from squamous cell cancer of the skin. In one patient cauda equina metastases appeared 6 years after initial presentation; the tumor from radical neck dissection demonstrated perineural invasion suggesting a possible route for subarachnoid dissemination. The other patient presented 2 years after initial diagnosis with confusion and cranial nerve seven and twelve palsies. Both patients died from complications of leptomeningeal metastases.

Aged↗

Genetic modeling of glioma formation in mice.

In addition to the histological features that define gliomas, mutations and other alterations in gene expression and signal transduction are classically found in these tumors. Some of these alterations are likely to be the effects of the neoplastic phenotype, while others may be causative agents essential to the etiologic origin of the disease. The determination of whether specific genetic alterations, either individually or in combination, can serve as the etiology of gliomas requires modeling in animals with the fulfillment of Koch's postulates. Animal modeling studies not only provide information on the potential causes of glioma formation, they also identify novel candidate targets for therapy and provide tumor-bearing animals for preclinical trials. Recently, remarkable strides have been made in the generation of mouse models of the diffuse gliomas that provide unparalleled opportunities for advancing our knowledge of the etiology, maintenance, and treatment of this lethal class of tumors.

Animals↗