Medulloblastoma Simulating Acute Myeloid Leukemia: Case Report With a Review of “Myeloid Antigen” Expression in Nonhematopoietic Tissues and Tumors

Etzell, Joan; Keet, Corinne A.; McDonald, William C.; Banerjee, Anuradha

doi:10.1097/01.mph.0000243647.66734.0f

Cited by 16 publications

(9 citation statements)

References 32 publications

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“…To determine whether DAOY and UW228 were intrinsically more immunogenic or if this was specific to the PD-1 pathway, we also evaluated these tumors for the expression of human MHC class II ligands; DR, DQ, and DB. MB has been previously described as having the ability to express MHC class II [ 24 – 26 ], and indeed all cell lines expressed it in response to stimulation except for D283-MED ( Supplementary Figure 5 ). No cell lines displayed intrinsic expression of MHC class II, consistent with prior reports, suggesting that the observed pattern of PD-L1 and PD-L2 was unique to molecules of the PD-1 pathway.…”

Section: Resultsmentioning

confidence: 92%

PD-L1 expression in medulloblastoma: an evaluation by subgroup

et al. 2018

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BackgroundThis study evaluated the expression of PD-L1 and markers of immune mediated resistance in human medulloblastoma (MB), the most common malignant pediatric brain tumor.ResultsOverall levels of PD-L1 in human MB were low; however, some cases demonstrated robust focal expression associated with increased immune infiltrates. The case with highest PD-L1 expression was a sonic hedgehog (SHH) MB. In cell lines, SHH MB, which are low-MYC expressing, demonstrated both constitutive and inducible expression of PD-L1 while those in Group 3/4 that expressed high levels of MYC had only inducible expression. In vitro, IFN-γ robustly stimulated the expression of PD-L1 in all cell lines while radiation induced variable expression. Forced high MYC expression did not significantly alter PD-L1.MethodsHuman MB tumor samples were evaluated for expression of PD-L1 and immune cell markers in relation to molecular subgroup assignment. PD-L1 expression was functionally analyzed under conditions of interferon gamma (IFN-γ), radiation, and MYC overexpression.ConclusionsMB expresses low levels of PD-L1 facilitating immune escape. Importantly, TH1 cytokine stimulation appears to be the most potent inducer of PD-L1 expression in vitro suggesting that an inflamed tumor microenvironment is necessary for PD-1 pathway activation in this tumor.

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Section: Resultsmentioning

confidence: 92%

PD-L1 expression in medulloblastoma: an evaluation by subgroup

et al. 2018

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“…More recently, expression of CD34 in conjunction with other hematopoietic markers has been reported in a case of medulloblastoma. 18 Taken together, this may indicate that expression of such a stem cell marker reflects progression toward a more primiby guest on http://neuro-oncology.oxfordjournals.org/ Downloaded from tive phenotype. Furthermore, it is possible that CD34-positive cells in gliomas are recruited into the tumor from circulating bone marrow-derived hematopoietic progenitors.…”

Section: Mesenchymal and Hematopoietic Stem Cell And Invasion Markersmentioning

confidence: 96%

High-grade glioma before and after treatment with radiation and Avastin: Initial observations

Fischer¹,

Cunliffe²,

Bollo³

et al. 2008

Neuro-Oncology

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We evaluate the effects of adjuvant treatment with the angiogenesis inhibitor Avastin (bevacizumab) on pathological tissue specimens of high-grade glioma. Tissue from five patients before and after treatment with Avastin was subjected to histological evaluation and compared to four control cases of glioma before and after similar treatment protocols not including bevacizumab. Clinical and radiographic data were reviewed. Histological analysis focused on microvessel density and vascular morphology, and expression patterns of vascular endothelial growth factor-A (VEGF-A) and the hematopoietic stem cell, mesenchymal, and cell motility markers CD34, smooth muscle actin, D2-40, and fascin. All patients with a decrease in microvessel density had a radiographic response, whereas no response was seen in the patients with increased microvessel density. Vascular morphology showed apparent "normalization" after Avastin treatment in two cases, with thin-walled and evenly distributed vessels. VEGF-A expression in tumor cells was increased in two cases and decreased in three and did not correlate with treatment response. There was a trend toward a relative increase of CD34, smooth muscle actin, D2-40, and fascin immunostaining following treatment with Avastin. Specimens from four patients with recurrent malignant gliomas before and after adjuvant treatment (not including bevacizumab) had features dissimilar from our study cases. We conclude that a change in vascular morphology can be observed following antiangiogenic treatment. There seems to be no correlation between VEGF-A expression and clinical parameters. While the phenomena we describe may not be specific to Avastin, they demonstrate the potential of tissue-based analysis for the discovery of clinically relevant treatment response biomarkers.

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“…MB CTCs display positivity for CD56 (NCAM), which, coupled with CD45 exclusion (to exclude white blood cells) and morphological examination, allows the identification of such cells. CD56+ve MB cells are also found in the blood of patients that display overt extraneural disease at progression, indicating that the expression of the antigen is conserved at relapse and could be useful for tracking MB CTCs during the entire course of the disease (17,23,92). However, efforts to characterize the surfaceome of MB CTCs should be undertaken, because expression of CD56 is frequently focal in primary tumors.…”

Section: Anatomic Routes Of Metastatic Disseminationmentioning

confidence: 99%

The molecular biology of medulloblastoma metastasis

et al. 2020

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Medulloblastoma (MB) is the most common primary malignant brain tumor of childhood and a significant contributor to pediatric morbidity and death. While metastatic dissemination is the predominant cause of morbidity and mortality for patients with this disease, most research efforts and clinical trials to date have focused on the primary tumor; this is due mostly to the paucity of metastatic tumor samples and lack of robust mouse models of MB dissemination. Most current insights into the molecular drivers of metastasis have been derived from comparative molecular studies of metastatic and non-metastatic primary tumors. However, small studies on matched primary and metastatic tissues and recently developed mouse models of dissemination have begun to uncover the molecular biology of MB metastasis more directly. With respect to anatomical routes of dissemination, a hematogenous route for MB metastasis has recently been demonstrated, opening new avenues of investigation. The tumor micro-environment of the primary and metastatic niches has also been increasingly scrutinized in recent years, and further investigation of these tumor compartments is likely to result in a better understanding of the molecular mediators of MB colonization and growth in metastatic compartments.

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Medulloblastoma Simulating Acute Myeloid Leukemia: Case Report With a Review of “Myeloid Antigen” Expression in Nonhematopoietic Tissues and Tumors

Cited by 16 publications

References 32 publications

PD-L1 expression in medulloblastoma: an evaluation by subgroup

PD-L1 expression in medulloblastoma: an evaluation by subgroup

High-grade glioma before and after treatment with radiation and Avastin: Initial observations

The molecular biology of medulloblastoma metastasis

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