Introduction There are a number of prognostic markers (methylation, CDKN2A/B) described to be useful for the stratification of meningiomas. However, there are currently no clinically validated biomarkers for the preoperative prediction of meningioma grade, which is determined by the histological analysis of tissue obtained from surgery. Accurate preoperative biomarkers would inform the pre-surgical assessment of these tumours, their grade and prognosis and refine the decision-making process for treatment. This review is focused on the more controversial grade II tumours, where debate still surrounds the need for adjuvant therapy, repeat surgery and frequency of follow up. Methods We evaluated current literature for potential grade II meningioma clinical biomarkers, focusing on radiological, biochemical (blood assays) and immunohistochemical markers for diagnosis and prognosis, and how they can be used to differentiate them from grade I meningiomas using the post-2016 WHO classification. To do this, we conducted a PUBMED, SCOPUS, OVID SP, SciELO, and INFORMA search using the keywords; 'biomarker', 'diagnosis', 'atypical', 'meningioma', 'prognosis', 'grade I', 'grade 1', 'grade II' and 'grade 2'. Results We identified 1779 papers, 20 of which were eligible for systematic review according to the defined inclusion and exclusion criteria. From the review, we identified radiological characteristics (irregular tumour shape, tumour growth rate faster than 3cm3/year, high peri-tumoural blood flow), blood markers (low serum TIMP1/2, high serum HER2, high plasma Fibulin-2) and histological markers (low H3K27me3, low SMARCE1, low AKAP12, high ARIDB4) that may aid in differentiating grade II from grade I meningiomas. Conclusion Being able to predict meningioma grade at presentation using the radiological and blood markers described may influence management as the likely grade II tumours will be followed up or treated more aggressively, while the histological markers may prognosticate progression or post-treatment recurrence. This to an extent offers a more personalised treatment approach for patients.

Biomarkers for differentiating grade II meningiomas from grade I: a systematic review.

Neuro-oncology biobanks are critical for the implementation of a precision medicine program. In this perspective, we review our first year experience of a brain tumor biobank with integrated next generation sequencing. From our experience, we describe the critical role of the neurosurgeon in diagnosis, research, and precision medicine efforts. In the first year of implementation of the biobank, 117 patients (Female: 62; Male: 55) had 125 brain tumor surgeries. 75% of patients had tumors biobanked, and 16% were of minority race/ethnicity. Tumors biobanked were as follows: diffuse gliomas (45%), brain metastases (29%), meningioma (21%), and other (5%). Among biobanked patients, 100% also had next generation sequencing. Eleven patients qualified for targeted therapy based on identification of actionable gene mutations. One patient with a hereditary cancer predisposition syndrome was also identified. An iterative quality improvement process was implemented to streamline the workflow between the operating room, pathology, and the research laboratory. Dedicated tumor bank personnel in the department of neurosurgery greatly improved standard operating procedure. Intraoperative selection and processing of tumor tissue by the neurosurgeon was integral to increasing success with cell culture assays. Currently, our institutional protocol integrates standard histopathological diagnosis, next generation sequencing, and functional assays on surgical specimens to develop precision medicine protocols for our patients. This perspective reviews the critical role of neurosurgeons in brain tumor biobank implementation and success as well as future directions for enhancing precision medicine efforts.

/pdf/brain-tumor-biobank-development-for-precision-medicine-role-19cmbj8jt8.pdf

Brain Tumor Biobank Development for Precision Medicine: Role of the Neurosurgeon.

Meningioma, one of the most common primary central nervous system tumors, are classified into three grades by the World Health Organization (WHO) based on histopathology. The gold-standard treatment, surgical resection, is hampered by issues such as incomplete resection in some cases and a high recurrence rate. Alongside genetic alterations, DNA methylation, plays a crucial role in progression of meningiomas in the occurrence and development of meningiomas. The epigenetic landscape of meningioma is instrumental in refining tumor classification, identifying robust molecular markers, determining prognosis, guiding treatment selection, and innovating new therapeutic strategies. Existing classifications lack comprehensive accuracy, and effective therapies are limited. Methylated DNA markers, exhibiting differential characteristics across varying meningioma grades, serve as invaluable diagnostic tools. Particularly, combinatorial methylated markers offer insights into meningioma pathogenesis, tissue origin, subtype classification, and clinical outcomes. This review integrates current research to highlight some of the most promising DNA and promoter methylation markers employed in meningioma diagnostics. Despite their promise, the development and application of DNA methylation biomarkers for meningioma diagnosis and treatment are still in their infancy, with only a handful of DNA methylation inhibitors currently clinically employed for meningioma treatment. Future studies are essential to validate these markers and ascertain their clinical utility. Combinatorial methylated DNA markers for meningiomas have broad implications for understanding tumor development and progression, signaling a paradigm shift in therapeutic strategies for meningiomas.

DNA methylation meningioma biomarkers: attributes and limitations

The present study aimed to investigate the role and mechanism of action of ribonucleotide reductase M2 (RRM2) in lung adenocarcinoma and its potential as a therapeutic target. Data of patients with lung adenocarcinoma from The Cancer Genome Atlas database were collected and analyzed to evaluate the potential of RRM2 as a biomarker. The expression of RRM2 was evaluated in the A549 cell line and its cisplatin-resistant A549/DDP cell line derivative by western blot and reverse transcription-quantitative PCR. The study also investigated cell proliferation and the mechanism by which RRM2 controls cellular cisplatin resistance using CCK-8 and colony-formation assays. In addition, cell migration was assessed using Transwell assays, and the cell cycle and apoptosis were examined using flow cytometry. RRM2 was highly expressed in lung adenocarcinoma and was associated with the clinical TMN stage. Functional enrichment analysis showed that RRM2 was enriched in the cell cycle. Immune cell infiltration analysis identified 12 types of immune cell that exhibited differences between patients expressing different levels of RRM2. Cellular assays revealed higher levels of RRM2 expression in A549/DDP cells than A549 cells, and its expression was induced by cisplatin. RRM2 knockdown decreased cell proliferation and migration, accelerated apoptosis and caused cell cycle arrest in the S-phase, increasing the sensitivity of A549 and A549/DDP cells to cisplatin through the Wnt/β-catenin signaling pathway. Overexpression of β-catenin reduced the effects of RRM2 knockdown on A549 cells. Lung adenocarcinoma growth may be influenced by RRM2 through the Wnt/β-catenin signaling pathway, suggesting a potential pathway for cancer progression.

RRM2‑mediated Wnt/β‑catenin signaling pathway activation in lung adenocarcinoma: A potential prognostic biomarker.

Volumetric growth of residual meningioma – A systematic review

Meningioma is the most common intracranial tumor, and recent studies have drawn attention to the importance of further research on malignant meningioma. According to the World Health Organization (WHO) grading, meningioma is classified into 15 subtypes with three grades of malignancy. However, due to a lack of descriptions of molecular subtypes, genetic mutations, or other features, there were deficiencies in the WHO classification. The DNA methylation-based meningioma classification published in 2017 used DNA copy number analysis, mutation profiling, and RNA sequencing to distinguish six clinically relevant methylation classes, which contributed to a better prediction of tumor recurrence and prognosis. Further studies indicated that gene variation and gene mutations, such as those in neurofibromin 2 (NF2) and BRCA1, were related to the high WHO grade, malignant invasion, and recurrence. Among the mutant genes described above, some have been associated with differential DNA methylation. Herein, we searched for articles published in PubMed and Web of Science from January 2000 to May 2020 by entering the keywords "meningioma," "methylation," and "gene mutation," and found a number of published studies that analyzed DNA methylation in meningiomas. In this review, we summarize the key findings of recent studies on methylation status and genetic mutations of meningioma and discuss the current deficits of the WHO grading. We also propose that a methylation-based meningioma classification could provide clues in the assessment of individual risk of meningioma recurrence, which is associated with clinical benefits for patients.

/pdf/is-dna-methylation-a-ray-of-sunshine-in-predicting-kmfadxne68.pdf

Is DNA Methylation a Ray of Sunshine in Predicting Meningioma Prognosis

Fibroadenomas (FAs) are the most common breast tumors in women. No pharmacological agents are currently approved for FA intervention owing to its unclear mechanisms and a shortage of reproducible human models. Here, using single-cell RNA sequencing of human FAs and normal breast tissues, we observe distinct cellular composition and epithelial structural changes in FAs. Interestingly, epithelial cells exhibit hormone-responsive functional signatures and synchronous activation of estrogen-sensitive and hormone-resistant mechanisms (ERBB2, BCL2 and CCND1 pathways). We develop a human expandable FA organoid system and observe that most organoids seem to be resistant to tamoxifen. Individualized combinations of tamoxifen with ERBB2, BCL2 or CCND1 inhibitors could significantly suppress the viability of tamoxifen-resistant organoids. Thus, our study presents an overview of human FA at single-cell resolution that outlines the structural and functional differences between FA and normal breast epithelium and, in particular, provides a potential therapeutic strategy for breast FAs. 

/pdf/single-cell-profiling-of-female-breast-fibroadenoma-reveals-3voaqbeg.pdf

Single cell profiling of female breast fibroadenoma reveals distinct epithelial cell compositions and therapeutic targets

Ribonucleotide reductase M2 subunit silencing suppresses tumorigenesis in pancreatic cancer via inactivation of PI3K/AKT/mTOR pathway.

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Is DNA Methylation a Ray of Sunshine in Predicting Meningioma Prognosis

Single cell profiling of female breast fibroadenoma reveals distinct epithelial cell compositions and therapeutic targets

Ribonucleotide reductase M2 subunit silencing suppresses tumorigenesis in pancreatic cancer via inactivation of PI3K/AKT/mTOR pathway.