MYBL1 (MYB Proto-Oncogene Like 1)

These findings provide preliminary evidence supporting further investigation of sex-specific approaches to BC management.

Thus, familiarity with relevant tumor mutations and radiogenomic features of LEATs is important for radiologists caring for affected patients. This article will review the genetic alterations and imaging characteristics of LEATs, formatted according to the three categories defined by the World Health Organization (WHO): glioneuronal and neuronal tumors (ganglioglioma, dysembryoplastic neuroepithelial tumor, papillary glioneuronal tumor, multinodular and vacuolating neuronal tumor); circumscribed astrocytic gliomas (pilocytic astrocytoma, pleomorphic xanthoastrocytoma); and pediatric-type diffuse low-grade gliomas (diffuse astrocytoma MYB or MYBL1-altered, angiocentric glioma, diffuse low-grade glioma MAPK pathway-altered, polymorphous low-grade neuroepithelial tumor of the young).

Combined use of LEF1 and β-catenin improved sensitivity (90%) but resulted in a medium specificity (93%). In conclusion, the proposed immunohistochemical panel can improve diagnostic accuracy in basaloid tumors of the salivary glands.

Our data support the clinical implementation of a tailored, histology-driven MP algorithm, potentially optimizing the genomic testing resources in SGCs.

We report here an exceedingly rare case of a benign neoplasm diagnosed as benign tubular SG adenoma that was unexpectedly found to harbor a MYBL1::NFIB fusion gene. This case expands the spectrum of SG tumors driven by fusions of MYBL1, and challenges the specificity of MYBL1 fusions for cutaneous AdCC.

Emerging data support the use of immune checkpoint inhibitors in squamous BGC and targeted agents (e.g., mTOR/CDK4/6 inhibitors) in adenocarcinoma. We propose a practical molecular testing algorithm and highlight the urgent need for prospective, multinational collaboration to establish BGC-specific guidelines.

Imaging Mass Cytometry (IMC) reveals no significant changes in immune cells, but a notable shift in the distribution patterns of cancer-associated hepatic stellate cells in the metastatic niche, when YAP is ablated in the cancer cells. The results demonstrate a novel metastasis-driving cell signaling pathway mediated by the functional interaction between HDAC4 and MybL1, which regulates YAP expression and metastasis.

Herein, we describe the epidemiologic, imaging, and molecular features of these pediatric diffuse glioma. In addition, we review current knowledge regarding management approach and treatment outcomes, including potential therapeutic implications of prevalent molecular alterations within this family of tumors.

While surgical resection remains curative for small, superficial tumors, deeper or more infiltrative variants may recur following subtotal resection. A thorough understanding of the clinicopathological and molecular features of these gliomas is imperative for accurate classification and appropriate therapeutic intervention.

This novel observation raises the question of whether this case represents an aggressive form of MYB/MYBL1-altered LGGs driven by an oncogenic MYB fusion, or if they are actually high-grade gliomas that coincidentally exhibit alterations near the MYB locus. Further reports are needed to confirm the existence of malignant forms of LGG, MYB/MYBL1-altered, potentially correlated with a higher grade.

These radiology-molecular correlations offer potential clinical utility in treatment planning and prognostication, especially as targeted therapies against the MAPK pathway emerge. Continued research is needed to refine our understanding of genotype-phenotype correlations in less common molecular alterations and to validate these imaging biomarkers in larger cohorts.

This review synthesizes recent advances in breast AdCC molecular genetics, encompassing MYB/MYBL1 rearrangements or amplifications, NOTCH pathway gene mutations, and chromatin remodeling gene alterations. We critically evaluate contemporary methodologies for MYB assessment and discuss their clinical implications.