ATRX immunohistochemistry can help refine ‘not elsewhere classified’ categorisation for grade II/III gliomas

Burford, Charlotte; Laxton, Ross C.; Sidhu, Z.; Aizpurua, Miren; King, Andrew; Bódi, István; Ashkan, Keyoumars; Al‐Sarraj, Safa

doi:10.1080/02688697.2019.1600657

Cited by 1 publication

(1 citation statement)

References 23 publications

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“…As a result, diagnostic algorithms are undergoing substantial changes for many tumor types: this molecular revolution has been fully undertaken by the latest 2016 World Health Organization (WHO) classification of central nervous system (CNS) neoplasms, as molecular markers (e.g., IDH1/IDH2 (Isocitrate dehydrogenase 1/2), 1p/19q codeletion, ATRX (transcriptional regulator ATRX), TP53 (tumor protein p53) etc.) have become mandatory for a conclusive diagnosis of many specific tumor entities [6][7][8][9]. Moreover, in the following few years since its publication, the diagnostic/prognostic/predictive importance of many additional molecular traits have been demonstrated and they are now being quickly translated into the routine clinical practice [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

NTRK Fusions in Central Nervous System Tumors: A Rare, but Worthy Target

Gambella

Senetta

Collemi

et al. 2020

IJMS

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The neurotrophic tropomyosin receptor kinase (NTRK) genes (NTRK1, NTRK2, and NTRK3) code for three transmembrane high-affinity tyrosine-kinase receptors for nerve growth factors (TRK-A, TRK-B, and TRK-C) which are mainly involved in nervous system development. Loss of function alterations in these genes can lead to nervous system development problems; conversely, activating alterations harbor oncogenic potential, promoting cell proliferation/survival and tumorigenesis. Chromosomal rearrangements are the most clinically relevant alterations of pathological NTRK activation, leading to constitutionally active chimeric receptors. NTRK fusions have been detected with extremely variable frequencies in many pediatric and adult cancer types, including central nervous system (CNS) tumors. These alterations can be detected by different laboratory assays (e.g., immunohistochemistry, FISH, sequencing), but each of these approaches has specific advantages and limitations which must be taken into account for an appropriate use in diagnostics or research. Moreover, therapeutic targeting of this molecular marker recently showed extreme efficacy. Considering the overall lack of effective treatments for brain neoplasms, it is expected that detection of NTRK fusions will soon become a mainstay in the diagnostic assessment of CNS tumors, and thus in-depth knowledge regarding this topic is warranted.

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