Improving precise counting of mitotic cells in mantle cell lymphoma using phosphohistone H3 (PHH3) antibody

Medani, Hanine; Elshiekh, Mohamed; Naresh, Kikkeri N.

doi:10.1136/jclinpath-2020-206956

Cited by 4 publications

(2 citation statements)

References 23 publications

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“…57 Indeed, mitotic figures are unevenly distributed across the tumour tissue, with large random effects, and unfortunately the current guidelines do not suggest any preferential method for mitotic counting. A possible solution for precise mitotic counting is IHC for phosphohistone H3 (PHH3), a marker of mitotic figures, which has been suggested to reduce interobserver variability in many tumour entities, including lung carcinoids, [58][59][60][61][62] but its use in routine grading requires validation.…”

Section: Diagnostic Reproducibilitymentioning

confidence: 99%

Updates on lung neuroendocrine neoplasm classification

Vocino Trucco,

Righi,

Volante

et al. 2023

Histopathology

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Lung neuroendocrine neoplasms (NENs) are a heterogeneous group of pulmonary neoplasms showing different morphological patterns and clinical and biological characteristics. The World Health Organisation (WHO) classification of lung NENs has been recently updated as part of the broader attempt to uniform the classification of NENs. This much‐needed update has come at a time when insights from seminal molecular characterisation studies revolutionised our understanding of the biological and pathological architecture of lung NENs, paving the way for the development of novel diagnostic techniques, prognostic factors and therapeutic approaches. In this challenging and rapidly evolving landscape, the relevance of the 2021 WHO classification has been recently questioned, particularly in terms of its morphology‐orientated approach and its prognostic implications. Here, we provide a state‐of‐the‐art review on the contemporary understanding of pulmonary NEN morphology and the potential contribution of artificial intelligence, the advances in NEN molecular profiling with their impact on the classification system and, finally, the key current and upcoming prognostic factors.

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Section: Diagnostic Reproducibilitymentioning

confidence: 99%

Updates on lung neuroendocrine neoplasm classification

Vocino Trucco,

Righi,

Volante

et al. 2023

Histopathology

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“…In the study of Chakhachiro et al, of 11 patients with a Ki-67 level > 30%, seven experienced disease recurrence within the first 3 years, while only 3 of 16 patients with a Ki-67 level ≤ 30% experienced relapse. However, Medani et al indicated that it is easier to perform precise counts and accurately evaluate proliferation indices via immunohistochemistry for phosphohistone H3 (PHH3), a reliable mitosis-specific marker in MCL, than via the Ki-67 index [24]. Moreover, Schrader and colleagues found that during early G1 phase, Ki-67 is undetectable, whereas minichromosome maintenance protein 6 (MCM6) is expressed throughout the entire G1 phase.…”

Section: The Difference In the Ki-67 Index Between Indolent MCL And Classical Mclmentioning

confidence: 99%

Progress in molecular feature of smoldering mantle cell lymphoma

Jiang

Desai

2021

Exp Hematol Oncol

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Mantle cell lymphoma (MCL) is considered one of the most aggressive lymphoid tumors. However, it sometimes displays indolent behavior in patients and might not necessitate treatment at diagnosis; this has been described as “smoldering MCL” (SMCL). There are significant differences in the diagnosis, prognosis, molecular mechanisms and treatments of indolent MCL and classical MCL. In this review, we discuss the progress in understanding the molecular mechanism of indolent MCL to provide insights into the genomic nature of this entity. Reported findings of molecular features of indolent MCL include a low Ki-67 index, CD200 positivity, a low frequency of mutations in TP53, a lack of SOX11, normal arrangement and expression of MYC, IGHV mutations, differences from classical MCL by L-MCL16 assays and MCL35 assays, an unmutated P16 status, few defects in ATM, no NOTCH1/2 mutation, Amp 11q gene mutation, no chr9 deletion, microRNA upregulation/downregulation, and low expression of several genes that have been valued in recent years (SPEN, SMARCA4, RANBP2, KMT2C, NSD2, CARD11, FBXW7, BIRC3, KMT2D, CELSR3, TRAF2, MAP3K14, HNRNPH1, Del 9p and/or Del 9q, SP140 and PCDH10). Based on the above molecular characteristics, we may distinguish indolent MCL from classical MCL. If so, indolent MCL will not be overtreated, whereas the treatment of classical MCL will not be delayed.

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