PubMed · 8841012
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R L Prentice. 1996-10-16. Tumor marker utility grading system.. https://doi.org/10.1093/jnci%2F88.20.1424
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Next-generation sequencing data is fundamentally changing the clinical management of patients with cancer. The most frequent genomic alterations in malignancy are mutations and amplifications, with a subset of tumors having multiple amplifications - "amplificators". We sought to understand the molecular correlates of high tumor amplification burden in a pan-cancer context. Using both national registries and a single-institution dataset, our results demonstrate that cancers with TP53 mutations (as compared to those with wild-type TP53) exhibited significantly higher tumor amplification burden across all datasets. Amplifications, generally associated with overexpression, may be potentially actionable secondary consequences of TP53 mutations.
BACKGROUND: While 2-4% of lung cancers possess alterations in BRAF, little is known about the immune responsiveness of these tumours. METHODS: Clinical and genomic data were collected from 5945 patients with lung cancers whose tumours underwent next-generation sequencing between 2015 and 2018. Patients were followed through 2020. RESULTS: In total, 127 patients with metastatic BRAF-altered lung cancers were identified: 29 tumours had Class I mutations, 59 had Class II/III alterations, and 39 had variants of unknown significance (VUS). Tumour mutation burden was higher in Class II/III than Class I-altered tumours (8.8 mutations/Mb versus 4.9, P < 0.001), but this difference was diminished when stratified by smoking status. The overall response rate to immune checkpoint inhibitors (ICI) was 9% in Class I-altered tumours and 26% in Class II/III (P = 0.25), with median time on treatment of 1.9 months in both groups. Among patients with Class I-III-altered tumours, 36-month HR for death in those who ever versus never received ICI was 1.82 (1.17-6.11). Nine patients were on ICI for >2 years (two with Class I mutations, two with Class II/III alterations, and five with VUS). CONCLUSIONS: A subset of patients with BRAF-altered lung cancers achieved durable disease control on ICI. However, collectively no significant clinical benefit was seen.
AIMS: Myxomas are thought to be slowly growing benign neoplasms. Presentation is often due to embolic phenomena, though rapid increase in size is sometimes seen. Such an increase may be due to proliferation of cellular components, an increase in matrix due to synthesis or oedema, haemorrhage into the lesion, or the addition of surface thrombus. Routine microscopy suggests a low proliferation rate. The aim of this study was to investigate cellular proliferation, and to assess its contribution to tumour growth. METHODS: The antibodies JC1, Ki67, PC10, and MIB1 were used to make an immunohistochemical assessment of proliferation in five cases of cardiac myxoma. RESULTS: A significant difference was seen between number and type of cells stained with PC10 and the other markers. Whilst PC10 stained the nuclei of most (60 - 95%) endothelial and stromal cells in all cases, the other markers stained far fewer cells (up to 5%). All markers stained varying numbers of lymphoid cells. CONCLUSIONS: Proliferation in cardiac myxomas is unlikely to be rapid. The widespread positivity for PC10 suggests that PCNA is not a reliable marker in such tissues. Clinical cases in which myxomas have grown rapidly are probably due to changes in intercellular matrix rather than cellular proliferation.