Oncogene-addicted metastatic non-small-cell lung cancer: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up

Hendriks, Lizza; Kerr, Keith M.; Menis, Jessica; Mok, T.; Nestle, Ursula; Passaro, Antonio; Peters, Solange; Planchard, David; Smit, Egbert F.; Solomon, Benjamin J.; Veronesi, Giulia; Reck, Martin

doi:10.1016/j.annonc.2022.12.009

Cited by 316 publications

(273 citation statements)

References 101 publications

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“…In line with this concept, BRAFi/MEKi should be maintained ‘beyond progression’ in case of slow, asymptomatic disease progression and in the case of oligoprogression, in addition to local treatments. 95 …”

Section: Reviewmentioning

confidence: 99%

Non-small-cell lung cancer: how to manage BRAF-mutated disease

Guaitoli¹,

Zullo²,

Tiseo³

et al. 2023

DIC

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BRAF mutations are reported in about 3–5% of non-small-cell lung cancer (NSCLC), almost exclusively in adenocarcinoma histology, and are classified into three different classes. The segmentation of BRAF mutations into V600 (class 1) and non-V600 (classes 2 and 3) relies on their biological characteristics and is of interest for predicting the therapeutic benefit of targeted therapies and immunotherapy. Given the relative rarity of this molecular subset of disease, evidence supporting treatment choices is limited. This review aims to offer a comprehensive update about available therapeutic options for patients with NSCLC harbouring BRAF mutations to guide the physician in the choice of treatment strategies. We collected the most relevant available data, from single-arm phase II studies and retrospective analyses conducted in advanced NSCLC, regarding the efficacy of BRAF and MEK inhibitors in both V600 and non-V600 BRAF mutations. We included case reports and smaller experiences that could provide information on specific alterations. With respect to immunotherapy, we reviewed retrospective evidence on immune-checkpoint inhibitors in this molecular subset, whereas data about chemo-immunotherapy in this molecular subgroup are lacking. Moreover, we included the available, though limited, retrospective evidence of immunotherapy as consolidation after chemo-radiation for unresectable stage III BRAF -mutant NSCLC, and an overview of ongoing clinical trials in the peri-operative setting that could open new perspectives in the future.

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Section: Reviewmentioning

confidence: 99%

Non-small-cell lung cancer: how to manage BRAF-mutated disease

Guaitoli¹,

Zullo²,

Tiseo³

et al. 2023

DIC

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“…Für Patient*innen mit metastasierten kolorektalen Karzinomen gehört exemplarisch die Bestimmung des KRAS-, NRAS und BRAF-Mutationsstatus sowie des Mismatch-Re-pair-Status zum diagnostischen Standard [14]. Auch beim nichtkleinzelligen Lungenkarzinom ist die Testung von PD-L1, EGFR, ALK, ROS1, BRAF, RET, MET, KRAS, NTRK und HER2 empfohlen [15].…”

Section: Präzisionsonkologie: Von Selektionierten Gruppen Zu Breiter ...unclassified

Molekulare Onkologie – wo stehen wir heute?

Bamopoulos,

Knödler,

Joosten

et al. 2023

TumorDiagnostik & Therapie

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“…Based on the probability of finding a therapeutic target, comprehensive molecular testing for these predictive biomarkers is recommended for all non-squamous NSCLC (when considering a systemic therapy) as well as for SCC in selected situations, in which a slight enrichment in targetable oncogenic drivers is to be expected: patients aged below 50 years, never smokers, former light smokers or long-term ex-smokers (who have quit smoking for more than 15 years). 84 This applies particularly to biopsies and cytological specimens where a diagnosis of SCC may actually represent an under-sampled adenosquamous carcinoma, with frequencies of oncogenic drivers more similar to adenocarcinoma. 82 Of note, in one study investigating 337 consecutive MET dysregulated stage IIIB/IV NSCLC, 6.8% of NSCLC with MET exon 14 skipping mutations were shown to be SCC, without age or histological particularities, favouring molecular testing regardless of histological subtype.…”

Section: Molecular Alterations and Their Clinical Significancementioning

confidence: 99%

“…Conversely, several mutations and fusion genes that represent approved drug targets in pulmonary adenocarcinoma may also be detected in SCC, although at lower frequencies. Table 1 compares the prevalence of targetable oncogenic drivers in both NSCLC entities, including mutations in EGFR , KRAS (in particular the G12C mutation), MET (exon 14 skipping mutations), ERBB2 , BRAF (V600E mutation) and fusion genes involving ALK , ROS1 , RET or NTRK 77–101 . Based on the probability of finding a therapeutic target, comprehensive molecular testing for these predictive biomarkers is recommended for all non‐squamous NSCLC (when considering a systemic therapy) as well as for SCC in selected situations, in which a slight enrichment in targetable oncogenic drivers is to be expected: patients aged below 50 years, never smokers, former light smokers or long‐term ex‐smokers (who have quit smoking for more than 15 years) 84 .…”

Section: Molecular Alterations and Their Clinical Significancementioning

confidence: 99%

Pulmonary squamous cell carcinoma and lymphoepithelial carcinoma – morphology, molecular characteristics and differential diagnosis

Berezowska,

Maillard,

Keyter

et al. 2023

Histopathology

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Squamous cell carcinoma (SCC) comprises one of the major groups of non‐small‐cell carcinoma of the lung, and is subtyped into keratinising, non‐keratinising and basaloid SCC. SCC can readily be diagnosed using histomorphology alone in keratinising SCC. Confirmatory immunohistochemical analyses should always be applied in non‐keratinising and basaloid tumours to exclude differential diagnoses, most prominently adenocarcinoma and high‐grade neuroendocrine carcinoma, which may have important therapeutic consequences. According to the World Health Organisation (WHO) classification 2015, the diagnosis of SCC can be rendered in resections of morphologically ambiguous tumours with squamous immunophenotype. In biopsies and cytology preparations in the same setting the current guidelines propose a diagnosis of ‘non‐small‐cell carcinoma, favour SCC’ in TTF1‐negative and p40‐positive tumours to acknowledge a possible sampling bias and restrict extended immunohistochemical evaluation in order to preserve tissue for molecular testing. Most SCC feature a molecular ‘tobacco‐smoke signature’ with enrichment in GG > TT mutations, in line with the strong epidemiological association of SCC with smoking. Targetable mutations are extremely rare but they do occur, in particular in younger and non‐ or light‐smoking patients, warranting molecular investigations. Lymphoepithelial carcinoma (LEC) is a poorly differentiated SCC with a syncytial growth pattern and a usually prominent lymphoplasmacytic infiltrate and frequent Epstein–Barr virus (EBV) association. In this review, we describe the morphological and molecular characteristics of SCC and LEC and discuss the most pertinent differential diagnoses.

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Oncogene-addicted metastatic non-small-cell lung cancer: ESMO Clinical Practice Guideline for diagnosis, treatment and follow-up

Cited by 316 publications

References 101 publications

Non-small-cell lung cancer: how to manage BRAF-mutated disease

Non-small-cell lung cancer: how to manage BRAF-mutated disease

Molekulare Onkologie – wo stehen wir heute?

Pulmonary squamous cell carcinoma and lymphoepithelial carcinoma – morphology, molecular characteristics and differential diagnosis

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