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A model for the biological rationale for rechallenge therapy: clonal selection in heterogeneous baseline RAS a wt tumours during anti-EGFR therapy. aAdditional.

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Presentation on theme: "A model for the biological rationale for rechallenge therapy: clonal selection in heterogeneous baseline RAS a wt tumours during anti-EGFR therapy. aAdditional."— Presentation transcript:

1 A model for the biological rationale for rechallenge therapy: clonal selection in heterogeneous baseline RAS a wt tumours during anti-EGFR therapy. aAdditional or secondary acquired mechanisms of resistance can also be driven by mutations in the extracellular domain of the EGFR, and other potential biomarkers continue to be investigated. A model for the biological rationale for rechallenge therapy: clonal selection in heterogeneous baseline RASa wt tumours during anti-EGFR therapy. aAdditional or secondary acquired mechanisms of resistance can also be driven by mutations in the extracellular domain of the EGFR, and other potential biomarkers continue to be investigated. EGFR, epidermal growth factor receptor; mut, mutant; wt, wild-type. Richard M Goldberg et al. ESMO Open 2018;3:e000353 Copyright © European Society for Medical Oncology. All rights reserved.

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Figure 1. (A) Forest plot of common odds ratios (adjusted for ECOG PS) for best overall response by a priori subgroups in patients with KRAS wild-type.
(A) Programmed cell death ligand-1 (PD-L1) expression score was significantly higher in pulmonary adenocarcinomas with grade G2/G3 differentiation as compared.

(A) Programmed cell death ligand-1 (PD-L1) expression score was significantly higher in pulmonary adenocarcinomas with grade G2/G3 differentiation as compared.
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A proposed treatment model for the decision-making process when choosing between cetuximab continuation vs rechallenge. aTypically patients with left-sided,

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Immunohistochemistry of CD8 (A and B) and PD-L1 (C–F).

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Male patients with non-small cell lung cancer (NSCLC) have a 24% reduction in the risk of disease progression (A). Male patients with non-small cell lung.

Male patients with non-small cell lung cancer (NSCLC) have a 24% reduction in the risk of disease progression (A). Male patients with non-small cell lung.
Schematic representation of main EGFR-TKIs resistance mechanisms.

Schematic representation of main EGFR-TKIs resistance mechanisms.
The chimeric Trk protein, composed by the TK domain with ATPase activity and a TM loop along with a fusion partner. The chimeric Trk protein, composed.

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(A) Frequency of synchronous diagnosis of primary tumour and BM according to primary tumour type (B) Frequency of patients with asymptomatic BM at first.

(A) Frequency of synchronous diagnosis of primary tumour and BM according to primary tumour type (B) Frequency of patients with asymptomatic BM at first.
Progesterone receptor nuclear morphology patterns in breast cancer.

Progesterone receptor nuclear morphology patterns in breast cancer.
Invasion front (pushing margin) of the patient's tumour from the primary resection showing a high number of tumour-infiltrating leucocytes, which is characteristic.

Invasion front (pushing margin) of the patient's tumour from the primary resection showing a high number of tumour-infiltrating leucocytes, which is characteristic.
Programmed cell death ligand-1 (PD-L1) expression of alveolar macrophages. Programmed cell death ligand-1 (PD-L1) expression of alveolar macrophages. (A)

Programmed cell death ligand-1 (PD-L1) expression of alveolar macrophages. Programmed cell death ligand-1 (PD-L1) expression of alveolar macrophages. (A)
Recurrence pattern after initial treatment of brain metastases and cause of death. Recurrence pattern after initial treatment of brain metastases and cause.

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Flow chart of the used methodology adapted from Moher et al

Flow chart of the used methodology adapted from Moher et al
The decision tree with the two alternatives.

The decision tree with the two alternatives.
Choice of the study design (superiority vs non-inferiority design) for postregistration trials comparing different treatments for the same therapeutic.

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Detection rate for EGFR mutations in cfDNA.

Detection rate for EGFR mutations in cfDNA.
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Histological and molecular heterogeneity of triple negative breast cancer (TNBC). Histological and molecular heterogeneity of triple negative breast cancer (TNBC).

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