Figure 1. Heterogeneous HER2 immunostaining in two gastric cancer samples classified as HER2 3+. (A) Complete ... Figure 1. Heterogeneous HER2 immunostaining.

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Figure 1. Heterogeneous HER2 immunostaining in two gastric cancer samples classified as HER2 3+. (A) Complete ... Figure 1. Heterogeneous HER2 immunostaining in two gastric cancer samples classified as HER2 3+. (A) Complete basolateral membranous immunoreactivity with strong intensity in all tumour cells. (B) Strong basolateral immunostaining restricted to a tumour cell area. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) 2019. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Annals of Oncology, Volume 30, Issue 8, 02 May 2019, Pages 1254–1264, https://doi.org/10.1093/annonc/mdz143 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 2. Intra-tumour heterogeneity: a role for clonal evolution Figure 2. Intra-tumour heterogeneity: a role for clonal evolution. Primary tumours are made up by different cell ... Figure 2. Intra-tumour heterogeneity: a role for clonal evolution. Primary tumours are made up by different cell populations bearing diverse molecular alterations. Those molecular changes can be reproduced or not in metastatic sites. Moreover, some specific molecular abnormalities can be found only in metastatic spots. HER2 amplification may be heterogeneously distributed in different areas of the primary tumours. This feature can be weakened or lost in metastatic sites. Some other molecular alterations may exclusively appear in metastasis (as EGFR amplification and PIK3CA mutations). Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) 2019. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Annals of Oncology, Volume 30, Issue 8, 02 May 2019, Pages 1254–1264, https://doi.org/10.1093/annonc/mdz143 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 3. Different mechanisms of resistance to anti-HER2 drugs: (A) Structural abnormality of HER2 receptor such as ... Figure 3. Different mechanisms of resistance to anti-HER2 drugs: (A) Structural abnormality of HER2 receptor such as p95HER2 or MUC4 co-expression physically impairing HER2 accessibility to trastuzumab-binding epitope; (B) presence of HER2 homo and heterodimers. HER2–HER3 is the most potent driver of PI3K/Akt/mTOR activation leading to resistance to anti-HER2 blockade; (C) co-expression of several tyrosine kinase receptors interfering with HER2 blockade. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) 2019. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Annals of Oncology, Volume 30, Issue 8, 02 May 2019, Pages 1254–1264, https://doi.org/10.1093/annonc/mdz143 The content of this slide may be subject to copyright: please see the slide notes for details.

Figure 4. Different mechanisms of action of conventional and novel anti-HER2 treatments. Unless provided in the caption above, the following copyright applies to the content of this slide: © The Author(s) 2019. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com.This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) Annals of Oncology, Volume 30, Issue 8, 02 May 2019, Pages 1254–1264, https://doi.org/10.1093/annonc/mdz143 The content of this slide may be subject to copyright: please see the slide notes for details.