Dortmund, 25th August 2026
How metastatic cancer cells adapt to new microenvironments is one of Prof. Dr Dr Alpaslan Tasdogan’s areas of research. The oncologist is Head of the Institute for Tumour Metabolism at the Clinic fpr Dermatology at University Hospital Essen, and he heads the research group Preclinical Metabolomics at ISAS. In a study published in Cancer Discovery, he and his fellow researchers investigated metastatic breast cancer cells in the lung. In this interview, he explains why these tumour cells survive in the lung and what therapeutic prospects there are for patients.
Your publication shows that metastatic tumour cells utilise certain protective mechanisms against oxidative stress to successfully establish themselves in the lung. Why did you choose to investigate lung metastases specifically in the context of breast cancer?
Tasdogan: The lung is one of the first and most common target organs to which breast cancer cells metastasise. In many patients, the tumour cells spread further throughout the body from there. That is why we wanted to gain a better understanding of the mechanisms that help metastatic tumour cells to survive in the lung and successfully establish themselves there. By better understanding these early stages of metastasis, we can, in the long term, develop new ways to intervene specifically and prevent further spread.

Prof. Dr Dr Alpaslan Tasdogan is an oncologist and Head of the Institute for Tumour Metabolism at University Hospital Essen. Together with his research group there, he conducts research into metastases and the metabolism of malignant melanoma. At ISAS, the doctor and scientist has been leading a second research group since May 2024. Tasdogan has already received several awards for his research, including, for example an ERC Starting Grant, an Emmy Noether Junior Research Group and the Peter Hans Hofschneider Endowed Professorship for Molecular Medicine.
© Dave Kittel / Universitätsklinikum Essen
What do your findings mean for the current and future treatment of lung metastases in different types of breast cancer?
Tasdogan: Our findings reveal new therapeutic targets for the early phase of metastasis. When tumour cells migrate to the lung, they are exposed to particularly severe oxidative stress there. To survive and establish themselves, they activate protective mechanisms that counteract this stress. If we succeed in specifically blocking these mechanisms, the tumour cells would no longer be able to compensate for the oxidative stress and would undergo apoptosis – that is programmed cell death – even before a metastasis forms.
Future therapies could aim to influence specific metabolic pathways in such a way that the tumour cells can no longer counteract the oxidative stress. Should effective compounds be identified in preclinical studies, these could open new treatment options for patients with metastatic breast cancer in long term.
What role might glutathione play in breast cancer, particularly regarding metastases in other organs – such as the liver, brain or bones?
Tasdogan: Glutathione helps the cell to counteract oxidative stress. Our findings suggest that tumour cells utilise this protective function to overcome the stressful conditions of early metastasis. As the lung is one of the first and most common target organs for metastatic breast cancer cells, the stress adaptation acquired there could be crucial for further spread. We suspect that tumour cells which have already developed effective stress-defence strategies in the lung are also better able to cope with the stressful conditions in other organs. We therefore regard the lung as a kind of gatekeeper of metastasis – a waystation that can influence and facilitate the further spread of tumour cells.
Considering your findings, to what extent is it relevant where the primary tumour originated? Or to put it another way: Could one expect similar effects in colorectal cancer cells that have metastasised to the lungs?
Tasdogan: What matters is not so much where the primary tumour originated, but rather the challenges tumour cells face in a new organ. When tumour cells colonise the lungs, they must adapt to a hostile environment. We assume that metastasising tumour cells utilise, to some extent, similar adaptation mechanisms in this process. These fundamental processes of metastasis can be analysed using comparable technologies across different types of cancer. We are currently investigating this, for example, in melanoma and colorectal cancer. In this context, we aim to gain a better understanding of the common principles of metastasis and to identify the adaptive mechanisms tumour cells use to colonise new organs.
(The interview was conducted by Saskia Schlesinger.)
Publication
Yeh, H.W., DelGaudio, N. L., Uygur, B., Millet, A., Khan, A., Unlu, G., Xiao, M., Timson, R. C., Li, C., Ozcan, K., Smith, K. W., Martins Nascentes Melo, L., Allies, G., Basturk, O., Sickmann, A., Bayraktar, E. C., Possemato, R., Tasdogan, A., Birsoy, K.
(2025) Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling.
Cancer Discovery. 15 (12), 2437–2449.
