News RESEARCH & EVENTS Breast cancer
remodels lymphatic vessels to spread
Breast cancer doesn’t just travel through the body — it actively remodels the lymphatic vessels that carry it to nearby lymph nodes, a new study [1] from the University of Turku, Finland, reveals. Understanding this process could open the door to therapies that stop cancer in its tracks.
Metastasis, the spread of cancer to other organs, is the most dangerous aspect of breast cancer. Typically, the fi rst sign is cancer cells appearing in the lymph nodes that drain the tumour site, located in the armpit.
The Finnish team analysed these lymphatic
vessels and discovered that breast cancer triggers molecular changes that make it easier for tumour cells to travel into lymph nodes. Central to this process is a protein called Matrix Gla Protein (MGP), previously known for its role in bone formation. The researchers found MGP was highly expressed in lymph nodes affected by metastasis but absent in distant, healthy nodes.
“These results reveal a new perspective on why breast cancer spreads and why stopping it is diffi cult,” said Academician Sirpa Jalkanen, head of the InFLAMES research
A lymph node in which cancer cells are marked with yellow. The blue veins are lymphatic vessels. Credit: Akira Takeda
consortium. “By understanding how cancer alters lymphatic vessels, we can work toward targeted therapies that block this process and improve patient outcomes.”
The study relied on lymph node samples from breast cancer patients at Turku University Hospital, highlighting the importance of close collaboration between clinicians and researchers.
Breast cancer remains one of the most common cancers worldwide, with thousands of new cases diagnosed each year in Finland alone.
Early detection remains key, as survival rates are highest when the disease is caught promptly.
The fi ndings appear in Nature Communications, offering a new molecular target in the fi ght against breast cancer metastasis.
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1. Breast cancer remodels lymphatics in sentinel lymph nodes published in Nature Communications
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Researchers at the CiRA Foundation in Kyoto, Japan, have published a detailed study [1] showing how carefully defi ned culture conditions can play a decisive role in directing human induced pluripotent stem cell (hiPSC) differentiation. Using Amsbio’s StemFit™ Basic03 medium alongside the iMatrix-511 matrix, the team demonstrates how pre- culture choices infl uence cell behaviour and downstream differentiation effi ciency.
The study examines how different combinations of iPSC culture media and extracellular matrices affect both the maintenance of pluripotency and the subsequent differentiation of hiPSCs into cardiomyocytes - cells essential for heart tissue formation. By comparing multiple culture setups, the researchers reveal that conditions applied before differentiation begins can signifi cantly infl uence lineage
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Pre-culture conditions guide cardiac differentiation in iPS cells commitment and developmental outcomes.
StemFit Basic03 is an animal-origin-free, chemically defi ned medium designed for feeder-free culture of human ES and iPS cells. Widely referenced in both clinical research and GMP-aligned manufacturing, the medium supported stable maintenance of undifferentiated hiPSCs in this study while also enabling effi cient progression into cardiac lineages. Notably, the results suggest that even subtle cues within the pre- culture environment can bias developmental trajectories - an important consideration for laboratories fi ne-tuning differentiation workfl ows.
The matrix component, iMatrix-511, is optimised for pluripotent stem cell culture and supports consistent adhesion and colony morphology under feeder-free conditions. In the CiRA experiments, its use helped
maintain uniform cell growth and contributed to reproducible differentiation outcomes. Combined with a defi ned medium such as StemFit Basic03, the matrix illustrates how coordinated culture systems can improve reliability and control in stem cell research.
Commenting on the fi ndings, Philipp Boder, CGT Business Manager at Amsbio, said: “This work clearly shows that pre-culture conditions have a measurable impact on the differentiation potential of hiPSCs.
Even modest changes in medium composition before differentiation can alter gene expression patterns and markers associated with the three germ layers. These insights are highly relevant for regenerative medicine and cell therapy research, where consistent and effi cient cardiac differentiation is essential.”
The full study is available at
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HiPSCs cultured on iMatrix Laminin-511 with StemFit® Basic03.
1. Effect of iPS cell culture medium on the differentiation potential of induced cardiac tissues published in Scientifi c Reports
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New fellow aims to decode hidden HIV reservoirs
The Wistar Institute has appointed Vincent Wu, PhD, as a Caspar Wistar Fellow in its Vaccine & Immunotherapy Center, bringing expertise in molecular biology and computational analysis to tackle one of HIV research’s most challenging problems: the persistent viral reservoir.
Wu, who fi rst studied HIV-2 as an undergraduate, has spent a decade investigating how the virus survives immune defences and hides in infected cells. During his postdoctoral work in Michael Betts’ lab at the University of Pennsylvania, he mastered single- cell profi ling and computational tools to analyse complex datasets, providing a high-resolution view of cellular changes during infection.
Vincent Wu. Credit The Wistar Institute
“The molecular biology and bioinformatics sides often speak different languages,” Wu
explained. “My goal is to build a lab where both approaches work together harmoniously, allowing experiments to directly inform data analysis and interpretation.”
A central focus of Wu’s research is the HIV reservoir - a heterogeneous population of cells that persists despite therapy. Using single-cell methods, he aims to map its composition, uncover what regulates it, and understand how it changes over time or after interventions. He is also pursuing ‘shock-and-kill’ strategies to activate dormant virus, making infected cells vulnerable to immune therapies. Recent work with mRNA–LNP approaches complements Wistar collaborations with CAR-T cell and broadly neutralising antibody researchers.
“Dr Wu’s integration of experimental and
computational approaches places him at the forefront of HIV and immunology research,” said David Weiner, PhD, Wistar Executive Vice President and Director of the Vaccine & Immunotherapy Center. Wu’s tools will support studies across Wistar’s HIV and immunotherapy programmes, advancing efforts to understand protective immunity and identify new therapeutic targets.
As a Caspar Wistar Fellow, Wu will receive institutional support to establish his lab and advance an ambitious research programme aimed at decoding and ultimately disrupting HIV reservoirs.
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