New research from Princeton University uncovers why bone metastasis often leads to anemia

Cancer specialists have long known that anemia, caused by a lack of healthy red blood cells, often arises when cancer metastasizes to the bone, but it’s been unclear why. Now, a research team led by Princeton University researchers Yibin Kang and Yujiao Han has uncovered exactly how this happens in metastatic breast cancer, and it involves a type of cellular hijacking. The discovery aims to help slow down bone metastasis – one of cancer’s deadliest forms.

In a study forthcoming in the journal Cell on September 3, Kang and Han reveal that cancer cells effectively commandeer a specialized cell that normally recycles iron in the bone, known as an erythroblast island (EBI) macrophage. This both deprives red blood cells of necessary iron and helps the tumor continue to grow in the bone. What’s more, when the tumor takes up the iron from the macrophage, it starts to behave as if it’s the normal recipient – a red blood cell – producing hemoglobin and helping the tumor survive in the bone’s hostile oxygen-deficient environment. 

Understanding metastatic cancer – or cancer that grows and spreads in other parts of the body beyond the original tumor site – is critically important. It is one of the deadliest forms of cancer and there is no cure. Of patients who die from breast and prostate cancer, 70% have bone metastasis. 

For the past two decades, Kang and much of the cancer biology field, have focused on studying the tumor cells. With the advent of single-cell sequencing and advanced cell labeling technologies, now Kang has shifted to studying the surrounding environment that nurtures or restrains the cancer, moving from investigating the ‘seeds’ to the ‘soil.’ Although the current study focuses on metastatic breast cancer, the findings have been extended to other major cancer types and carry broad implications. By revealing how tumors manipulate their surroundings, the work opens new avenues for therapies designed to slow or stop bone metastasis and relieve the debilitating anemia that often comes with it.

Jie Chen et al. from Sun Yat-Sen Memorial Hospital, of Sun Yat-sen University published a paper entitled "Psychological effects of virtual reality intervention on breast cancer patients with different personalities: A randomized controlled trial" in the International Journal of Nursing Sciences. A randomized controlled trial was conducted to systematically investigate the efficiency and safety of VR intervention with natural landscape content in alleviating negative emotions, aiming to provide new ideas and empirical evidence for psychological care of breast cancer patients.

An international team led by researchers at Lund University in Sweden has identified the molecular tools needed to reprogram ordinary cells into specialised immune cells. The discovery, published in Immunity, could pave the way for more precise and personalised cancer immunotherapies.

The study investigates the interaction between the human epidermal growth receptor 2 (HER2) and amygdalin, a compound found in peaches, almonds, and apples. To assess the potential of amygdalin, the interaction between HER2 and amygdalin was explored using molecular docking and molecular dynamics simulations. Binding energies were evaluated for both the crystal and equilibrated HER2 structures. The effects of water on binding were also assessed. Molecular dynamics simulations analyzed structural changes in HER2, including interdomain distances, hydrogen bond fluctuations, dihedral angle shifts, and residue-residue distances at the dimerization arm. The free energy landscape was constructed to evaluate stability. Binding energies of −33.472 ​kJ/mol and −36.651 ± 0.867 ​kJ/mol were observed for the crystal and equilibrated HER2 structures, respectively, with water further enhancing binding to −41.212,4 ​± ​1.272,7 and −53.513 ± 1.452,3 ​kJ/mol. Molecular dynamics simulations revealed significant conformational changes in HER2, including a reduction in interdomain distance, fluctuations in hydrogen bond lengths, and a shift in dihedral angles from 60° to −30°. The residue-residue distance at the dimerization arm decreased, indicating conformational changes upon binding. The free energy landscape showed a deeper and more defined minimum in the bound state, reflecting enhanced stability. These findings highlight amygdalin’s potential as a therapeutic agent targeting HER2.