Breast cancer drugs could help treat resistant lung cancers

A class of drugs used to treat certain breast cancers could help to tackle lung cancers that have become resistant to targeted therapies, suggests a new study in mice from the Francis Crick Institute and the Institute of Cancer Research (ICR).

The research, published in Cell Reports, found that lung tumours in mice caused by mutations in a gene called EGFR shrunk significantly when a protein called p110α was blocked.

Drugs to block p110α are currently showing promise in clinical trials against certain breast cancers, so could be approved for clinical use in the near future. The new findings suggest that these drugs could potentially benefit patients with EGFR-mutant lung cancers whose tumours have become resistant to treatment.

"At the moment, patients with EGFR-mutant lung cancers are given targeted treatments that are very effective for the first few years," explains study leader Professor Julian Downward, who has labs at the Crick and the ICR. "These drugs are improving, but unfortunately after a couple of years the cancer usually becomes resistant and starts to grow and spread again. The second line of treatment is currently conventional chemotherapy, which is not targeted and has substantial side-effects.Our new study suggests that it would be worth investigating whether p110α inhibitors could be used as a second-line therapy. As our research is at such an early stage, more research in mice and patient cells would be needed before even considering clinical trials, but it opens up a promising avenue of investigation."

For this research, the team targeted a specific interaction between the RAS protein and p110α. The RAS gene is mutated in around one in five cancers, causing uncontrolled growth, and is a key focus of Downward's research. When they blocked this interaction in genetically modified mice with EGFR mutations, their tumours shrank significantly.

Before the intervention, the tumours filled around two thirds of the space inside the lung. When the interaction between RAS and p110α was genetically blocked, this shrank significantly to about a tenth of the space inside the lung. The intervention also had very few side-effects.

"As we wanted to pinpoint the specific interaction responsible, we used a genetic technique that would not be practical in a patient treatment," says Downward. "We're looking to develop ways to do this with drugs, as blocking this specific pathway would significantly reduce side-effects, but this work is many years from the clinic. In the medium-term, investigating existing drugs that inhibit p110α will be the next step. While these have side-effects, including temporary diabetes-like symptoms during treatment, they are still less toxic than chemotherapy."

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Bone marrow-derived fibroblasts shown to promote breast cancer growth

A new study has revealed that breast cancer cells recruit bone marrow-derived fibroblasts to enhance their growth. It is hoped that the discovery will lead to the development of new treatments that target the cells in and around the tumor.

Many breast cancers show the presence of abundant fibroblasts from neighboring breast tissue and other body tissues.

Fibroblasts are typically associated with malignant solid tumors and are among the cell types that are not actually cancerous but enhance tumor progression.

For instance, fibroblasts within breast tumors secrete growth factors that increase the rate of proliferation of the cancer cells.

They also induce inflammation and tumor neovascularization (the formation of new blood vessels growing deep into the tumor).

Neovascularization of the tumor is essential to provide an adequate supply of oxygen and nutrients for its growth.

In the current experiment breast cancers in mice were shown to contain a high percentage of fibroblasts recruited from mesenchymal stromal cells (MSCs).

These cells originate in the bone marrow and show significant differences from other fibroblasts present in cancerous growths.

One important difference is the absence of an important cytokine, a protein called PDGFRα. The lack of PDGFRα, therefore, acts as a marker for such cells.

Bone marrow-derived fibroblasts are strong promoters of tumor neovascularization (the formation of new blood vessels to supply a tumor) because they secrete high amounts of the protein clusterin.

The presence of such fibroblasts was associated with faster tumor growth rates due to improved vascularization, compared to other breast tumors which contain only fibroblasts derived from surrounding breast tissue.

The same team discovered that human breast cancers also showed the presence of fibroblasts which were negative for PDGFRα.

When the tumor concentration of PDGFRα was lower, the tumors were significantly more likely to be fatal.

In effect, therefore, breast tumors that recruit bone marrow-derived fibroblasts have taken a very important step towards more rapid growth and distant spread.

Gaining insight into how these cells work could well lead to the emergence of new treatments which selectively target not just the cancer cells but also the bone marrow-derived fibroblasts that support tumor progression.

Our study shows that the recruitment of bone marrow-derived fibroblasts is important for promoting tumor growth, likely by enhancing blood vessel formation. Understanding the function of these cancer-associated fibroblasts could form the basis of developing novel therapeutic manipulations that cotarget bone marrow-derived fibroblasts as well as the cancer cells themselves."

Neta Eretz, Lead Author

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatment and many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

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Scientists uncover hidden estrogen receptors in epithelial breast cells

Estrogens are hormones that play central roles in the development and the physiology of the breast, but also are involved in breast cancer. Like all hormones, estrogens exert their biological effects by binding to dedicated receptors in the target cell.

Scientists led by Cathrin Brisken at EPFL have now uncovered that half of the luminal epithelial breast cells that appear not to express the estrogen receptor actually express it at low levels. Publishing in Nature Communications, they show that different parts of the estrogen receptor play different roles in the luminal breast cells that give rise to cancer. Depending on whether a cell has low or high levels of the estrogen receptor, the hormone-dependent or the hormone-independent activities are more or less important for its function.

In addition, the researchers found that the action of the estrogen receptor is biphasic: it stimulates the expansion and growth of breast cells in young mice but inhibits it during pregnancy.

The discovery has immediate implications for the role of ERα in the development of breast cancer. "This begs the question whether these ER-pseudo-negative breast cells will ultimately turn into estrogen receptor-positive or -negative breast cancers," says Cathrin Brisken.

We welcome researchers from different part of the to submit abstract on their latest research at our upcoming conference Cell Tissue Science 2019 which is mainly focuses on the complications the consequences of Stem Cell, Regenerative Medicine, Stem Cell Therapy, Cancer Cell Biology , Technical Advancements in cancer treatmentand many more.We welcome you to the our upcoming conference “ 12th World Congress on Cell & Tissue Science” . 

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