Dr. Alice Turdo winner of the fellowship “Fondazione Carlo Chianello 2016”

Italian and foreign scholars in the field of experimental clinical oncology and computer engineering were awarded on the 12th of December 2016, in the Sala Magna of the Monumental Complex of the Steri. The award ceremony was held for Italian and foreign scholars who distinguished themselves in the field of clinical and experimental oncology and in the disciplines of computer engineering.
The parchments to the winners of the prizes and scholarships were presented by the Rector of the University Fabrizio Micari who expressed great satisfaction with the role of the "Carlo Chianello" foundation in the development of cancer research. Alice Turdo has been declared winner of the "C.Chianello ” scholarship, which has been established to encourage young researchers and support research in the field of cancerology and oncology disciplines.

The dott. Simone Di Franco selected for the scholarship award “Fondazione Carlo Chianello 2018”

Simone Di Franco, PhD Research Fellow at the Laboratory of Cellular and Molecular Physiopathology at Di.Chir.On.S., was selected for the “Fondazione Carlo Chianello 2018” scholarship, awarded to the most deserving young researchers in the field of clinical and experimental oncology (Announcement of 08-10-2018, prot. n ° 75240). The research activity proposed by Dr. Di Franco will take place within the Laboratory of Cellular and Molecular Physiopathology, directed by Prof. Giorgio Stassi, and will address the theme of “the role of adipose tissue in the progression of colorectal cancer”.

A new collaboration has been established between the University of Palermo and the National Institutes of Health (NIH)

A new collaboration has been established between the Laboratory of Cellular and Molecular Oncology, headed by Prof. Giorgio Stassi, at the Department of Surgical, Oncological and Oral Sciences (DICHIRONS), University of Palermo and the National Institutes of Health (NIH), Bethesda, Maryland, USA. The strenght of this scientific collaboration between DICHIRONS and the NIH is confirmed by the following points:

  1. Published papers in collaboration with Dr. Ettore Appella, Chief of Chemical Immunology Section, Laboratory of Cell Biology, National Cancer Institute (NCI), and Dr. Carol J. Thiele, Deputy Director of Center for Cancer Research and Deputy Chief of the Pediatric Oncology Branch, at NIH.
  2. DICHIRONS is provided with a “Special Volunteer” agreement with the NIH in the years 2016-2018.
  3. Expertise in TP53, stem cell biology and molecular oncology fields is integrated in these two laboratories.

The outcome of the ongoing cooperation is a scientific project based on the role of TP53 in cancer stem cells freshly isolated from patients affected by colorectal cancer (CRC). This project is aimed to develop novel therapies as a precision medicine approach in the oncology field.

SPV Agreement

AIRC scholarship assigned to a young graduate

Turdo Alice

Dr Pier Giuseppe Torrani, President of the Italian Association for Cancer Research has announced the renewal, for the third consecutive year, of an AIRC scholarship for the year 2018 to Dr Alice Turdo. The Doctor carries out her research activity in the Cellular and Molecular Oncology Laboratory of the University of Palermo directed by Prof Giorgio Stassi, professor of “Surgical, Oncological and Stomatological Disciplines”.

“It is a great pride for me to be able to carry out this research activity at our University – says Alice Turdo – who is giving me the opportunity to deepen our study in oncology, which is a research field of great interest for public health”.

The Rector Fabrizio Micari congratulated the new scholarship holder. “Having known about the important award that was once again conferred – states the rector – I formulate my best wishes for the excellent result achieved”.

Source Unipa.it

Breast cancer: IL-4 identikit, the molecule that promotes metastasis

An all-Italian study shows that interleukin-4 produced by tumor cells and cells in the surrounding microenvironment favors the progression of breast cancer, paving the way for new therapeutic developments.

In oncological research it can happen that some results, in addition to being relevant in themselves, open the way to new lines of investigation that help to clarify the biology of the tumor. The group of Prof Matilde Todaro of the University of Palermo, has observed that several tumors are characterized by high concentrations of a molecule of the immune system called interleukin-4 (IL-4). The observation is the basis of a recent study that showed how, in breast cancer, IL-4 is essential for the development of metastases and resistance to anti-cancer therapies.

First, the researchers found higher concentrations of IL-4 in triple negative breast tumors, which are more aggressive and tend to give metastases. A long series of experiments in isolated cells and with laboratory animals has allowed to define the molecular mechanisms that lead this molecule to promote tumor progression. “IL-4 – explains Todaro – works by activating the transcription factor NF-kB, which in turn inhibits the DUSP-4 molecule”. In practice all this translates into a “push” favorable to the tumor. To confirm their hypothesis, the researchers conducted other experiments with laboratory animals, demonstrating that if the concentration of DUSP-4 is lowered it is possible to transform non-metastatic tumors into metastatic tumors and vice versa.

These results, obtained thanks to the fundamental support of AIRC and published in the journal Cancer Research, are significant for two reasons. Firstly, they underline once again the importance of the microenvironment for the progression of the tumor. “The IL-4 is in fact produced both by the tumor cells and by the cells present in the tumor microenvironment, for example by the cells of the adipose tissue. This discovery, therefore, reinforces the link already known between obesity and breast cancer, “explains Todaro. Secondly, it opens up a new therapeutic perspective. “There are already NF-kB inhibitors that could be tested in breast tumors that have elevated IL-4 concentrations: this could be the case if the risk of metastasis is reduced”.

Source Airc.it

Here is the key that triggers colon cancer metastasis

The fibroblasts of healthy connective tissue around the tumor push cancer stem cells to spread the disease at a distance. Once the mechanism has been discovered a possible system has also been identified to neutralize it

As long as the tumor cells proliferate in their initial location, they hardly put the patient’s life at risk. The problem are distant metastases to be countered if a cure for cancer is to be made. This is why many research groups all over the world are committed to understanding the mechanisms that allow cells to break away from the tumor and reproduce it in other parts of the body. Understanding the phenomenon will perhaps be possible to find ways to inhibit it. An important result recently published in the Cell Stem Cell magazine was obtained by Ruggero De Maria, the scientific director of the Regina Elena Cancer Institute of Rome, as part of the AIRC program of molecular clinical oncology. De Maria’s group has discovered a molecule that has a difficult name to remember, CD44v6, but a role that is easy to understand: the CD44v6 molecule is responsible for the ability of cancer stem cells to migrate from the intestine and implant into other organs, giving place of relapse and metastasis and thus aggravating the prognosis of the disease; but the CD44v6 is also a kind of label that is on the surface of these cells and allows its presence to recognize them from the others.

“On the surface of stem cells of more aggressive colon tumors, which will give rise to metastasis, this molecule abounds, which is expressed only in very small quantities in primitive tumors” explains Giorgio Stassi, from the University of Palermo, who coordinated the work . “The paradox is that increasing the production of CD44v6, which then determines a negative turn of the disease, is not the tumor, but a series of substances, called cytokines, which are produced by the healthy cells of the surrounding connective”.

The research goes further: “We have also identified an enzyme, phosphatidylinositol 3-kinase (PI3K), which is the Achilles’ heel of these cells and which can be blocked to prevent the formation of metastases”. Laboratory observation was also confirmed in the study with patients: those whose cells expressed the lowest CD44v6 levels survived longer.

Source Airc.it

p63, the protein that causes breast cancer to spread

A new mechanism has been discovered that can make breast cancer metastatic. At the center there is a variant of the p63 protein whose presence is in turn closely linked to the characteristics of the tumor microenvironment.

To make a tumor dangerous is usually its ability to form metastases, that is to invade tissues and organs far from their place of origin. This is why it is important to understand the molecular mechanisms that guide its diffusion in the organism. In the case of breast cancer, one more step in this direction was made by the research group of Prof Matilde Todaro of the University of Palermo. Thanks to a study conducted with the irreplaceable funding of AIRC, Todaro and colleagues have described the fundamental role of a particular variant of p63 protein in making malignant cells, and therefore able to metastasize, breast cancer cells.

“It all started with the observation that different variants of the p63 protein (and relative RNA) are expressed in metastatic and non-metastatic tumor cells”, explains the researcher. “More precisely, we realized that metastatic tumor cells had a greater abundance than a particular variant of p63 called DeltaNp63. Conversely, the cells in which another variant was more abundant – TAp63 – were less invasive “.

The next step was to try to understand the reasons for the abundance of DeltaNp63 in the most malignant cells. The experiments conducted, described in the pages of Oncotarget, show that the game is the tumor microenvironment, e.g. the set of cells and substances in which the tumor is immersed. It is precisely the particular molecules present in this environment that drive the higher expression of DeltaNp63 to the detriment of TAp63.

The researchers also found that DeltaNp63 increases the expression of PI3K and CD44v6, two molecules already known for their involvement in the proliferative and metastatic capacity of colon cancer cells. DeltaNp63 is therefore upstream of a molecular cascade that increases tumor malignancy. “In practice – Todaro makes clear – this molecule does nothing but activate a very convenient path for the tumor itself”. The good news is that there are already inhibitors of these molecules and Todaro and colleagues have shown their effectiveness, in isolated cells and with laboratory animals, in blocking the proliferation and spreading capacity of tumor cells with DeltaNp63 variant. An observation that opens up to the possible development of new therapeutic strategies.

Source Airc.it