Antonio Giordano, who led the study that showed whole tomato extracts can slow the growth of stomach cancer, says Italian cuisine inspired him to investigate the dietary staple’s cancer-fighting ability.
Retinoblastoma family, Rb2 gene, tumor suppressor gene, senescence, mesenchymal stem cells
The mouse is the most widely used model organism to understand human genetics, biology, and diseases in the research setting. Aspects of gene function in humans can be predicted by studies of the corresponding gene in mice, but new research findings have revealed important divergences between the species which scientists will need to understand better through further investigation.
The research group that made this discovery was lead by Professor Umberto Galderisi at the Department of Experimental Medicine, Campania University “Luigi Vanvitelli” in Naples, Italy, and Antonio Giordano at the Sbarro Institute for Molecular Medicine department of Biology at Temple University in Philadelphia. Their paper, “Misidentified Human Gene Functions with Mouse Models: The Case of the Retinoblastoma Gene Family in Senescence” by Nicola Alessio et al., has been published in the journal Neoplasia.
These differences can have a significant impact on the efficacy of research findings to infer gene function in humans by means of the so-called knock-out, or in situexperiments carried out in mouse models. In their paper, the authors describe how the retinoblastoma gene family may represent an illustrative example of this possible gene divergence between humans and mice. This gene family comprises three members (RB1, RB2/P130, and P107), which regulate several aspects of cell life, such as cell cycle, apoptosis, senescence, and differentiation.
Researchers analyzed differences in functions between mice and humans in this gene family that cannot be overlooked, if scientists are to be able to interpret mouse model experiments for purposes of diagnosis and treatment of human diseases.
“We decided to investigate the role of retinoblastoma gene family members in the regulation of the senescence process,” says Galderisi. “Senescence, or cellular aging, is the deterioration of activities that can occur in the cells. This process may have either anti- or pro-cancer functions, depending on context. For this reason, studying molecular mechanisms governing senescence is of great importance for human diseases,” Gladerisi says.
“Our interest resides on the fact that, in human mesenchymal stromal cells (MSCs), the acute silencing of RB1 did not induce unrestricted proliferation as had been described mouse model studies,” says Giordano, “but, rather, resulted in cell cycle arrest and cellular senescence.” In other words, the effect of silencing the RB1 gene had the opposite effect in the mouse model versus human, indicating that the well-known RB1-P16 axis involved in senescence may not have a general role.
The authors believe their study demonstrates that the function of a protein has many aspects that are context-dependent, such as species and cell type.
These findings could be useful as a general paradigm for caution when inferring the role of a gene in humans, based on animal studies. Furthermore, human MSCs are being studied in several ongoing clinical trials, and the drivers of senescence described in this study should be thoroughly understood in order to maintain strict control for their safe and effective use in research.
Newswise — Neurodegenerative disorders such as Alzheimer’s Disease, Parkinson’s Disease, amyotrophic lateral sclerosis (ALS), and Huntington’s Disease are typically characterized by progressive apoptotic death of neurons. Apoptosis, or programmed cell death, in these neurodegenerative disorders is believed to be triggered by a process of cell cycle reactivation, however, the mechanisms involved in this phenomenon remain largely unsolved. Researchers studying the role of inflammation as well as the expression of Rb family proteins (RB1/p105, RBL1/p107 and Rb2/p130) in neuronal death, have discovered a clue to the mechanism for neuronal degeneration and possible target for a therapeutic approach to these disorders.
The research was conducted by a team of scientists lead by Dr. Antonio Giordano, Director of the Sbarro Institute for Cancer Research and Department of Biology at Temple University, Philadelphia in collaboration with University of Siena Italy. Their study was published online on August 2017, in the international journal Cell Cycle. The study was funded in part by a grant from the Ken and Ann Douglas Charitable Foundation.
These findings are significant because mature neuronal cells are in a permanent state of cell cycle arrest, and they do not undergo the same process of cell death and replacement as other tissues throughout the body. Shedding light on the cause for the neurodegeneration occurring in diseases like Alzheimer’s and Parkinson’s, the study authors found that inflammation induced cell cycle re-entry, causing neurons to resume the cell cycle and undergo apoptotic cell death.
The study was performed in an in vitro model of brain inflammation, which revealed an aberrant expression of p107 and p105 following the inflammatory insult, leading researchers to conclude a possible implication of these factors in the reactivation of the cell cycle in neurons.
The pRB family is comprised of factors well known for their ability to regulate the cell cycle, and has been largely explored in cancers for their role as tumor suppressors.
Dr. Giordano’s team provides novel information on the pleiotropic activity of pRB proteins extending the investigation to fields outside of oncology. The concept emerging from their study could help in formulating innovative therapeutic approaches to halt neurodegenerative processes like Alzheimer’s Disease.
“Alzheimer’s Disease, similar to other neurodegenerative diseases, is an incurables disorder affecting populations worldwide,” Dr. Giordano says. “However, in recent years, scientists have made great advances in uncovering the cause of these pathologies. As we discover novel elements correlated to the pathways involved in these diseases, we are confident that we will be able to treat and prevent them. Albeit it is still at an early stage, our study brings to light an important aspect of this mechanism that will speed our progress toward this common goal,” Dr. Giordano concludes.
In frail patients with cancer who are to undergo contrast-enhanced CT, the choice of iodated contrast medium can be key to reducing risk for impaired renal function and the development of contrast-induced nephropathy (CIN).
In a head-to-head comparison of two contrast media, iodixanol (Visipaque, GE Healthcare) appeared to have a better safety profile than iopromide (Ultravist, Bayer Healthcare).
The results come from the blinded, randomized COMEDIANS trial, which was conducted in 504 cancer patients at low risk for CIN who underwent chest-abdomen-pelvic CT. The trial was conducted by Maddalena Barba, MD, of the Regina Elena National Cancer Institute in Rome, Italy, and colleagues.
The study was published online August 4 in the Journal of Cellular Physiology.
Currently, there is no evidence to support the use of a specific contrast medium in cancer patients, the study authors note. They point out that CT is one of the imaging techniques most frequently used in cancer management, from diagnosis and disease staging to evaluation of treatment response and follow-up.
Although CIN can be minor ― defined by the study investigators as a 25% increase in serum creatinine level ― more severe cases can lead to renal failure, the need for dialysis, or death. Patients with cancer who are weakened by disease or treatment may be particularly vulnerable.
“It is our responsibility to focus on the safety of fragile patients, such as those affected by cancer,” coauthor Irene Terrenato, PhD, of the Regina Elena National Cancer Institute in Rome, said in a statement. “Iodated contrast media is essential, and, unfortunately, we often observe adverse events on renal function due to contrast media use, such as CIN.”
“To understand which one [contrast medium] minimizes the incidence of CIN is fundamental, and this study arises from the need to protect our patients as much as possible,” added Stefano Canitano, MD, who is also at the Regina Elena National Cancer Institute.
Cancer Patients Develop CIN
The cancer patients taking part in this study were at low risk of developing neuropathy. At baseline, the patients’ estimated glomerular filtration rate (eGFR) was >60 mL/min.
The researchers report that CIN developed at 24 hours in seven patients in the iopromide group compared to two patients in the iodixanol group (P = 0.34).
The same trend was seen with late-occurrence events, with eight patients in the iopromide group developing CIN at 72 hours compared to two in the iodixanol group (P = .11).
Overall, 17 patients developed CIN. Among those patients, the event rate was higher in the iopromide arm (P = .045), although no cases of permanent CIN or significant differences in adverse events or GFR were observed.
“The distribution of CIN events across the study arms seemed to provide a suggestion in support of the use of iodixanol in light of the more favourable toxicity profile,” the study authors say. “However,” they add, “none of these results reached the predefined cut off for statistical significance.” These findings need to be confirmed and the underlying biological mechanisms clarified in larger trials with a similar design, they emphasize.
“Our results can represent a first indication for radiologists who are responsible for performing CT scans on very compromised patients daily,” commented coauthor Antonio Giordano, MD, PhD, from the University of Siena and Istituto Toscano Tumori, in Siena, Italy, who is also the president of the Sbarro Institute for Cancer Research and Molecular Medicine, Temple University, in Philadelphia, Pennsylvania.
He emphasized that “further studies are strongly recommended to confirm these results.”
Specifically, biomarkers associated with increased risk for CIN need to be identified, Dr Giordano told Medscape Medical News. He noted that “sera from the participants in the COMEDIANS trial are stored at our biorepository.”
Importantly, these results are consistent with those from previously published randomized controlled trials demonstrating less patient discomfort, lower frequency of adverse events, and equivalent or higher CT image quality with iodixanol compared with low-osmolar contrast media, Dr Giordano said.
The study enrolled patients from four cancer enters who were to undergo a chest-abdomen-pelvis CT with iodated contrast media. A total of 247 patients were centrally randomly allocated to receive iodixanol; 250 patients received iopromide. Although patients and nurses were blinded to group assignment, the pharmacologist, radiologists, technicians, and statisticians were not.
CIN was defined as a decrease of baseline eGFR of >25%. Serum creatinine was used to assess CIN development in addition to eGFR.
The study design, with its focus on cancer patients at very low risk of developing CIN, “renders our findings worthy of attention,” the study authors say. Previous studies have been largely observational and have varied in size, design, and patient characteristics, they note.
Limitations of the study include its low power and failure to reach the recruitment target of 2868 patients, the study authors acknowledge.
This study was funded by the Italian Agency of Drugs. GE Healthcare provided educational support to the biostatistical and methodologic core of the research group.
Researchers analyzed data confirming the improved outcomes in both short- and long-term survival in patients that underwent neoadjuvant chemotherapy prior to surgery for triple-negative breast cancer. The study included 213 patients at 8 Italian cancer centers whose diagnoses were characterized by clinical, molecular, and therapeutic features of triple-negative breast cancer, an aggressive form of cancer with limited treatment options.
The study, “Neoadjuvant chemotherapy in triple-negative breast cancer: Multicentric retrospective observational study in real-life setting,” was recently published in the Journal of Cellular Physiology, an international, peer-reviewed journal focused on cancer-related issues. The study is authored by a multidisciplinary Italian-American team of scientists who have a long and productive history of collaboration with Prof. Antonio Giordano, Director of the Sbarro Institute for Cancer Research and Department of Biology at Temple University.
“Triple-negative breast cancers account for about 10-15% of breast cancer cases. Their aggressive behavior is well exemplified by the large tumor volume at presentation, along with the quite frequent involvement of regional lymph nodes, and high histological grade,” says co-author Dr. Maddalena Barba, researcher at the IRCCS Regina Elena National Cancer Institute of Rome, Central Italy.
“Currently, there are no approved targeted therapies for triple-negative breast cancers and chemotherapy remains the mainstay of treatment. When compared with other and more frequent breast cancer subtypes, these tumors show higher chemosensitivity, especially when chemotherapy is administered prior to surgery,” adds co-author Dr. Patrizia Vici, clinical researcher at the division of Medical Oncology 2 of the IRCCS Regina Elena National Cancer Institute.
“Results from our study confirmed previous findings from randomized clinical trials on the advantage conferred by more than 6 six cycles of a well characterized regimen of neoadjuvant chemotherapy, that is, the sequential antracycline-taxane regimen,” explains Prof. Antonio Giordano. “In addition, we confirmed the predictive role of some features related to the disease and its potential spread, namely Ki-67 absolute value and its relative measures, on treatment outcomes. Our work on triple negative breast cancer is thus confirmative in nature.
“But, what I would strongly underline, is the need for this sort of confirmative evidence to implement the scientific knowledge stemming from large, well designed and absolutely needed randomized clinical trials. Indeed, breast cancer patients who participate in these trials are selected on the basis of well codified demographic, clinical, and molecular characteristics, which do not necessarily reflect those of patients from the real-world setting who represent the final recipients of our gains in cancer-related knowledge.” concludes Dr. Giordano, a scientist with widely recognized expertise in cancer with a specific focus on translational research.
Philadelphia, PA (Scicasts) – A new study of non-diabetic women with ovarian cancer reveals a potential correlation and area for further study regarding the expression of the GLUT1 glucose transporter receptor at the cancer tissue level.
GLUT1 is a receptor protein involved in the absorption of glucose, or sugar, in the bloodstream and across membranes in the body. Physiologically, GLUT1 is not traceable in the ovaries. However, in patients diagnosed with ovarian cancer, use of immunohistochemical methods revealed the presence of this receptor, which tends to be intensely expressed in the most aggressive cases.
The study, titled, “GLUT1 receptor expression and circulating levels of fasting glucose in high grade serous ovarian cancer,” appeared recently in the journal entitled Journal of Cell Physiology, an international, peer reviewed journal focused on cancer-related issues. The authors belong to a multidisciplinary Italian-American team, which has long collaborated with Prof. Antonio Giordano, Director of the Sbarro Institute for Cancer Research and Molecular Medicine at Temple University in Philadelphia.
“Ovarian cancer is the leading cause of death among gynecological cancers. Despite remarkable achievements in terms of diagnoses and therapeutics, patient outcomes in terms of survival rates have remained largely unchanged. This is largely due to our limited understanding of the underlying mechanisms and pathways,” says Dr. Maddalena Barba, researcher at the IRCCS Regina Elena National Cancer Institute of Rome, Central Italy.
“This study revealed a higher expression of the glucose transporter 1 in cancer samples of patients with lower glucose levels in non-diabetic women. These findings provide evidence in support of our prior results from this same study population. Indeed, we have recently observed an association between cancer stage at diagnosis and circulating levels of fasting glucose,” explains Dr. Vici, clinical researcher at the division of Medical Oncology 2 of the IRCCS Regina Elena National Cancer Institute.
The study included 40 randomly selected patients from a larger cohort of 147 women diagnosed with high-grade, advanced stage ovarian cancer.
“The findings from the immunohistochemical assessment of this population are key to understanding a variety of factors and determinants related to glucose metabolism in ovarian cancer. In addition, our findings establish a link between fasting glucose, and the expression of the glucose transporter GLUT1.
“We thus provide support to the hypothesis stated in our prior work within this same pipeline and, at the same time, ascertain the existence of a relation between a systemic and a local tissue biomarker related to energy metabolism. If confirmed in future studies, this may translate into the identification and characterization of innovative drug targets in ovarian cancer patients,” concludes Prof. Antonio Giordano, a scientist with widely recognized expertise in cancer with a specific focus on translational research.
A new study shows that whole tomato extracts from two different Southern Italy cultivars inhibit gastric cancer cell growth and malignant features, paving the way for future studies aimed at implementing lifestyle habits not only for prevention, but potentially as a support to conventional therapies.
“Their antitumoral effect seem not related to specific components, such as lycopene, but rather suggest that tomatoes should be considered in their entirety,” says Daniela Barone, researcher at the Oncology Research Center of Mercogliano (CROM), and one of the authors of the study.
Experiments analyzed whole tomato lipophilic extracts for their ability to tackle various neoplastic features of gastric cancer cell lines. Extracts of both the San Marzano and Corbarino tomato varieties were able to inhibit the growth and cloning behavior of malignant cells. Treatment with the whole tomato extracts affected key processes within the cells hindering their migration ability, arresting cell cycle through the modulation of retinoblastoma family proteins and specific cell cycle inhibitors, and ultimately inducing cancer cell death through apoptosis.
The study, published in theJournal of Cellular Physiology, details findings by Daniela Barone and Letizia Cito, from the research group at the National Cancer Institute of Naples, Pascale Foundation-CROM, coordinated by Prof. Antonio Giordano from the Sbarro Institute, College of Science and Technology at Temple University.
“Our results prompt further assessment of the potential use of specific nutrients not only in the cancer prevention setting but also as a supportive strategy along with conventional therapies,” says Prof. Antonio Giordano, Director of the Sbarro Institute for Cancer Research and Molecular Medicine, College of Science and Technology, Temple University.
“Distinct species may exert different effects, in different stages of a certain neoplasm,” adds Barone.
Gastric cancer is the fourth most common type of cancer worldwide and has been associated with genetic causes, Helicobacter pylori infection, and eating habits, such as consumption of smoked and salted food.
Tomatoes are consumed worldwide and are a staple of the Mediterranean diet, which is popularly thought to lower cancer risk. Various tomato components have also been analyzed for their ability to counteract tumor growth in experimental systems, although few studies have analyzed the effects of tomatoes in their entirety.
The study authors worked in collaboration with researchers from Prof. Barbara Nicolaus‘ group and Dr Rocco De Prisco at the National Research Council of Pozzuoli, Italy.
“This work stems from the SHRO research programme performed through a longstanding collaboration with the Department of Medicine, Surgery and Neuroscience, University of Siena, and the Pascale Institute, CROM of Mercogliano. On the wake of these results Dr Attilio Bianchi, General Director of the Pascale Institute and CROM, and I teamed up to renew the collaboration with SHRO implementing the nutrigenomics studies for the benefit of cancer patients,” concludes Giordano.
Cancer expert Antonio Giordano, MD, PhD, Director of the Sbarro Institute for Cancer Research and Molecular Medicine at Temple University, describes the recent progress and future possibilities of treating SCLC. Giordano was recently quoted in the Italian news outlet Il Mattino
Newswise — Small cell lung cancer (SCLC) is an aggressive disease characterized by quick growth and spread. While there has been a gradual decrease in incidence of SCLC in recent years, likely reflecting the decreased prevalence of tobacco use, little progress has been made in treating SCLC due to its complex pathogenesis.
The majority of patients, including those with limited-stage disease and those who initially respond to chemo- and radiation- therapy (two traditional pillars of cancer therapy), become resistant to treatment resulting in a very small percentage (approximately 6%) who survive 5 years after being diagnosed.
Smoking is the main risk factor for SCLC, with only 2-3% of patients categorized as never-smokers.
Identifying Therapeutic Targets in Small-Cell Lung Cancer
From the molecular point of view, SCLC is characterized by a multitude of alterations, owing to the fact that cells are exposed to a myriad of carcinogens contained in cigarette smoke, which bind and mutate DNA. These alterations affect numerous genes and pathways, but among these there are few obvious therapeutic targets. This means that the driver genes responsible for most SCLC development and progression have yet to be identified with any certainty.
However, new high-throughput technologies, which allow comprehensive gene profiling, have revealed promising findings. For example, 20% of SCLC patient tumors bear alterations in the MYC gene family. This discovery has helped to identify a subset of patients sensitive to an oncogenic kinase downstream in the MYC pathway, allowing for better designed, biomarker-driven clinical trials for these, often repurposed, therapeutic agents.
Similarly, PARP1 and Notch have been found overexpressed in SCLC. In order to target PARP1, an enzyme which, when it malfunctions, leads to replication of damaged DNA, researchers are currently evaluating the efficacy of PARP inhibitors for treatment of SCLC. And, to investigate targeting of the Notch signaling pathway, which influences the cellular life-cycle, the FDA is in the process of approving Tarextumab, a selective Notch inhibitor, in the treatment of SCLC.
Another issue with SCLC tumors is that they are mostly characterized by the loss of two crucial oncosuppressor genes, named RB, RB2\p130 i and TP53, which are less actionable pharmaceutically because it is much more difficult to restore a loss of function rather than block an oncogenic gain of function. Although challenging, researchers are nonetheless trying to develop strategies in this direction.
Repurposing Existing Drugs
Also important to the progress of SCLC therapies, more effective drug identification and testing, through the use of powerful mouse models of the human disease, put researchers in a good position to tackle this cancer type and attempt better defined targeted approaches.
Recent immunotherapy approaches have emerged as a significant new pillar in cancer therapy and are being assessed in numerous clinical trials for a multitude of tumors, including SCLC. In particular, two new agents, nivolumab and ipilimumab, have recently been developed to treat other forms of cancer, such as unresectable or metastatic malignant melanoma, advanced non-small-cell lung cancer (NSCLC), and advanced renal-cell carcinoma. These agents have also been tested for applications in SCLC. Nivolumab and ipilimumab are constituted by monoclonal antibodies functioning through direct inhibition of CTLA4 and PD1, respectively, which are key negative regulators of the antitumoral immune function. Bristol-Myers Squibb (BMS) was able to obtain the National Comprehensive Cancer Network indication for use of nivolumab and nivolumab plus ipilimumab in patients with SCLC who progressed after one or more previous regimens. The indication was achieved upon the publication on Lancet Oncology by Scott Antonia and colleagues, who reported the efficacy of nivolumab monotherapy and nivolumab plus ipilimumab, achieving antitumour activity with durable responses and manageable safety profiles in previously treated SCLC patients, enrolled in the CheckMate-032 clinical trial.
Data was also presented at the World Lung Cancer Congress on the immunotherapy drug pembrolizumab, another therapeutic antibody against PD1, already approved for other diseases, which showed good efficacy.
One additional drug in this category is rovalptizumab teserine, a first-in-class antibody-drug conjugate comprised of a humanized monoclonal antibody against DLL3 and a toxin. DLL3 is a Notch ligand found to be expressed on 80% of SCLC. There is a 3rd line trial which is biomarker driven, meaning that they test for DLL3 expression and patients are eligible if they have “high” DLL3.
In conclusion, with careful evaluation, a doctor can use immunotherapy as a second phase or combination therapy, but many factors should be considered. For example, the issue of whether a patient should have some time to recover after a course of chemotherapy before starting immunotherapy is still debated among colleagues. Also, some combinations, such as nivolumab plus ipilimumab, seem to work better but can be more toxic.
About the Expert
Antonio Giordano, MD, PhD, Director of the Sbarro Institute for Cancer Research and Molecular Medicine and Center of Biotechnology, College of Science and Technology, Temple University and Professor of Pathology at the University of Siena, Italy
About Sbarro Health Research Organization
Sbarro Health Research Organization conducts research in cancer, diabetes, and cardiovascular disease. Based in Philadelphia, Pennsylvania on the campus of Temple University, our programs train young scientists from around the globe.
Dr. Giordano is joined on the board by Corporation for Public Broadcasting President and CEO Patricia de Stacy Harrison and former Talk America President, Chairman and CEO Gabriel A. Battista who will serve as co-chairperson of the Foundation
The National Italian American Foundation (NIAF) met this week to elect its Board of Directors for the 2017-2021 term. Board members for the new term will include re-elected member Antonio Giordano, president and founder of the Sbarro Health Research Organization (SHRO) at Temple University in Philadelphia, who has served on the Board since 2011.
“It has been an honor working with NIAF,” says Dr. Giordano, “especially in creating our annual medical research conference highlighting the contribution of Italian-Americans to science.” The conference, a collaboration of the NIAF and SHRO, is held each October, and includes the presentation of the annual Giovan Giacomo Giordano NIAF Lifetime Achievement Award for Ethics and Creativity in Medical Research.
Giordano serves with newly elected co-Chairpersons Patricia de Stacy Harrison, president and ceo of the Corporation for Public Broadcasting, and Gabriel A. Battista, former president, chairman, and CEO of Talk America.
“Certainly our new co-Chairs have some big shoes to fill, but I’m very excited for the opportunity to work with two of the most dedicated Italian Americans I’ve come to know during my time at the Foundation. Pat and Gabe have been tireless advocates for our community for so many years and I really look forward to the next phase of the NIAF story under their leadership,” said NIAF President and COO John M. Viola.
Giordano is proud to serve on the NIAF Board of Directors, continuing a lifelong mission of service to the Italian-American community. The Sbarro Health Research Organization began with a mission to foster international research collaboration with Italian and American scientists.
“I look forward to promoting the work of NIAF among my colleagues at the top Italian and American universities, to make our mission known among the next generation of Italian-American scientists,” says Dr. Giordano.
The NIAF Board of Directors includes other Italian-Americans from a wide variety of fields in the public and private sector, including a former Major League Baseball player; an executive vice president at the Wildlife Conservation Society; a venture capitalist; and an executive in higher education. More information about the NIAF and the newly elected Board of Directors can be found at www.niaf.org.
About the National Italian American Foundation
The National Italian American Foundation (NIAF) is a non-profit, non-partisan organization dedicated to preserving, promoting and protecting the Italian American heritage and culture. To learn more about the Foundation and become a member, please visit www.niaf.org.
About the Sbarro Health Research Organization
The Sbarro Health Research Organization (SHRO) is non-profit charity committed to funding excellence in basic genetic research to cure and diagnose cancer, cardiovascular diseases, diabetes and other chronic illnesses and to foster the training of young doctors in a spirit of professionalism and humanism. To learn more about the SHRO please visit www.shro.org
The most recent global cancer data from the WHO highlights the growing differences in mortality rate among regions of the world bearing very different economic circumstances. Given that cancer has been globally responsible for the death of 8.8 million individuals in 2015 and that the number of new cases is expected to rise by about 70% over the next two decades, these new figures are cause for concern looking at the rise of Cancer among economically weak regions.
In fact, according to the most recent reports, about 70% of deaths from cancer occur in low and middle-income countries. Furthermore, only 35% of low income countries carry pathology services generally available to the public sector while treatment services are available in less than 30% of low income countries as compared to 90% of high income countries.
“It is not surprising that only one in five of these low- and middle-income countries have the necessary data to drive cancer policies and health interventions,” comments Prof. Antonio Giordano, Director of Sbarro Health Research Organization, a cancer and biomedical research institute based in Philadelphia.
“This problem,” adds prof. Giordano, “is a major driver for the expected increase of cancer cases and deaths, especially among children and children-bearing women in these countries also due to the higher risk connected to specific infective agents for which there are no widespread prevention programs as well as limited access for women and children to what we now consider basic care in other parts of the world.”
“The Limited access to sustainable diagnosis and treatment in economically weak regions disclosed by these reports,” states prof. Pierluigi Scalia, director of ISOPROG Onlus, an Italian non profit research organization, “is not only restricted to third world countries, but it is likely to be witnessed within countries with higher income when comparing different regions of the same country.” “For example,” says prof. Scalia, “we could expect the same trend due to lack of access to basic sustainable care when comparing large cities to the peripheries such it can be seen throughout the US and as it is still a problem in countries like Italy between the northern and the southern regions. In all these cases, the incidence of cancer in children and economically weak part of our society is expected to rise.”
“Research as well as new social entrepreneurial models to manage healthcare,” concludes prof. Giordano, “are desperately needed to face this growing problem.”