Hormone signalling and inflammation of fat influences breast cancer development

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breast cancer tumour_oncology news australiaNew research led by York University Professor Michael Connor highlights how fat cells could help determine the most effective way to fight breast cancer; including using exercise to combat the disease.

The research published in the Journal of Applied Physiology points to exercise – which has none of the harmful side-effects of many cancer drugs – as being a potentially beneficial therapy in some breast cancer patients.

This contributes to a growing body of evidence linking exercise to cancer outcomes.

Connor and his research team set out to determine whether the hormones, or adipokines, found in body fat can account for the observed association between obesity and breast cancer.

obese woman_oncology news australia“Our research has found that the characteristics of hormones produced by fat cells in obese people can promote breast cancer growth, whereas in lean people it prevents growth,” said Connor. “The characteristics of those hormones differ depending on whether the person is lean or obese and that determines whether the cancer grows or not.”

Using a rodent model, Connor and his team looked at whether the fat cells play a role in the link between obesity and breast cancer, and whether interventions targeted at obesity counteract any of the life-threatening effects of breast cancer.

“Our study shows that voluntary and rigorous exercise can counteract, and even completely prevent the effects on cancer growth that are caused by obesity. We also show that even moderate exercise can lead to slowing of breast cancer growth and that the more exercise you do, the greater the benefit.” said Connor.

For nearly a half century, researchers have studied the links between obesity and breast cancer.

exercise concept_oncology news australia_800x1200This recent study has revealed specifically that adiponectin and leptin are possible reasons for poorer response to therapy and higher risk of death in obese persons than in others.

Meanwhile, a second study published in the Journal of Cell Physiology describes how inflammation that characterizes fatty tissue is one of the main microenvironment actors responsible for promoting cancer.

The authors also describe the involvement of steroid hormones and others factors produced by adipose tissue in breast cancer development.

The authors belong to a multidisciplinary Italian-American-Tunisian team with a long and productive history of collaboration with Prof. Antonio Giordano, Director of the Sbarro Institute for Cancer Research, Temple University of Philadelphia, Pennsylvania, USA.

A novel approach was developed to analyze cell culture systems by professor Pietro Formisano from the University of Naples “Federico II” (NA, Italy), in order to study interactions between adipose tissue and tumors, and the molecular mechanism of insulin action.

The contribution of professor Angelina Di Carlo, University of Rome “La Sapienza” (Rome, Italy), was to underline the role of matrix metalloproteinases in obesity-related mechanisms of breast carcinogenesis.

The work by Professor Soumaya Kouidhi, of Manouba Thabet University (Aryanah,Tunisia), suggests that the small circulating RNA could be important in the diagnosis and prognosis of breast cancer.

Finally, professor Marina Di Domenico from the Second University of Naples (Italy) and PI of IRCCS “La salute della donna” of “Malzoni Clinic ” (AV, Italy), describes the “non genomic” actions of estrogen receptors in relation to breast cancer, with particular reference to the main roles of p85 / PI3K, in differentiation and cell migration.

This publication, resulting from an excellent exchange of worldwide knowledge, represents an important contribution in the studies of molecular mechanisms regulating breast cancer pathogenesis.

SourceJournal of Applied Physiology and Journal of Cell Phsyiology

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The ONA Editor curates oncology news, views and reviews from Australia and around the world for our readers. In aggregated content, original sources will be acknowledged in the article footer.

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