Posts Tagged ‘diagnostic’

Minimally invasive, high-performance intervention for staging lung cancer

Endoscopic biopsy of the lymph nodes is a minimally invasive, non-surgical intervention that has recently begun to be used to stage lung cancer. The study conducted by Dr. Liberman’s team involved 166 patients with confirmed or suspected non small cell lung cancer, and was designed to compare the new approach to surgical staging under general anesthesia, as prescribed in current guidelines for this type of cancer. The findings, which were recently published in CHEST Journal, the official publication of the American College of Chest Physicians, show that the endoscopy approach is not only sensitive and accurate, but also leads to improved staging compared to surgical staging due to its ability to biopsy lymph nodes and metastases not attainable with surgical techniques.

Research protocol

All patients underwent endobronchial ultrasound (EBUS), endoscopic ultrasound (EUS) and surgical mediastinal staging (SMS) during a single procedure. Each subject served as his or her own control. The results of the EBUS, EUS and combined EBUS/EUS were compared to SMS (gold standard) results and, in patients with negative lymph node staging, to lymph node sampling at pulmonary resection.

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Carcinogenic role of protein in liver decoded

The EGF Receptor (Epidermal Growth Factor Receptor, EGFR) is a protein which, as a transmembrane receptor, controls a multitude of vital processes in the cell. In human beings, the EGF Receptor is present in many cells types and plays an important role in many types of cancer. It is present in various kinds of tumors in excessive amounts and/or in mutated form, which causes the tumor cells to grow and multiply. For this reason the EGFR serves as a point of attack in many treatment strategies. In the process, its function is inhibited with the objective of slowing down the growth of the tumor cell.

The liver cell carcinoma (hepatocellular carcinoma, short HCC) is one of the most frequent malignant tumors worldwide. Approximately six percent of all cancers in men and about three percent in women are liver cell carcinomas. It is the second most frequent cause of death associated with cancer. Risk factors for HCC include liver diseases through Hepatitis B and C infections as well as alcohol abuse or the classic “fatty liver.”

Up to now, the tumor-promoting role of EGFR has only been linked with its expression directly in the tumor cells. However, the study group of Maria Sibilia, Manager of the Institute for Cancer Research at the Medical University of Vienna and Deputy Manager of the Comprehensive Cancer Centre, in cooperation with the research groups of Michael Trauner and Markus Peck-Radosavljevic at the clinical division for gastroenterology and hepatology (Manager: Michael Trauner) as well as the Eastern Hepatobiliary Surgery Institute/Hospital in Shanghai discovered that EGFR plays a more decisive role in the macrophages of the liver (these are important cells of the immune system which are called Kupffer cells in the liver) with respect to the growth of the liver cell carcinoma than previously assumed.

“In this study we were able to prove that the inhibition of EGFR has a tumor inhibiting effect on the macrophages and not its inhibition on the tumor cell itself,” explains Maria Sibilia. However, if the EGFR conversely exists on these macrophages in an excessive number, it can promote the growth of the tumor. Its existence on the macrophages reduces the chance of survival for HCC patients.

This could explain why EGFR inhibitors utilised for cancer treatment and aiming directly for the tumor cells have achieved clinically disappointing results in the fight against the liver cell carcinoma in the past. For the first time, this study proves the tumor-promoting mechanism for EGFR in non-tumor cells, which could lead to more effective and precise treatment strategies with macrophages as a point of approach in the future.

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Promising new cancer therapy uses molecular ‘Trash Man’ to exploit a common cancer defense

Cancer therapies cause unwanted proteins to accumulate in cancer cells, which can trigger a form of cell suicide known as apoptosis. To survive, the cells break down the excess proteins through autophagy, from a Greek term meaning “self eating.” In a study recently published in the journal Molecular and Cellular Biology, scientists induced autophagy using the anti-tumor drug obatoclax while simultaneously blocking the production of p62 using a drug known as a cyclin-dependant kinase (CDK) inhibitor. Several experiments involving animal models and cultured multiple myeloma cells demonstrated that blocking p62 disrupted autophagy and killed far more cancer cells than administering the anti-cancer agents alone.

“Therapies that are designed to block the early stages of autophagy do not offer the possibility of exploiting its potentially lethal effects,” says Steven Grant, M.D., Shirley Carter Olsson and Sture Gordon Olsson Chair in Cancer Research, associate director for translational research and program co-leader of Developmental Therapeutics at VCU Massey Cancer Center. “Our strategy turns autophagy from a protective process into a toxic one, and these results suggest it could increase the effectiveness of a variety of cancer therapies that induce autophagy.”

Critical to the success of this therapy is Bik, a protein that plays a significant role in governing cell death and survival. During cancer treatments, Bik accumulates in cancer cells until it triggers apoptosis. Normally, the cancer cells would induce autophagy and p62 would rid the cells of Bik by loading the proteins into degradation chambers known as auotophagosomes for disposal. However, blocking p62 production results in an inefficient form of autophagy and the accumulation of Bik eventually causes the cancer cells to undergo apoptosis.

This research builds upon more than a decade of work by members of Grant’s laboratory investigating novel treatment strategies and combination therapies that selectively kill multiple myeloma and other blood cancer cells. The technology in his study has been made available for licensing through the VCU Office of Research.

“We are now working to identify additional CDK inhibitors that can be used to disrupt autophagy,” says Grant. “The ultimate goal will be to translate these findings into a clinical trial to test the therapy in patients with various blood cancers.”

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