Latest Research Offerings on Novel Treatment Options For Various Cancers

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Highlights:

• The Experimental Biology conference provides a unique platform for scientists across the United States to present the latest and game changing treatments and concepts for various cancers
• Cancer is one of the leading causes of mortality globally and scientists are constantly striving to create better and more effective cancer treatments and prevention.

The Experimental Biology 2018 meet held from April 21-25 at the San Diego Convention Center is a premier annual meeting of five host scientific societies and several guest societies. It offers an unparalleled opportunity for scientists from the US and across the world to share and exchange ideas on path breaking developments in cancer research.

Highlighted below are four of the many new developments that are being show cased in the EB meeting 2018

‘The annual Experimental Biology meet offers scientists from across the US and the world a platform to present the latest developments in various fields and translating their research to clinical patients’

1. New Treatment for Pancreatic Cancer

Pancreatic ductal adenocarcinoma (PDAC), makes up for about 90 percent of all pancreatic cancers, and has a 5-year survival rate of onlyless than five percent. Pancreatic cancer is very often difficult to detect, and therapy is additionally complicated by p53 tumor suppressor gene mutations that render the tumor cells resistant to treatment.

Scientists from the Human BioMolecular Research Institute, University of California San Diego and ChemRegen, Inc. have created a novel compound that could be potentially useful in treating pancreatic cancer

• In earlier research, the team demonstrated that this compound killed PDAC cells both expressing and not having the p53 mutation. The compound was also found to inhibit tumor growth in a mouse model of invasive PDAC
• In their latest work, the scientists have showed that the compound works by uniquely targeting two human cell death pathways namely programmed cell death (apoptosis), and the intracellular scavenging system referred to as autophagy
• They have demonstrated that the compound exerts its effects through its ability to induce crosstalk PDAC cell death pathways.

Jiongjia Cheng will be presenting this work at the American Society for Pharmacology and Experimental Therapeutics (ASPET) annual meeting.

2. Understanding Mechanisms of Chemotherapy Induced Nerve Pain

Patients receiving chemotherapy drugs often experience crippling pain due to the occurrence of chemotherapy-induced peripheral neuropathy. The reason for its occurrence remains unclear and there is no effective treatment.

• In a new study, research teams from the University of Texas Health Science Center at San Antonio found that exposure to taxanes and vinca alkaloids anticancer agents led to an immediate pain response mediated through the peripheral nerve receptors that detect pain impulses
• They showed that the chemotherapy drugs cause over excitation of sensory neurons by specificactivation of an ion channel (TrpA1) involved in perception of pain.
• The study is among the first to demonstrate direct activation of sensory neurons by anti-cancer drugs and suggests a possible role for developing treatments for chemotherapy induced neuropathy by targeting TrpA1.

The findings could lead to creation of novel and effective treatments to combat this debilitating condition. Nina Boiko will present this work at the American Physiological Society annual meeting.

3. Role of NSAID in Treatment of Colon Cancer

Indomethacin is a potent nonsteroidal anti-inflammatory drug (NSAID) found to have anticancer properties in animal models and in clinical trials.

A research team from University of Texas Health Sciences Center in Houston conducted a study using unmodified indomethacin and indomethacin modified with phosphatidylcholine (to counter NSAID induced injury in the gastrointestinal tract) to test its ability to inhibit colonic cancer cells.

• In mice-derived cultivated cancer cells, doses of both forms of indomethacin significantly suppressed colon tumor cell growth, with the phosphatidylcholine containing formulation found to be slightly more potent at the lowest dose that was tested
• Similarly, in mice injected with colon cancer cells, both forms of indomethacin brought about significant decrease in the amount of tumor compared to mice that got no treatment

Thus the results suggest that indomethacin and phosphatidylcholine-indomethacin are effective inhibitors of colon cancer cell growth and may have a role in the treatment and prevention of colon cancer in persons as well. This work will be presented by Lenard Lichtenberger at the ASPET annual meeting.

4. Decoding the Mechanisms of Breast Cancer Growth and Spread

Cold-inducible RNA binding protein (CIRP) plays a critical part in regulating gene expression and response of cells to stress

• A research team from the University of New Mexico Health Sciences Center studied a mouse model of breast cancer that expresses higher levels of CIRP than normal to test its role in growth and spread of breast cancer
• They found that increased levels of CIRP inhibited the growth and spread of tumor cells
• These anti-cancer effects were associated with changes in the levels of cytokines (chemical mediators of the immune system). Specifically, the mice secreted lesser amounts of cytokines that promote tumor growth and progression; at the same time they secreted increased levels of cytokines that suppress cancer growth and metastasis.

The team continues to study CIRP's ability to influence signaling between the tumor and immune cells and how this information could be used to create even more effective immunotherapies for breast cancer. Daniel Lujan will present this study during the Cell Biology Award Hybrid Symposium at the American Association of Anatomists annual meeting.

Reference:

1. A Conserved Pain Syndrome Resulting from the Acute Activation of TrpA1 by Chemotherapy Drugs - (https:plan.core-apps.com/eb2018/abstract/4a709b89-d3ff-46af-a215-42ebfc852802)

Source: Medindia

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