Arthritis Drug Auranofin With an Agent Can Knock Off Gene-Mediated Lung Cancer

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Arthritis Drug Auranofin With an Agent Can Knock Off Gene-Mediated Lung Cancer

According to a study published in Cancer Cell and researchers at Mayo Clinic's Florida campus conveyed that rheumatoid arthritis drug "auranofin" and targeted experimental agent's worked as a combination therapy, which can halt the fatal and common types of lung cancer. This combination therapy showed the potential to treat and cease the lung adenocarcinoma which takes place due to mutation of the KRAS gene.

"If our approach works in KRAS-mediated lung adenocarcinoma, it may work in other KRAS-mediated cancers, such as pancreatic and colon cancers, as well as other cancer types," said Alan P. Fields, a cancer biologist and the Monica Flynn Jacoby Professor of Cancer Research, Department of Cancer Biology at Mayo Clinic in Florida.

Mayo Clinic is conducting early-phase trials to check the effectiveness of auranofin alone and in targeted combinations owing to this recent research and many other preclinical research from Dr. Fields' team. It is scheduled to conduct in KRAS-mediated lung adenocarcinoma, ovarian cancer and lung squamous cell carcinoma patients.

The current study:

1. Identified cancer stem cells that lead cancer cells development in KRAS-mediated lung adenocarcinoma

2. Identified a major signaling pathway and encourages the growth of those cancer stem cells

3. Disclosed how auranofin and experimental agent combination stop down the pathway and may be an effective treatment approach

"Cancer stem cells are the really bad actors in many cancers," Dr. Fields said. "Cancer stem cells initiate cancer development, drive its growth and metastasis, and also develop resistance to treatments."

"Conventional chemotherapy can effectively kill non-stem cancer cells, but cancer stem cells often survive," Dr. Fields conveyed. "Then, once therapy is stopped, these cancer stem cells can re-establish the tumor and cause a relapse."

The current research study made upon previous research from Dr. Fields' laboratory that:

1. Identified protein kinase C iota as an oncogene, a gene with the ability to cause cancer

2. Showed that auranofin hinder PKCiota and may be beneficial in the treatmant of cancer

3. A second oncogene " SOX2" activated by PKCiota

4. PKCiota activates a second oncogene, known as SOX2, to boost the cancer stem cell growth in lung squamous cell carcinoma.

Dr. Fields reveals that the current study astonishingly found protein kinase C iota which regulates cancer stem cells through a different pathway in KRAS-mediated lung adenocarcinoma than in lung squamous cell carcinoma. It also activates NOTCH3, a different oncogene. "Using this knowledge, we treated KRAS-mediated lung adenocarcinoma tumors in mice with auranofin and a NOTCH3 inhibitor," says, Syed A. Ali, a postdoctoral researcher in Fields' lab. "We found that these two drugs work better together than either drug did alone."

"This research indicates auranofin might be useful in treating many different cancer types," Dr. Fields said. "By combining it with a second agent targeted to the specific signaling pathway, we hope to fin-tune therapy to the particular vulnerabilities of each type of tumor," Dr. Fields said. He added, "This approach may be useful in multiple forms of lung, ovarian, pancreatic, and possibly head and neck, cervical, and several other cancers."

Therapeutic, Auranofin, Cancer, Lung, Chronic, Chrysotherapeutic, Phase 1, Efficacy, Oral
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