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Jane Antony, postdoctoral researcher, Stanford Medicine, Stem Cell Biology and Regenerative Medicine, delivers an important and thorough overview of the current state of cancer research and methods that may lead to promising new discoveries.

Antony worked toward her Ph.D. through a unique joint program of the National University of Singapore and Imperial College London to bolster her study and understanding of cancer cell biology. She has been an active member of various research groups in Singapore and the UK that focus their efforts primarily on cancer biology, ovarian cancer, metastasis, signal transduction, and therapeutics. Her current work pertains to the identification of innovative therapeutic targets in invasive breast cancer illuminating differential signaling schemas in tumor heterogeneity. Antony is constantly curious, with a passion for understanding the link between metastasis and cancer stem cells.

Antony discusses her current cancer research. She states since cancer is an intrinsic disease, whatever you use to target it will impact the normal healthy tissue as well. Generally, a disease’s etiology, or cause, can be classified as intrinsic, extrinsic, or idiopathic. Antony’s particular interest is in regard to metastasis and how cancer spreads. Antony states that many cancers can be removed surgically and can utilize therapies that shrink the cancer cells, but if it spreads to other organs it becomes more difficult to treat. Antony gives a detailed analysis of what is currently known about DNA as it relates to cancer growth. She describes the different types of cancers, how they metastasize, and typically where they travel to, or could. Additionally, she provides an in-depth overview of the current therapies such as radiation and chemotherapy. In regard to radiation therapy, it certainly has an effect on normal cells as well, and chemotherapy, unfortunately, becomes less effective over time and multiple treatments.

Antony talks about some of her work and areas of particular interest such as tumor suppressors. Understanding how tumor suppressors are involved in the development of cancer, specifically genes that regulate Receptor Tyrosine Kinases (RTKs) can quite possibly provide some important answers. A gene of great interest is the OPCML, which is present in healthy, normal cells but is switched off in cancer, which makes treatment very difficult with lowered chances for recovery. Understanding how this gene functions in cells is a critically important issue. Targeting genes that regulate RTKs can lead to possible gene-based cancer therapies for patients.

Antony details other important developments in research, such as limiting dilution assays (LDA). LDA is designed to define an undetermined frequency of effector cells within a population. They are dose-response assays that enable detection of a positive or negative immunoresponse in each unique culture within replicates that vary in the number of actual responder cells tested. By calculating stem cell frequencies researchers can study how stem cells are evolving throughout treatment.

Antony describes her findings in regard to stem cells and various types of cancers. She states that in blood cancers, the methods are somewhat different, in that bone marrow is removed and then reinstated after treatment has flushed out the affected area. Obviously, this is a treatment advantage of liquid cancers, for solid tumor cancers cannot benefit in the same way due to their form. And she talks about an assortment of other interesting trials that are underway that may provide further answers of great benefit to science and medicine.

Antony is a postdoctoral member of the American Society for Cell Biology (ASCB), as well as a member of the EMT International Association, and an associate member of the American Association for Cancer Research. She holds a Doctor of Philosophy from the National University of Singapore, a Bachelor of Engineering from the National University of Singapore, and a Doctor of Philosophy from Imperial College of Science, Technology & Medicine.

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