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Elephants and cancer

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

In 1992, I moved to the Washington DC area and attended a conference on new and projected trends in cancer care at the National Institutes of Health.

Researchers in Texas are now reporting that there may be a smarter way to combat cancer-associated KRAS (Kirsten rat sarcoma viral oncogene homolog) mutations and possibly attack specific tumor types in a new targeted manner.

A new study at a single center in Japan found no significant differences in the rate of BRCA mutations between ovarian cancer patients with or without family histories of the mutations and recommends that BRCA1/2 testing be required for all ovarian cancer patients

 

Why Elephants Don’t Get Cancer

Blog | October 30, 2015 | Cancer and Genetics
By Deborah A. Boyle, RN, MSN, AOCNS, FAAN

Image © Marchenko Yevhen/ Shutterstock.com
In 1992, I moved to the Washington DC area and attended a conference on new and projected trends in cancer care at the National Institutes of Health. A pediatric immunologist who treated and studied rare genetically-based childhood illnesses told the audience of oncology nurses that in the future there will be no need for surgery, radiation, or systemic antineoplastic therapies to treat cancer. Rather, genetic molecular engineering will be used to stop and reverse early signs of cancer and counter carcinogenesis even at later stages. I sat in the audience and was awestruck by this forecast. I found it unfathomable that this could ever become a reality.
Fast forward to 2015, over 20 years later, and I read in the science column of the Los Angeles Times the story entitled, “Elephants’ Anti-Cancer Secret” (October 10, 2015, p.B2). Reporting on a study published in a recent issue of JAMA,1, 2 the columnist shares the finding that elephants (and other large mammals) rarely get cancer. Scientists recently revealed the potential reason for such.

African elephants have twenty copies of a gene called TP53, which produces a protein that suppresses tumor growth. Humans on the other hand, have only one copy of this gene. Collaborating with a zookeeper at Utah’s Hogle Zoo in Salt Lake City and the chief veterinarian for Ringling Bros. Barnum and Bailey Circus, the researchers also identified that elephants were able to make copies of TP53 such that they were incorporated into the genome over time. Additionally, when the elephants’ cells were exposed to radiation, cell death occurred at twice the rate of human cells.

In recent years, the advent of targeted therapies and the identification of genes associated with heightened cancer risk have put the spotlight on genetics in the management of cancer.

The implications of this research will undoubtedly help keep the focus on this critical area of cancer research. The scientists involved in this investigation posited that perhaps a drug could be created that mimics the actions of TP53 or that the insertion of TP53 genes into precancerous cells could reverse mutations. Since it took millions of years for the elephants of today to evolve, I guess waiting 20 years for this type of knowledge to come forth isn’t that long to wait.

I’ve become a believer in the profound possibility of genetics in cancer therapy. That physician I heard decades ago was “right on.”

REFERENCES

Abegglen LM, Caulin AF, Chan A, et al. (2015).
Potential Mechanisms for Cancer Resistance in Elephants and Comparative Cellular Response to DNA Damage in Humans.
JAMA, Oct 8:1-11. http://dx.doi.org:/10.1001/jama.2015.13134.
Greaves M, Ermini L. (2015).
Evolutionary Adaptation to Risk of Cancer: Evidence From Cancer Resistance in Elephants.
JAMA, Oct 8:1-3. http://dx.doi.org:/10.1001/jama.2015.13153.
– See more at: http://www.oncotherapynetwork.com/cancer-and-genetics/why-elephants-dont-get-cancer#sthash.5xGzcSFp.dpuf

 

Researchers Develop New Classification Model for Cancer-Associated KRAS Mutations

News | October 28, 2015 | Cancer and Genetics
By John Schieszer
Researchers in Texas are now reporting that there may be a smarter way to combat cancer-associated KRAS (Kirsten rat sarcoma viral oncogene homolog) mutations and possibly attack specific tumor types in a new targeted manner. They are reporting that the use of biochemical profiling and sub classification of KRAS-driven cancers may lead to a more rational selection of therapies targeting specific KRAS isoforms or specific RAS effectors.
KRAS is one of the main members of the RAS family. About one-third of all human cancers, including a high percentage of pancreatic, lung, and colorectal cancers, are driven by mutations in RAS genes, which also make cells resistant to some available cancer therapies, according to the National Cancer Institute.

The UT Southwestern Medical Center researchers have developed a new classification for cancers caused by KRAS. They are investigating a new strategy based on models that the researchers developed to classify cancers caused by KRAS mutations, which cause cells to grow uncontrollably. Although KRAS-driven cancer mutations have long been a focus of cancer research, effective targeted therapies are not available.

“This work further supports the idea that not all oncogenic KRAS mutations function in the same way to cause cancer. The model we developed may help in sub classifying KRAS-mutant cancers so they can be treated more effectively, using therapies that are tailored to each mutation,” said Kenneth Westover, MD, who is an as Assistant Professor of Radiation Oncology and Biochemistry at the University of Texas Southwestern Medical Center, in a news release.1 “Furthermore, this study gives new fundamental understanding to why certain KRAS-mutant cancers, for example those containing the KRAS G13D mutation, behave as they do.”

The researchers, who have published their findings in Molecular Cancer Research, have characterized the most common KRAS mutants biochemically for substrate binding kinetics, intrinsic and GTPase-activating protein (GAP)–stimulated GTPase activities, and interactions with the RAS effector, RAF kinase. They report that KRAS G13D appears to show rapid nucleotide exchange kinetics compared with other mutants analyzed.2

In this study, the researchers evaluated eight of the most common KRAS mutants for key biochemical properties including nucleotide exchange rates, enzymatic activity, and binding activity related to a key signaling protein, RAF kinase. The researchers observed significant differences between the mutants, including about a tenfold increase in the rate of nucleotide exchange for the specific mutant KRAS G13D, highly variable KRAS enzymatic activities, and variability in affinity for RAF. They also determined high-resolution, three-dimensional X-ray crystal structures for several of the most common mutants, which led to a better understanding of some of the biochemical activities observed.

The researchers now plan to test their models in more complex experimental systems, such as genetically engineered cancer cell lines.

REFERENCES

UT Southwestern Medical Center. (2015).
Researchers develop classification model for cancers caused by most frequently mutated cancer gene.
Hunter JC, Manandhar A, Carrasco MA, et al. (2015).

Biochemical and Structural Analysis of Common Cancer-Associated KRAS Mutations.
Molecular Cancer Research, Sep;13(9):1325-35.
– See more at: http://www.oncotherapynetwork.com/cancer-and-genetics/researchers-develop-new-classification-model-cancer-associated-kras-mutations#sthash.kkK8G0Mi.dpuf

 

 

 

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