Volume 14, Issue 2, December 2010
 
   
Troglodyte or Transformational Leader?
Genetic Nursing in 2010

Patricia Kelly, DNP, APRN, CNS, AOCN®
Dallas, TX
patriciakelly@texashealth.org


I faithfully read Joseph Simone’s column, "Simone's OncOpinion" in Oncology Times. Dr. Simone never fails to engage and inspire me with his written words.

In the August 2010 Oncology Times, Dr. Simone lists the six attributes of the successful Apple Inc. company and draws parallels to healthcare centers. I was drawn to attribute number 2, “Lead. Don’t follow.” Dr. Simone describes medical centers that are anchored in the past as “troglodytes.” My first thought was that the word troglodyte must be a frameshift mutation of letters—in other words, a printing error. I went to Merriam-Webster (n.d.) online, looked up the word troglodyte, and found the following.

  1. Member of any of various peoples (as in antiquity) who lived or were reputed to live chiefly in caves.
  2. Person characterized by reclusive habits or outmoded or reactionary attitudes.

The troglodyte is in contrast with Dr. Simone’s challenge to be a leader. Transformational leaders engage team members with shared values and common goals (Sherman & pross, 2010).

Currently, oncology nurses are facing challenges in the area of genetics education and standards. The American College of Surgeons Commission on Cancer (CoC) and the National Accreditation Program for Breast Centers (NAPBC) are revising standards and verbiage concerning who is a qualified genetics provider. Our professional organization, ONS, has a position statement that outlines the roles and expectations of the general oncology nurse, the advanced practice nurse in oncology, and the advanced practice nurse with specialty training in genetics and genomics. However, the position statement does not define genetics and genomics specialty training.

Are we leaders in defining CoC and NAPBC standards and genetics and genomics specialty training, or do we wait for others to set the standards and then respond?

Consider the following questions.

  • Did you know that ONS (2009) has official position statements for cancer predisposition genetic testing and risk-assessment counseling and the role of the nurse in cancer genetic counseling?
  • Are you familiar with the American Society of Clinical Oncology (ASCO) guidelines, CoC, and NAPBC standards for genetics services?
  • Are you actively involved in the ONS Cancer Genetics SIG, and do you encourage others to join? We have power in numbers both for the organization and for the Cancer Genetics SIG. It is significant that ONS appoints liaisons to the CoC and NAPBC.

One of the Cancer Genetics SIG goals for 2010–2011 is to survey SIG members concerning present cancer risk-assessment practices and the need for educational programs. To accomplish this goal, we need three to four SIG members to develop a short online survey, share survey results, and develop recommendations—a beginning assessment of shared values and goals.

As your new ONS Cancer Genetics SIG coordinator, I challenge you to be a visionary leader for genetics and genomics education and standard setting. A first step is to send me an e-mail saying that you’d like to volunteer for the risk assessment and educational assessment task force. Remember, it is dark and cold in the troglodyte’s home.

If you would like to share additional thoughts concerning the “Coordinator’s Message,” please visit the Cancer Genetics SIG Virtual Community Discussion Board.

Resources:

NAPBC standard for genetic evaluation and management (beginning Jan 2011)

American College of Surgeons CoC standard for risk assessment and genetic counseling (updated November 10, 2010)
 
References:

Merriam-Webster. (n.d.). Troglodyte. Retrieved from http://www.merriam-webster.com/dictionary/troglodyte

Oncology Nursing Society. (2009). The role of the oncology nurse in cancer genetic counseling. Retrieved
from http://www.ons.org/Publications/Positions/GeneticCounseling

Oncology Nursing Society. (2009). Cancer predisposition genetic testing and risk assessment counseling. Retrieved from http://www.ons.org/Publications/Positions/Predisposition

Sherman, R., & Pross, E. (2010). Growing future nurse leaders to build and sustain healthy work environments at the unit level. Online Journal of Issues in Nursing. Retrieved from http://www.nursingworld.org/MainMenuCategories/ANAMarketplace/
ANAPeriodicals/OJIN/TableofContents/Vol152010/No1Jan2010/
Growing-Nurse-Leaders.aspx

Simone, J.V. (2010).  Six things medical centers can learn from Apple. Oncology Times, p. 6.

 
The Cancer Genetics SIG Newsletter is produced by members of the
Cancer Genetics SIG and ONS staff and is not a peer-reviewed publication.

Special Interest Group Newsletter  December 2010
 
   

Pharmacogenetic Testing in the Oncology Setting

Julie Eggert, RN, PhD, GNP-C, APRN-BC, AOCN®
Greer, SC
jaegger@clemson.edu


Since the sequencing of the human genome in 2003, technology rapidly has advanced from identification of a few single nucleotide polymorphisms (SNP) over days, weeks, or months to a single microarray screening for 100,000 SNPs in less than 24 hours. Because of this, genetic testing now is available to determine how individuals will respond to a drug and therefore, allows for a benefit versus risk ratio analysis. Ultimately, pharmacogenetic testing of polymorphisms in the p450 cytochrome system can improve patient outcomes, decrease toxicities, and minimize the cost of treatment.

One example of a pharmacogenetic test currently recommended for use targets TPMT variants, which produce the thiopurine S-methyltransferase enzyme. This enzyme is important for breaking down the chemotherapeutic agent. If there is little or no enzyme, the patient is at risk for developing severe side effects from any of the thiopurine agents, such as 6-mercaptopurine (6-MP) and azathioprine (AZA), and the dose would need to be lowered or another chemotherapeutic agent identified for use. Multiple variants exist, but currently, three of them are responsible for about 95% of the enzyme deficiencies. While it is theorized that a high level of enzyme would mean increased degradation of the thiopurine and potentially a need for increased dosages, no studies currently document this need.

Multiple genomic biomarkers are available for pharmacogenomic testing. However, the FDA has documented that only three are required and six have been recommended for use in the clinical setting. This information is included in the package insert of the specific drugs that they affect and are found in Table 1.

Note. Adapted from “Table of Valid Genomic Biomarkers in the Context of Approved Drug Labels,” by Shin, Kayswer, & Langaee, 2009. Retrieved from http://www.fda.gov/Drugs/ScienceResearch/ResearchAreas/Pharmacogenetics/
ucm083378.htm

References:

Shin, J., Kayswer, S., & Langaee, T. (2009). Pharmacogenetics: From discovery to patient care. American Journal Health-System Pharmacology, 66, 625–637. doi: 10.2146/ajhp080170

Bibliography:

Clinical Pharmacogenetics. (2010). Table of valid genomic biomarkers in the context of approved drug labels. Retrieved from http://www.pharmgkb.org/clinical/index.jsp

 
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Special Interest Group Newsletter  December 2010
 
   

Cancer Genetics SIG Goals 2009–2012

Patricia Kelly, DNP, APRN, CNS, AOCN®
Dallas, TX
patriciakelly@texashealth.org


As your SIG coordinator, I would like to share the Cancer Genetics SIG goals. Goals are developed using the ONS pillars of advocacy, knowledge, and partnership as the framework and are written by the Cancer Genetics SIG officers. We welcome your input.

Advocacy

Promote awareness and advocate for genetics legislative issues, representation, competencies and standards, reimbursement, and other genetics- and genomics-related issues.

Action:

  1. Review and update ONS position statements concerning cancer genetics and the levels of oncology genetics nurses.
  2. Continue to review, update, and advocate for the advanced practice nursing role in the National Accreditation Program for Breast Cancer Centers (NAPBC) and the American College of Surgeons Commission on Cancer (CoC) standards.
  3. Advocate for increased genetic content on all levels of ONS certification examinations.
  4. Survey billing and reimbursement issues for risk-assessment programs.

Knowledge

Provide cancer genetic nurses (and all oncology nurses) with professional education on current genetics research, practice issues, and content.

Action:

  1. Publish three newsletters per year and include research, practice issues, and knowledge content.
  2. Establish networking and discussion among ONS cancer genetics SIG members through the Virtual Community and SIG page on Facebook.
  3. Submit a minimum of two genetics and genomics topic submissions for Congress 2011 and the Institutes of Learning.
  4. Survey ONS members concerning current cancer risk assessment practices and educational needs.
  5. Provide consultation for ONS-related genetics materials, courses, and newsletter articles

Partnership

Establish relationships with other organizations.

Action:

  1. Collaborate with the American Nurses Association and other organizations to set standards for essential genetic and genomic competencies for graduate nurses (master’s and doctoral level).
  2. Explore collaborative opportunities and relationships with the International Society of Nurses in Genetics (ISONG) and National Society of Genetic Counselors (NSGC).
  3. Continue to collaborate with the National Coalition for Health Professional Education in Genetics (NCHPEG) and provide input on selected projects (e.g., Genetic Information Nondiscrimination Act education and the Veterans Affairs Hospital Colon Cancer Educational Initiative).
  4. Collaborate with the Breast Care SIG, Nurse Practitioner SIG, etc., on Congress submissions, member surveys, newsletter articles, and special topics.
 
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Special Interest Group Newsletter  December 2010
 
   

BART Testing for Large Rearrangements in BRCA1 and BRCA2 Genes

Edie Smith, RN, MSN, CNM, WHNP
Corona del Mar, CA
edsmith@myriad.com

Lisa R. Miller, RN, BSN, OCN®
Corona del Mar, CA
lmiller@myriad.com


Cancer Genetics SIG members have requested additional information on BART testing. SIG members, Edie Smith and Lisa Miller submitted the following material.

What is BART?
Comprehensive BRACAnalysis is a highly reliable and accurate test that includes complete sequencing of the BRCA1 and BRCA2 genes and an additional procedure to identify five relatively common large rearrangements in the BRCA1 gene. The BRACAnalysis Large Rearrangement Test (BART) was launched to provide a way to detect additional large genomic rearrangements in both BRCA1 and BRCA2.

Although each patient must be evaluated individually based on his or her personal and family history, there is, on average, a less than 1% chance that BART will identify a mutation in a patient who already has had a negative result from Comprehensive BRACAnalysis.

How is BART ordered?
For patients who have an especially strong personal and family history of breast and ovarian cancer (see Table 1 for details of these criteria), Myriad Genetics Inc. includes BART testing at no additional charge as part of Comprehensive BRACAnalysis tests. Myriad identifies patients eligible for this free BART testing based on the clinical history provided on the test requisition form by the ordering healthcare provider. For patients who do not meet these clinical criteria, BART is available as a “reflex” test and is run when Comprehensive BRACAnalysis is negative.

How are BART results reported?
For patients who meet these criteria, BART is run concurrently with the standard Comprehensive BRACAnalysis and the results for both tests appear on a single report. When BART is run as a “reflex” test after Comprehensive BRACAnalysis is negative, the ordering healthcare provider will receive the negative Comprehensive BRACAnalysis results first, and the BART results will be sent separately, usually within one to two weeks.

Check out additional information and a list of frequently asked questions.

Bibliography:

Myriad Genetics Inc. (2010). Web site. Retrieved from https://www.myriadpro.com/

 
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Special Interest Group Newsletter  December 2010
 
   

From the National Cancer Institute News Bulletin

Jennifer T. Loud, RN, CRNP, DNP
Clinical Nurse Specialist, Research, Clinical Genetics Branch, Division of Cancer Epidemiology Genetics, National Institutes of Health


The following is reprinted with permission from the National Cancer Institute News Bulletin, volume 7, numbers 18 and 19.

Genetic Study Finds Clue to Gastrointestinal Stromal Tumors

Researchers have identified a gene called ETV1 that may contribute to the development of some types of gastrointestinal stromal tumors (GISTs). Although preliminary, the findings suggest that ETV1 could be a marker for diagnosing the disease and also may be a potential therapeutic target. Drs. Charles Sawyers of Memorial Sloan-Kettering Cancer Center (MSKCC) and C. David Allis of Rockefeller University and their colleagues reported their findings online in Nature in October 2010.

The researchers discovered the gene while searching gene expression data sets for GIST-specific genes. Among 11 such genes that appeared in three data sets was ETV1, which is a member of the ETS family of transcription factors—genes that regulate the activity of other genes. This gene was of immediate interest because overexpression of other ETS transcription factors has been associated with prostate and other cancers. ETV1 was highly active in all the GIST tumor samples and cell lines they examined and in the cells in which these tumors may originate. Further experiments then showed that ETV1 was essential for the growth and development of GISTs.

In addition, the researchers found that the transcription factor may cooperate with the product of the KIT gene in the development of GIST. Most GISTs harbor mutations that activate KIT, but these mutations alone are not sufficient to cause GIST. The reason could be that KIT mutations promote the development of cancer only in the presence of high levels of ETV1 expression, according to co-author Dr. Yu Chen of MSKCC.

These findings establish an oncogenic role for ETV1 in GIST, the authors concluded. Although transcription factors have been considered “undruggable,” recent studies have begun to challenge this idea, they noted (Chi et al., 2010).

Reference:

Chi, P., Chen, Y., Zhang, L., Guo, X., Wongvipat, J., Shamu, T., . . . Sawyers, C.L. (2010). ETV1 is a lineage survival factor that cooperates with KIT in gastrointestinal stromal tumours. Nature, 467, 849–853. doi: 10.1038/nature09409

Mutations Linked to Two Uncommon Forms of Ovarian Cancer

Mutations in a gene called ARID1A may play a key role in the development of two types of ovarian cancer, according to studies published online September 2010, in the New England Journal of Medicine (NEJM) and Science.

In the NEJM study, Canadian researchers found ARID1A mutations in 55 (46%) of 119 samples of ovarian clear-cell carcinoma, which accounts for about 12% of U.S. ovarian cancer cases, as well as in 10 (30%) of 33 samples of endometrioid carcinoma, another relatively uncommon type of ovarian cancer. No mutations were found in samples from patients with the most common type of ovarian cancer, serous carcinoma, which accounts for about 70% of U.S. ovarian cancers.

In the Science Express study, which was smaller but very similar, researchers from Johns Hopkins Sidney Kimmel Comprehensive Cancer Center reported ARID1A mutations in 57% of ovarian clear-cell carcinoma tumor samples.

Both ovarian clear-cell and endometrioid carcinoma are associated with endometriosis, a gynecologic condition in which cells that line the uterus proliferate in other nearby areas, often producing severe pelvic pain and other problems. Neither cancer subtype responds well to available therapies.

“Connecting ARID1A gene mutations to endometriotic lesions accelerates us toward the development of tools to determine which women with endometriosis are at increased risk for ovarian cancer,” said the NEJM study’s senior author, Dr. David Huntsman from the British Columbia Cancer Agency, in a news release.

His research team initially identified seven types of ARID1A mutations in a small (discovery) set of 19 clear-cell and endometrioid carcinoma samples and then confirmed the findings in an additional (validation) set of 211 ovarian cancer samples.

When the researchers looked more closely at two patients whose clear-cell carcinoma tumors had ARID1A mutations, they found the mutations in nearby endometriotic lesions but not in lesions farther away from the primary tumor. Taken together, the research team wrote, the evidence suggests that ARID1A mutations “may be pathogenic, rather than random, events” and are “an early event in neoplastic transformation” (Wiegand et al., 2010).

The findings, Dr. Huntsman said, via e-mail, suggest that earlier studies implicating the gene in cancer were correct and that ARID1A “appears to be a tumor-suppressor gene of considerable relevance."

Bibliography:

Jones, S., Wang, T.L., Shih, I.M., Mao, T.L., Nakayama, K., Roden, R., . . . Papadopoulos, N. (2010). Frequent mutations of chromatin remodeling gene ARID1A in ovarian clear cell carcinoma. Science, 330, 228–231. doi: 10.1126/science.1196333

Reference:

Wiegand, K.C., Shah, S.P., Al-Agha, O.M., Zhao, Y., Tse, K., Zeng, T., . . . Huntsman, D.G. (2010). ARID1A mutations in endometriosis-associated ovarian carcinomas. New England Journal of Medicine, 363, 1532–1543. doi: 10.1056/NEJMoa1008433

 
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Special Interest Group Newsletter  December 2010
 
   

Re:Connect

RE:Connect is a blog written by oncology nurses on a variety of topics of interest to other nurses in the specialty, including facing day-to-day challenges at work, juggling busy lives at home, and keeping up to date with the magnitude of information available for practicing nurses. This month on RE:Connect, you’ll find discussions titled What Do You Hide Beneath Your Smile?; Thanks to Technology, Professional Isolation Can Be Reduced; and State Cancer Plans: Yes, They’re for Nurses Too. As a reader, join in on the conversation and connect with other oncology nurse readers by posting your own stories, tips, ideas, and suggestions in the comments section at the end of each blog post.

 
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Special Interest Group Newsletter  December 2010
 
   

Five-Minute In-Service

In the latest issue of ONS Connect, the Five-Minute In-Service takes a look at how P6 Acupressure Can Help Patients Self-Manage Chemotherapy-Induced Nausea, which appeared in the November 2010 issue of the Oncology Nursing Forum.

 
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Special Interest Group Newsletter  December 2010
 
   

ONS Podcasts of Interest

ONF Podcasts

ONF Associate Editor Ellen Giarelli, EdD, RN, interviews Jeanne Erickson, PhD, RN, AOCN®, the lead author of the July 2010 ONF article “Patterns of Fatigue in Adolescents Receiving Chemotherapy.” Listen in as Dr. Erickson discusses her article and describes patterns of fatigue through the eyes of the adolescent.

CJONPlus Podcasts

In the first-ever installment of CJONPlus, Cindy Tofthagen, PhD, ARNP, AOCNP®, addressed questions based on a descriptive study she conducted with adults experiencing chemotherapy-induced peripheral neuropathy. Listen in as Dr. Tofthagen is interviewed about the study and her June 2010 CJON article "Patient Perceptions Associated With Chemotherapy-Induced Peripheral Neuropathy.”
 
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Special Interest Group Newsletter  December 2010
 
   

Make Sure You're Getting the Latest SIG Info!

All SIG newsletters and communiqués are posted to their respective SIG Virtual Community, and members with valid e-mail addresses receive notification when the latest newsletters and communiqués are posted. As of January 1, 2011, ONS will no longer distribute via U.S. mail hard copy printouts of the SIG newsletters and communiqués to members who have not provided a valid e-mail address.

If you currently are not receiving e-mails from ONS, please go to www.ons.org and select “login.” Enter your username and password (or, if you do not have a profile, select “Create One Now”). Once you are logged in, go to your profile and select “My Personal Info.”Here you can add or change your e-mail address in our database.

If you wish to receive SIG correspondence but not other e-mails from ONS, select “My Preferences” on the left, and then, select “Manage Subscriptions” under “E-mail Preferences.” From this page, you can select any kind of e-mail that you do NOT want to receive. You still will receive your SIG information as part of your membership as long as we have a valid e-mail address on file for you.

If you do not provide an e-mail address, you will not be notified when a new SIG newsletter or communiqué is posted. However, you always can access newsletters and communiqués by going to your SIG’s Virtual Community.

 
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Special Interest Group Newsletter  December 2010
 
   

Membership Information

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Join a Virtual Community

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Special Interest Group Newsletter  December 2010
 
   

Cancer Genetics SIG Officers

Coordinator (2010–2012)
Patricia Kelly, DNP, APRN, CNS, AOCN®
Dallas, TX
patriciakelly@texashealth.org

Ex-Officio (2010–2011)
Lisa Aiello-Laws, RN, MSN, APNG, AOCNS®
North Cape May, NJ
llaws@itapartners.com

Editor
Nancy Roehnelt, PhD, RN, ANP, BC
Glen Ridge, NJ
nancymgardner@msn.com

 

Co-Editor
Rose Bell, ARNP-C, MSN, OCN®
Gig Harbor, WA
Rosebl3@aol.com

Special Projects
Julie Eggert, RN, PhD, GNP-C, APRN-BC, AOCN®
Greer, SC
jaegger@clemson.edu

ONS Copy Editor
Emily Nalevanko, MFA
Pittsburgh, PA
enalevanko@ons.org

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View past newsletters.

ONS Membership & Component Relations Department Contact Information

Brian K. Theil, CAE, Director of Membership
btheil@ons.org
412-859-6244

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dscheuring@ons.org
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412-859-6230

The Oncology Nursing Society (ONS) does not assume responsibility for the opinions expressed and information provided by authors or by Special Interest Groups (SIGs). Acceptance of advertising or corporate support does not indicate or imply endorsement of the company or its products by ONS or the SIG. Web sites listed in the SIG newsletters are provided for information only. Hosts are responsible for their own content and availability.

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