Volume 15, Issue 1, May 2011
Mamma at the Bar
Understanding Genetically-Targeted Therapies

Patricia Kelly, DNP, APRN, CNS, AOCN®
Dallas, TX

Analogies and visuals are powerful tools. I learn this lesson daily from talented teachers. Many nurses say that their eyes glaze over when they hear the words genetics and genomics. For these nurses, trying to learn genetics is like memorizing the periodic table in chemistry class—it has no relevance and is boring. By connecting the genetics and genomics concepts to interpretative visuals, clinical practice, and everyday life examples, we can enhance learning and move beyond “boring”. Let’s see how this can be done.

In December 2010, at an ONS:Edge meeting, I heard Wendy Vogel, MSN, FNP, AOCNP®, discuss genetically-targeted therapies in a memorable way. When Wendy explained targeted therapies, I felt as if I had put on eyeglasses and could now see the blackboard. It made sense, and I could visualize the drugs in action. I share the following “Mamma at the Bar” analogy with Wendy’s permission. Wendy states that her examples are simplistic and not exact science, but they do help nurses and others to get it.

Mamma at the Bar
Think of the cell as a bar. The receptor sites and ligands are people in the bar wanting to hook up. When the receptor sites and ligands get together, a lot of lovin’ takes place in the cell (i.e., the cells reproduce, lose apoptosis, and metastasize). Mamma is the targeted therapy, and she wants to stop the lovin’. Mamma may try to intercept you and take you home at several places within the bar scene. If Mamma gets you in the parking lot before you even approach the bar, that is how bevacizumab (Avastin®) works (extracellularly) by hooking up with a ligand, preventing the ligand from getting to the receptor site, and blocking the vascular endothelial growth factor. If Mamma stops you from going in the door of the bar and takes you home, that is how trastuzimab (Herceptin®) and cetuximab (Erbitux®) work (at the cell surface level) by hooking up with the receptor site before its natural ligand does. If you make it all the way into the bar and Mamma gets you there (intracellularly), that is the action of dasatinib (Sprycel®), sorafenib (Nexavar®), and bortezomib (Velcade®), by stopping the signaling or (bar talk) already in action. What a great analogy! I will never think of these targeted therapies, the monoclonal antibodies (mabs), multikinase inhibitors (nibs), and proteosome inhibitors (mibs) again without imagining Mamma.

I also learn through pictures as many people do. “A picture is worth a thousand words” is a timeless, popular, and useful saying and is the basis for visual literacy. The National Cancer Institute recently released an educational package, Personalized Medicine for Cancer: Putting the Pieces in Place, which helps health professionals understand and share the context of genetics and genomics in clinical practice. Seventeen content areas exist with many genomic examples including Understanding the Cancer Genome, Understanding Genome-Wide Profiling of Cancer, Understanding a Cancer Patient’s Genetic Background, and Understanding Targeted Therapies of Cancer. The content areas have great visuals, and the authors and creators teach with pictures. The Understanding Cancer series is designed for self-study or classroom teaching, and the slides are available in a downloadable PowerPoint® format.*

As Cancer Genetics SIG members, we understand that personalized medicine is all about genetics and genomics. Understanding genetics and genomics is no longer optional; however, the concepts often seem complex and abstract. We need to use innovative strategies to demystify the science.
Using Wendy’s example and the National Cancer Institute visuals, we can infuse our teaching with pictures, analogies, and humor.

I welcome feedback and response to this “Coordinator’s Message.” To share additional thoughts, comments, resources, and analogies, please go to the Cancer Genetics Virtual Community SIG discussion board.


*National Cancer Institute. (2011). Understanding cancer. Retrieved from http://www.cancer.gov/cancertopics/UnderstandingCancer

A special thank you to Wendy H. Vogel, MSN, FNP, AOCNP®, oncology nurse practitioner, Kingsport Hematology Oncology Associates, Kingsport, TN, for sharing her analogies.

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  May 2011

Hereditary Ovarian Cancer:
Consider the Possibilities

Cristi Radford, MS, CGC*
Sarasota, FL

Patricia Kelly, DNP, APRN, CNS, AOCN®
Dallas, TX

Nancy Gardner Roehnelt, PhD, RN, ANP, BC
Temple Terrace, FL

This article and case study are a collaborative effort of the National Society of Genetic Counselors (NSGC) Familial Cancer Risk Counseling Special Interest Group (SIG) and the ONS Cancer Genetics SIG. The ONS Cancer Genetics SIG would like to recognize our NSGC colleagues and thank Cristi Radford, MS, CGC*, for her ongoing efforts to partner with ONS. Cristi Radford is lead author for this newsletter article and is a member of ONS and of the Cancer Genetics SIG. (*CGC stands for certification by the American Board of Genetic Counseling (ABGC). For more information about genetic counselors and to find an NSGC directory, visit their Web site.)

Several hereditary cancer syndromes are associated with increased ovarian cancer risk, and inherited gene mutations account for approximately 10% of all ovarian cancers. Hereditary breast and ovarian cancer (HBOC) syndrome and Lynch syndrome (LS) are the most common ovarian-related hereditary syndromes; however, other conditions exist, such as Peutz-Jeghers and Li-Fraumeni syndrome. HBOC syndrome, a mutation in the BRCA1 or BRCA2 gene, accounts for up to 85% of ovarian germline mutations (South et al., 2009). An approximate 20%–40% lifetime risk of ovarian cancer exists with HBOC syndrome. LS, also called hereditary non-polyposis colorectal cancer (HNPCC) syndrome, carries a lifetime ovarian cancer risk of about 13%.

When discussing hereditary syndromes with families, it is important to remember that genetic testing is most informative and cost-effective when it begins with the individual most likely to have a hereditary cancer syndrome. The patient with an ovarian cancer diagnosis is usually the best candidate for initial genetic testing. According to the 2011 National Comprehensive Cancer Network (NCCN) Guidelines for Genetic and Familial High-Risk Assessment, any woman with ovarian, fallopian tube, or primary peritoneal cancer should be referred to an expert in cancer genetics for further evaluation (NCCN, 2011a, 2011b). Family history is key to assessing patients for a hereditary cancer syndrome. Family history information should include (for each family member) current age, cancer diagnoses if appropriate (pathology reports if available), age of cancer onset, and age of death. When a hereditary ovarian cancer syndrome is suspected, it is important to know if female family members have an intact uterus and ovaries. For the patient with ovarian cancer who presents with a negative BRCA1/2 mutation report, it is essential to know if full sequence testing and BRAC Analysis® Rearrangement Test (BART) for large rearrangements was done and if the patient has had a formal genetic evaluation. Recent publications detail cases in which women with ovarian cancer and a negative BRCA1/2 mutation report were later found to have LS (Brierley, Campfield, Ducaine, & Dohany, 2010; South et al., 2009).

According to the American College of Surgeons (2010)

Cancer risk assessment and genetic counseling is performed by a cancer genetics professional who has extensive experience and educational background in genetics and cancer genetics, counseling, and hereditary cancer syndromes to provide accurate risk assessment and empathetic genetic counseling to patients with cancer and their families.

Cancer risk assessment and potential for referral may be discussed as part of the multi-disciplinary cancer conference.

Genetics professionals include the following.

  • An ABGC board certified or board eligible or (in some states) a licensed genetic counselor
  • An American College of Medical Genetics (ACMG) physician board certified in medical genetics
  • A genetics clinical nurse (GCN), credentialed through Genetics Nursing Credentialing Commission (GNCC) (GCN credentialing is obtained through successful completion of a professional portfolio review process.)
  • An advanced practice oncology nurse who is prepared at the graduate level (master’s or doctorate) with specialized education in cancer genetics and hereditary cancer predisposition syndromes; certification by the Oncology Nursing Certification Corporation is preferred.
  • A board-certified physician with experience in cancer genetics (defined as providing cancer risk assessment for at least 30 cases annually)

Case Study
Sally is a 52-year-old female with papillary ovarian cancer who presents to your office for follow-up care after total abdominal hysterectomy with bilateral salpingo-oopherectomy (TAH-BSO). She has two children, a 22-year-old daughter and a 25-year-old son. She asks you if her 22-year-old daughter should have genetic testing.

Risk Assessment
Your first step in assessing Sally’s risk for hereditary cancer is to determine if she has had a genetics consultation. Upon asking her, she replies, “My gynecologist drew some blood and told me my cancer isn’t related to my aunt’s breast cancer.” After reading her medical record, you see that her gynecologist tested her for BRCA1/2 mutations via Comprehensive BRAC Analysis®, and her result was negative.

Currently, you know Sally is concerned about her daughter, her aunt had breast cancer, and Sally’s BRCA1/2 test result was negative. However, you still have very limited information on her family history. How old was the aunt when she was diagnosed with breast cancer? Is she a maternal or paternal aunt? What about other family members?

Key Points

  • Obtain a detailed family history paying special attention to female relatives who may have had an oophorectomy. This surgery may prevent ovarian cancers and also may decrease the risk of breast cancer depending on the age at which the surgery was performed.
  • Current ages and ages of death are important details to obtain as these can affect risk assessment for a hereditary syndrome. For instance, if all of the female relatives died at early ages of other causes, the true hereditary cancer risk may be hidden.

Family history is essential in assessing Sally’s chance of having a hereditary cancer syndrome. Keep in mind that limitations exist to assessing family history. Clinicians must rely on patient report, which means that if the patient does not report accurate information, the assessment may also be inaccurate. Sometimes, the usual pattern for a hereditary cancer syndrome can be masked by limited family structure (few females in the family or very small family size), premature deaths (relatives who die young of other ailments or accidents), or surgeries (such as hysterectomy for fibroids).

You ask about Sally’s family history in more detail and learn that the aunt is actually a maternal great aunt, related through the maternal grandmother. In addition, this great aunt was diagnosed with breast cancer at age 81. You also learn that Sally’s brother had colon cancer at age 55, a paternal uncle had colon cancer at age 50, and the paternal grandmother died from “female or stomach cancer” in her 40s.

Red Flags in Sally’s Family

  • Multiple cancers on the same side of the family
  • Multiple generations affected with cancer
  • Early onset cancer and less common cancers

Based on these familial characteristics, you know that Sally is a candidate for genetic services. You recognize that her primary concern is her daughter’s risk, which a genetics professional can address. However, you also are concerned about Sally’s lifetime risk for other cancers. You begin to discuss the benefits of meeting with a trained genetics professional, such as a CGC or an advanced practice nurse (APN) with training in genetics.

Common Misconceptions

  • Receiving a cancer genetics risk assessment and genetic counseling means that a person HAS to have genetic testing.
    • A patient can seek information through risk assessment and counseling and ultimately decide not to undergo genetic testing. This is the patient’s decision.
  • Genetic counseling is not important prior to undergoing genetic testing.
    • Because genetic testing has implications for the patient and her family members, education and counseling are recommended (Robson, Storm, Weitzel, Wollins, & Offit, 2010).

Typically, a candidate for genetic testing receives education and counseling before testing to facilitate informed decision making and adaptation to the risk or condition. The initial step of genetic counseling is determining a patient’s knowledge, concerns, and beliefs surrounding a condition to guarantee that the patient’s needs are addressed. In Sally’s case, the CGC or APN would discuss the chance of her daughter having cancer. Sally also would receive information on how genetic testing might impact her son.

Genetic education and counseling gives an individual time to consider the possible uncertainties and medical management options based on varied test results and the risks, benefits, and limitations of genetic testing. Genetic counseling also helps to ensure the most appropriate test is ordered on the best candidate in the family.

Differential Diagnoses
Two syndromes to consider in evaluating a 52-year-old female with papillary serous ovarian cancer are

1) Hereditary breast and ovarian cancer (HBOC)—Two genes are associated with HBOC: BRCA1 and BRCA2. Females with BRCA1/2 mutations have a 15%–40% lifetime chance of developing ovarian cancer. Individuals are also at increased risk of cancers of the breast, skin, and pancreas.

When Sally’s family history is documented in the form of a pedigree, multiple unaffected maternal aunts, uncles, and cousins exist. The only individual with cancer was her maternal grandmother’s sister who had breast cancer at age 81. Based on this family history, Sally does not have a high likelihood of having a BRCA1/2 mutation.

2) LS, also called HNPCC—Five genes are associated with LS—MLH1, MSH2, MSH6, PMS2, and EpCAM/TACSTD1. Females with LS have up to a 13% risk of ovarian cancer. In addition, individuals are at an increased risk for colon, endometrial, gastric, and several other cancers. An individual has a clinical diagnosis of LS by having a mutation in one of the above genes or by meeting the Amsterdam I or II criteria. The Amsterdam II criteria states that at least three relatives must have a cancer associated with LS (colorectal, endometrial, small bowel, ureter, or renal-pelvis) and all of the following criteria should be present.

  • One must be a first degree relative of the other two.
  • At least two successive generations must be present.
  • At least one of the relatives with a cancer associated with LS should be diagnosed under age 50.
  • Familial adenomatous polyposis should be excluded in colorectal cases.
  • Tumors should be verified whenever possible.

Prior to Sally’s genetic counseling appointment, she learned that her paternal grandmother had stomach cancer. In addition, she found out that her paternal uncle’s daughter was diagnosed with endometrial cancer at the time of a routine hysterectomy for uterine fibroids. Sally’s completed family history now includes a brother diagnosed with colon cancer at age 55, a paternal uncle diagnosed with colon cancer at age 50, a paternal uncle’s daughter diagnosed with endometrial cancer at age 38, and a paternal grandmother diagnosed with gastric cancer at age 47. Sally’s personal and family history is now suggestive of LS.

Two main testing strategies exist for LS—tumor characteristic testing via microsatellite instability (MSI) and/or immunohistochemistry (IHC) or germline analysis of the mismatch repair genes. When selecting a testing method and laboratory, the provider must consider multiple factors, including sensitivity or specificity, cost of analysis, and the urgency of test results for treatment decisions. IHC has been demonstrated to be one of the most cost-effective testing approaches for LS. However, the sensitivity and specificity of MSI/IHC in tumors other than colon and endometrial have prevented it from being adequately validated as a screening tool. Additionally, the majority of mutations associated with LS are in MLH1 and MSH2. Because Sally’s test results would not affect immediate surgical decisions, a tiered approached was chosen beginning with germline analysis of the MLH1 and MSH2 genes. Ultimately, Sally was found to have a LS associated MSH2 mutation. This information is not only important for her own medical management but also for that of her children’s and paternal family members.

In summary, review all of the potential ovarian-related hereditary cancer syndromes for patients with a diagnosis of ovarian cancer. Assess carefully and refer patients to cancer genetics professionals for a discussion of risks, benefits, and the implications for family members. Testing results can induce strong emotions, whether or not a genetic mutation is found. Encourage the patient being counseled and/or tested to discuss feelings with friends and family and to share concerns with a healthcare provider or genetic counselor. The patient may find support through online or local groups for individuals with hereditary cancer syndromes. Hereditary cancer risk assessment is a complex, rapidly changing field; consider all possibilities.


American College of Surgeons. (2010). Cancer standards: Risk assessment and genetic counseling. Retrieved from https://www.socialtext.net/cancer_standards/index.cgi?clinical_services
Brierley, K.L., Campfield, D., Ducaine, W., & Dohany, L. (2010). Errors in delivery of cancer genetics services: Implications for practice. Connecticut Medicine, 74, 413–423.

National Comprehensive Cancer Network. (2011a). Colorectal cancer screening. NCCN clinical practice guidelines in oncology. Retrieved from http://www.nccn.org

National Comprehensive Cancer Network. (2011b). Genetic/familial high-risk assessment: Breast and ovarian. NCCN clinical practice guidelines in oncology. Retrieved from http://www.nccn.org/professionals/physician_gls/f_guidelines.asp

Robson, M., Storm, C.D., Weitzel, J., Wollins, D.S., & Offit, K. (2010). American Society of Clinical Oncology policy update: Genetic and genomic testing for cancer susceptibility. Journal of Clinical Oncology, 28, 893–901.

South, S.A., Vance, H., Farrell, C., DiCioccio, R.A., Fahey, C., Piver, M.S., & Roadabaugh, K.J. (2009). Consideration of hereditary nonpolyposis colorectal cancer in BRCA mutation-negative familial ovarian cancers. Cancer, 115, 324–333.

Special acknowledgement to Millie Arnold, RN, BSN, OCN®, CCRC, research nurse coordinator and ONS Cancer Genetics SIG member, for creating the family history pedigree that appears in this article.

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Special Interest Group Newsletter  May 2011

14th Annual Collaborative Group of the Americas on Inherited Colorectal Cancer Meeting

Millie Arnold, RN, BS, OCN®, CCRC
Dallas, TX

October 12–13, 2010, Dallas, TX

The Collaborative Group of the Americas on Inherited Colorectal Cancer (CGA-ICC) was established in 1995 to improve understanding of the basic science of inherited colorectal cancer and the clinical management of affected families. The CGA’s focus is families with rare forms of inherited colorectal cancer such as familial adenomatous polyposis (FAP), Peutz-Jeghers syndrome, juvenile polyposis, other hamartomatous polyposes, and hereditary nonpolyposis colorectal cancer. The 15th Annual CGA-ICC meeting will be October 10–11, 2011, Montréal, Canada.

(The following are Millie’s conference take-aways. This report is not a CGA-ICC document.)

“Herrera Lecture: Non-coding RNAs and Colon Cancer”—C. Richard Boland: Fecal microRNAs (miRNAs) are being researched as a genetic marker in colorectal screening tests. MicroRNAs are short RNA molecules that bind to messenger RNA transcripts (mRNAs), resulting in gene silencing. Each miRNA may regulate up to several hundred genes. MiRNAs are involved in multiple types of cancers and it appears that there are specific patterns of miRNA expression associated with different cancers. Fecal miRNAs are stable and extractable from feces to identify possible expression profiles associated with colorectal cancer. Feces from patients with colorectal neoplasia have different miRNA expression patterns from normal controls.

Link, A., Balaguer, F., Yan, S., Nagasaka, T., Lozano, J., & Boland, C.R. (2010). Fecal microRNAs as novel biomarkers for colon cancer screening. Cancer Epidemiology, Biomarkers, and Prevention, 19, 1766–1774.

“Update on Chemoprevention”—John Baron: Potential chemoprevention of colorectal neoplasia and high-risk genetic settings has been examined either without success to minimal success ranging from vitamin C, vitamin D, folic acid, fish oil, and hormones, to non-steroidal inflammatory drugs. Recent studies using low-dose aspirin have been reported to reduce the risk of developing colon cancer. Observational studies suggest that taking statin drugs over a long period of time may lower colon cancer risk. No vitamins or drugs reduce the risk of hereditary colorectal cancers (yet).

“InSIGHT, and the Human Variome Project and Collaborative Activities”—Finlay Macrae, Secretary of InSIGHT, presented information about the International Society for Gastrointestinal Hereditary Tumours (InSIGHT). InSIGHT has formed a consensus with the Human Genome Variation Society (HVP). HVP has a vision to document variants of all 2,600 human genes and associated phenotypic and other information to improve genetic healthcare and research outcomes. This organization encourages a national submission of mismatch repair (MMR) variant data to build and interpret variant data and volunteer to beta test phenotype data collection.

“Implementing Routine IHC/MSI Testing on Sporadic Tumors”—A panel discussion: The unanswered question remains as to which patient population routinely should complete tumor immunohistochemistry (IHC) and/or microsatellite instability (MSI). Approximately 15% of MSI results can be false-positive. Many institutions routinely complete IHC/MSI based on age less than 70 years; others use greater than 50 years. Discussion was held about having IHC/MSI incorporated as part of the surgery consent. In these instances, the patient is aware that genetic counseling may be involved depending on the results to obtain additional family history for possible germline testing to rule out hereditary colorectal cancer. Other institutions consider this tissue examination as pathological clinical information and do not include IHC/MSI as part of the surgical consent.

“Metachronous Colorectal Cancer (CRC) Risks for MMR Gene Mutation Carriers—The Advantage of More Extensive Surgery”—Susan Perry, of the New Zealand Familial Gastrointestinal Cancer Registry, presented study outcomes for 382 MMR gene mutation carriers from the Colon Cancer Family Registry who had their first diagnosis and curative colorectal cancer surgery. This study reported that one in six patients will have cancer recur within 10 years. The conclusion was that a high cumulative risk exists for metachronous CRC in MMR mutation carriers, indicating that these patients may benefit from a more extensive colon resection for risk reduction.

“Comparison of Family Health History to Personal Genomic Screening for Risk Assessment of Colon Cancer”—Brandie Leach, of Cleveland Clinic, presented a study examining family history risk assessment (FHRA) with Navigenics Personal Genomic Screen (PGS) for 44 eligible patients ages 18 or older for breast, prostate, and colon cancer. The conclusion—FHRA and PGS may be complementary tools for colon cancer risk assessment. Evaluation of family history remains the gold standard until PGS can be integrated to increase sensitivity.

“Colonic Resection in LS Too Much or Not Enough?”—Matthew Kalady and Jaime Bohl presented the pros and cons of prophylactic total colectomy versus segmental colectomy. One prospective for extended surgery is that it significantly reduces the risk of subsequence cancer because metachronous colorectal cancer risk is high after limited resection. Another is that extended resections can be done safely with low morbidity and reasonable quality of life. Two decision models were presented—total versus segmental colectomy. The two models considered age and increased mean survival along with quality of adjusted life being equivalent.

“LS and Gynecologic Operations: Proactive or Reactive?”—Karen Lu and Marta Crispens presented clinical cases about prophylactic gynecological surgery for confirmed LS. Lu reported that surgical considerations such as treating the colorectal cancer have a different urgency than a preventative cancer surgery. Delaying surgery until age 40 may allow women identified with LS to complete childbearing and may decrease the impact on quality of life. Recommended preoperative discussions  to have with patients include completion of child-bearing, performing surgery concurrently, removal of ovaries, and surgical menopause. Patients must be presented with the risks and supported in their choice of surveillance versus prophylactic surgery. More studies are necessary to examine efficacy of screening and chemoprevention.

“Lynch Lecture: The Extra-Intestinal Cancers of LS”—Henry Lynch presented information related to LS, Li-Fraumeni syndrome, MEN-2a and MEN-2b, familial atypical multiple mole–melanoma syndrome, and hereditary diffuse gastric cancer syndrome. Female MSH6 mutation carriers are at lower risk for colorectal cancer and greater risk for endometrial cancer. In male MSH6 carriers, the risk of colorectal cancer is lower, but the difference is not significant. The conclusion—female MSH6 mutation carriers to start screening colonoscopies from age 30 years. Hysterectomy might be considered for these carriers older than 50 years, but Lynch believes older than 40 years is better. He reinforced that gynecologists and gynecologic oncologists must be involved in the ongoing care of women identified with LS. Lynch discussed how prostate cancer should be included as a potential lesion in LS. He presented results of two clinical reports of neurofibromatosis in pediatric studies and discussed unusual tumors in LS presenting large kindred with adrenal cortical carcinoma. He discussed two studies of breast cancer and the close functional relation of CHEK2 and MSH6, suggesting that MSH6 mutations may be involved in CHEK2 polygenic cancer susceptibility. Lynch closed with discussion about the 2009 LS EPCAM mutation.

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Special Interest Group Newsletter  Month 2011


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 The Devil’s in the Details. Thankfully, Your Oncology Nurse Is There, Too, Contemplation Through Journaling, and New Healthcare Experiences Cause Fear and Anxiety, Even for Nurses. 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  May 2011

Five-Minute In-Service

In the latest issue of ONS Connect, the Five-Minute In-Service takes a look at Survivors Seeking Cancer Information Online Can Experience Disenchantment, Empowerment, which appeared in the May 2011 issue of the Oncology Nursing Forum.

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Special Interest Group Newsletter  May 2011

ONS Podcasts of Interest

ONF Podcasts
Listen in as ONF Associate Editor Ellen Giarelli, EdD, RN, interviews Barbara Cochrane, PhD, RN, FAAN, the lead author of the March 2011 ONF article “Exploring a Diffusion of Benefit: Does a Woman With Breast Cancer Derive Benefit From an Intervention Delivered to Her Partners?” In this podcast, Dr. Cochrane elaborates on the role of partners and the promise of an indirect effect of a nursing intervention on the psychosocial well-being of women with breast cancer.

CJONPlus Podcasts
This podcast features CJON Associate Editor Mallori Hooker, RN, MSN, NP-C, AOCNP®, interviewing CJON author Kathryn Trotter, MSN, CNM, FNP, about this innovation in healthcare delivery and the April 2011 CJON article on this topic titled “Innovation in Survivor Care: Group Visits.”

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Special Interest Group Newsletter  May 2011

Help Improve Evidence-Based Practice: Get Involved in PEP

Do you want to help make evidence readily available to nurses in oncology practice? Do you want to easily stay up to date with all of the evidence in particular PEP topic areas or learn more about summarizing and critically appraising evidence? Become a PEP topic contributor or reviewer today. Those who participate in PEP activities are eligible for ONC-Pro points on an annual basis. Contact us to learn more about how you can become involved today.

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Special Interest Group Newsletter  May 2011

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Special Interest Group Newsletter  May 2011

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Special Interest Group Newsletter  May 2011

Cancer Genetics SIG Officers

Coordinator (2010–2012)
Patricia Kelly, DNP, APRN, CNS, AOCN®
Dallas, TX

Coordinator-Elect (2011–2012)
Jacqueline Hale, RN, APN-C, AOCN®
Flemington, NJ

Rose Bell, ARNP-C, MSN, OCN®
Gig Harbor, WA

Robin Stevens, ARNP-BC, OCN®
Jupiter, FL


Web Administrator
Lisa Aiello-Laws, RN, MSN, APNG, AOCNS®
North Cape May, NJ

Special Projects
Julie Eggert, PhD, APRN-BC, AOCN®
Greer, SC

ONS Copy Editor
Emily Nalevanko, MFA
Pittsburgh, PA

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ONS Membership & Component Relations Department Contact Information

Brian K. Theil, CAE, Director of Membership and Component Relations Department

Diane Scheuring, MBA, CAE, CMP, Manager of Member Services

Carol DeMarco, Membership Specialist—SIGs

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.

Oncology Nursing Society
125 Enterprise Dr.
Pittsburgh, PA 15275-1214

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