Cancer Genetics
Volume 13, Issue 2, June 2009
     
Coordinator's Message
Greetings SIG Members!

Greetings SIG Members!Lisa Aiello-Laws, RN, MSN, APNG, AOCNS®
North Cape May, NJ
llaws@itapartners.com


When this newsletter comes out, ONS Congress will be over. I hope everyone had a chance to sight-see in San Antonio, TX, and enjoy the Riverwalk. I am sure the keynote address, “Why I Wore Lipstick to My Mastectomy” by Geralyn Lucas, was fabulous! Maybe you were able to go to the Witte Museum and see the exhibit “Genome: The Secret of How Life Works” made possible by Pfizer.

Our SIG sponsored a session titled “The Nurse's Role When Drugs Are Designed With the Patient in Mind: Individualized Treatment in Breast Cancer.” Speakers were Loretta Williams, RN, DSN, OCN®, AOCN®, Julie Eggert, RN, PhD, GNP-C, AOCN®, and Patricia Jolley, RN, BS.

Our SIG displayed a Cancer Genetics SIG poster, which described who we are, what we do, and topics we may cover. I hope everyone had a chance to see it. It will be posted on our Virtual Community (VC) if you missed it.

At the SIG Planning/Networking meeting, we met up with many of our colleagues for an interactive discussion.

  • The meeting started with an educational session about Direct-to-Consumer marketing of genetic testing. Our SIG was charged with developing a position statement to submit to the ONS Board. If you would like to be a part of this project, please e-mail me.
  • We discussed the National Accreditation Program for Breast Centers, which began in 2008. We discussed their definition of genetic counseling and education and which professionals they expect to perform these services. More information on this will be available in the future.
  • The SIG has been quite active lately because many members are acting as advocates for our professional responsibilities. We need to stay abreast of issues that develop in health care that may affect our practice. We need to work collaboratively with our International Society of Nurses in Genetics (ISONG) colleagues, as we have the same goals to preserve our practice and will be stronger in numbers.
  • Another topic that typically is discussed is credentialing in genetics. For those of you who are not aware, ISONG offers credentialing at two levels, one for advanced practice nurses and one for nurses with bachelors’ of science in nursing degrees. I recommend you check out ISONG’s Web site and the Genetic Nursing Credentialing Commission’s Web site for more information.
  • We also discussed the long-standing issues with billing and coding for genetic services. We would like to put a work group together that will survey how this is being addressed across the country. We need to gather this information as it may be a vital part of keeping a genetic program alive. Again, please contact me if you are interested in being involved with this work group.

I hope everyone has returned home with a new sense of vigor and a desire to get involved! Many ways exist to get involved, including working on one of our work groups, volunteering for a position within the SIG, writing an article for the newsletter, or posting a question on the discussion board. Please remember that to receive automatic e-mails from the SIG VC, you must go to the VC and sign up. I recommend signing up for the announcements, discussion board, and newsletter e-mails. If you can think of any topics that you would like us to address in the newsletter or information you would like posted to the VC, please contact me.

I look forward to our successes this year!

 

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

Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

Using Family History to Identify High-Risk Individuals and Families

Using Family History to Identify High-Risk Individuals and FamiliesJennifer Loud, RN, CRNP, DNP
Clinical Genetics Branch, National Cancer Institute
Derwood, MD
LoudJ@mail.nih.gov


The National Institute of Health, the Center for Disease Control, and the United States’ Surgeon General have launched an initiative to encourage all families to know their family histories and all healthcare providers to document family history. The mission is to identify patterns of chronic diseases—not only cancer but also cardiovascular disease and diabetes—and to catch these diseases early to provide treatment before the diseases progress. All oncology nurses promote efforts to improve the health and well-being among members of high-risk families and to reduce the incidence and burden of cancer. The hope is that by identifying individuals who are at higher risk for cancer, early detection and cancer prevention services will reduce their risk of the developing cancer. The family history tool, My Health Portrait, can be used by families to document family history and by healthcare providers to perform an initial family history assessment.

Patterns of Cancer Development
The majority of cancers diagnosed in the United States (lung, prostate, breast, and colon) are sporadic cancers. These cancers are thought to occur because of aging and/or environmental exposures and occur late in life (after 60 years) (Lindor, McMaster, Lindor, Greene, & National Cancer Institute, Division of Cancer Prevention, Community Oncology and Prevention Trials Research Group, 2008). Sporadic cancers are caused by somatic errors in DNA replication that occur in genes (tumor suppressor genes and proto-oncogenes) that normally function to promote cell growth and development.

A familial cancer pattern is characterized by an increase in the number of cancers within a family; however, the pattern of cancers identified does not fit a hereditary cancer syndrome pattern (Lindor et al. 2008). Cancer cases within family clusters most likely represent complex interactions of low-penetrance susceptibility genes and/or environmental factors. Unaffected, close relatives are considered to be at increased risk of developing the cancers seen within the family when compared to the general population.

Hereditary cancers, in contrast, are attributable to mutations in specific genes that are inherited from either parent (mother and/or father) in an autosomal dominant or recessive pattern. Only about 5%–10% of all cancers are hereditary (Lindor et al. 2008). Individuals who inherit a highly penetrant cancer susceptibility gene are much more likely to develop cancer within their lifetime than individuals who do not inherit a cancer susceptibility gene. Family health history can identify individuals at risk of a hereditary cancer syndrome. The challenge for busy healthcare providers is to select appropriate candidates for hereditary cancer risk assessment and to provide, or refer, patients for comprehensive cancer genetic risk assessment, counseling, and testing.

Identifying Hereditary Cancer Risk
Hereditary forms of cancer are identified by evaluating a three-generation pedigree (American Society of Clinical Oncology, 2003). First-degree relatives (parents and siblings) share 50% of their genes; second-degree relatives (aunts, uncles, and grandparents) share 25% of their genes; and third-degree relatives (cousins) share approximately 12.5% of their genes. The pedigree consists of each family member (both affected and unaffected), the types of cancer, and the ages at the time of the cancer diagnoses. Most hereditary cancer syndromes exhibit an autosomal dominant inheritance pattern and, therefore, typically occur on one side of the family. Other signs of a hereditary cancer pattern include the following.

  • Cancer in two or more relatives (on the same side of the family)
  • Early age of onset (younger than age 50)
  • Multiple primary tumors in the same individual
  • Bilateral or multiple rare cancers
  • Constellations of tumors consistent with specific cancer syndrome (e.g., breast and ovary)
  • Evidence of autosomal dominant transmission
    • Multiple affected generations
    • Presence of congenital anomalies or syndrome-associated benign lesions.

For example, a 30-year-old woman whose mother developed ovarian cancer at age 45 could be at greater risk of developing cancer because ovarian cancer diagnosed at the age of 45 is a “red flag” of a hereditary cancer. Once identified, a comprehensive cancer genetic risk assessment can be performed.

All oncology nurses are encouraged to review the recently updated ONS position statements on the role of the oncology nurse in cancer genetic counseling.

The Role of the Oncology Nurse in Cancer Genetic Counseling

Cancer Predisposition Genetic Testing and Risk Assessment Counseling

References

American Society of Clinical Oncology. (2003). American Society of Clinical Oncology policy statement update: Genetic testing for cancer susceptibility. Journal of Clinical Oncology, 21(12), 2397–2406.

Lindor, N.M., McMaster, M.L., Lindor, C.J., Greene, M.H., & National Cancer Institute, Division of Cancer Prevention, Community Oncology and Prevention Trials Research Group. (2008). Concise handbook of familial cancer susceptibility syndromes—Second edition. Journal of the National Cancer Institute. Monographs, (38), 1–93.

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

What Is DNA Banking and What Does it Entail?

What Is DNA Banking and What Does it Entail?Lisa Aiello-Laws, RN, MSN, APNG, AOCNS®
North Cape May, NJ
llaws@itapartners.com


DNA Banking is the extraction and storage of genetic material (DNA) through a blood sample, which is saved for future genetic testing. It may be stored, waiting for more genetic discoveries, so it will be accessible for testing when new tests are developed and available.

Genetic testing should start with the affected person. The testing will then help to identify if a hereditary cause exists for the disease. If testing is begun on an unaffected family member only, the value of the test is limited. If the unaffected person tests negative for a mutation, is this because no hereditary cause was present, or did this person not inherit the mutation? The patient would walk away with no more information than he or she had at the beginning of the process.

Therefore, it is appropriate to test the affected family member first. If a mutation was found, then the family members could be tested to identify if they also inherited the mutation. The goal then would be to develop a medical management plan, which could assist in early diagnosis and/or risk reduction.

DNA banking can cost from $50–$350 and usually is not covered by health insurance. The DNA can be stored from five years to as long as you’d like, depending on the DNA bank. An initial fee might be charged at the time of storage. The person can define who may or may not use their genetic information in the future and for what purposes, if they are deceased.

As oncology nurses (and as RNs), our scope of practice includes the following.  

  • Conducting a genetic health assessment
  • Identifying patients who may benefit from genetic information
  • Identifying ethical, cultural, and societal issues related to genetic information and technology
  • Educating patients and families regarding genetic health information
  • Advocating for patient’s access to genetic services
  • Facilitating referrals for specialized genetic services.
For information on the role of the nurse in genetics, please refer to the International Society of Nurses in Genetics (ISONG) Web site. Here you can access the Essential Nursing Competencies and Curricula Guidelines for Genetics and Genomics, which was published in 2006.

Another resource for professionals and patients includes the National Society of Genetic Counselors (NSGC) Web page. A DNA banking brochure that can be downloaded and printed as educational material for patients is available.

The Cancer Genetics (CAG) SIG is also a resource for information, education, and networking. The CAG SIG Virtual Community (VC) has important links for family risk assessment tools and educational materials. Join the discussion group, which is a good forum to bring up genetic questions and its ethical implications. We invite you to join our VC.

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

Advances in Pharmacogenomics: K-Ras Mutations and Resistance to Targeted Agents

Advances in Pharmacogenomics: K-Ras Mutations and Resistance to Targeted AgentsLisa Aiello-Laws, RN, MSN, APNG, AOCNS®
North Cape May, NJ
llaws@itapartners.com


Targeted agents have changed cancer care. Treatment now focuses on changing the intracellular signaling pathways involved with carcinogenesis. Primarily, targeted agents block tumor growth and spread.

In normal cell growth, when old cells die, new cells are replicated. However, sometimes during replication, errors occur, leading to abnormal cell growth. These cells can grow without regulation, invade, and spread to other body organs. Typically, tumor suppressor genes, which normally slow down cell growth, cause these cells to die. If these cells do not die, their DNA makes abnormal proteins. Cancer develops when these abnormal proteins signal a cell to reproduce excessively.

Many targeted therapies are directed at these proteins, thus blocking the signaling that drives tumor cell growth and division.

Many targeted agents are now standards of care for cancer treatment. These include trastuzumab, which attaches to HER-2 positive cancer cells and slows or stops their growth; and Bevacizumab, which binds to vascular endothelial growth factor (VEGF) and signals a tumor to develop new blood vessels to feed and sustain the tumor. When VEGF is blocked, newly formed microvasculature disintegrates. Cetuximab and panitumumab act on the epidermal growth factor receptor (EGFR), which are signaling molecules involved in multiple cell functions, including cell proliferation, differentiation, motility, survival, and tissue development. Among other cellular interactions of EGFR is a cell membrane receptor tyrosine kinase (TK). TK is an activator of the intracellular signaling pathway. Gefitinib and erlotinib (TK inhibitors—TKIs) are small molecule EGFR inhibitors of TK enzymatic activity. (Cascone, Morelli, & Ciardiello, 2006)

New findings indicate that the K-Ras gene in tumor cells, when mutated, leads to activation of the signaling pathways of EGFR and VEGF. K-Ras mutations are found in 65%–100% of pancreatic carcinomas, 36% of colorectal cancers, and 20% of non-small cell lung (NSCL) cancers. (Saif & Shah, 2009) When K-Ras is tested in the lab, the results are reported as “mutation” or “wild-type” (which implies a normal, nonactivated protein).

Recent studies of cetuximab and panitumumab in the treatment of metastatic colorectal cancer have found that patients with a “wild-type” K-Ras (no mutation present) in the tumor cells have an improved progression-free survival and overall response rate when compared with patients whose tumor has a mutated K-Ras gene.

Studies of patients with NSCL cancer and response to TKIs has stratified response by EGFR and K-Ras mutations. The cumulative findings indicate that patients with EGFR mutations in the tumor cells exhibit impressive outcomes when given EGFR-TKIs. Patients with K-Ras mutations did not show a significant benefit. Patients whose tumors were wild-type for both EGFR and K-Ras did not exhibit significant difference in response from those with K-Ras mutations. (Jackman et. al, 2008)

The National Comprehensive Cancer Network (NCCN) continually updates its Clinical Practice Guidelines in Oncology. The most recent edition (v.2.2009) of the Colon Cancer Guidelines has been updated to recommend K-Ras tumor testing prior to treatment with cetuximab or panitumumab, which only should be considered for patients whose tumor has the wild-type gene. This has become standard of care.

NCCN also has updated its Non-Small Cell Lung Cancer Guidelines (v.2.2009) to recommend that patients with K-Ras mutation-positive tumors should be considered for therapy other than erlotinib. The findings in lung cancer are not strong enough at this time to make a stronger recommendation.

Research continues on pancreatic tumor tissue. Still unknown  is whether K-Ras mutations in the tumor cells will indicate a response to treatment.

References

Cascone, T., Morelli, M.P., & Ciardiello, F. (2006). Small molecule epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in non-small cell lung cancer. Annals of Oncology, 17(Suppl. 2), ii46–ii48.

Jackman, D., Sequist, L.V., Cioffredfi, L., Janne, P.A., Riely, G.J., Gallegos Ruiz, M., et al. (2008). Impact of EGFR and K_Ras genotype on outcomes in a clinical trial registry of NSCLC patients initially treated with erlotinib or gefitinib. ASCO abstract # 89.

Saif, M.W., & Shah, M. (2009). K-Ras mutations in colorectal Cancer. A practice changing discovery. Clinical Advances in Hematology and Oncology, 7(1), 45–64.

www.avastin.com

www.bio-itworld.com

http://www.cancer.gov/cancertopics/factsheet/Therapy/targeted

http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=131550

http://www.researchvegf.com/researchvegf/privacy/index.m

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

News to Use From the National Cancer Institute

News to Use From the National Cancer InstituteResearchers Identify Genetic Variations That May Increase Risk of Breast Cancer

Researchers have identified new genetic variations in two regions of DNA—located on chromosomes 1 and 14—that may be associated with the risk of sporadic breast cancer. This study also confirms some of the previously identified associations between specific regions in the genome and breast cancer risk. The findings are reported by the Cancer Genetic Markers of Susceptibility (CGEMS) team, which includes researchers at the National Cancer Institute (NCI), part of the National Institutes of Health.

Nearly every cell in your body contains 46 chromosomes—tightly packed bundles of DNA—half of which came from your mother and half from your father. Although the DNA of any two people is more than 99% the same, the fraction of DNA that varies among individuals can play an important role in risk of disease. The most common type of variation, called a single nucleotide polymorphism (SNP), affects just a single building block of DNA. SNPs are used in genome-wide association studies to identify chromosome regions that are associated with disease.

"By studying large populations of individuals with and without disease, CGEMS research can provide powerful indicators as to which SNP variations are associated with breast cancer," said Stephen Chanock, MD, director of NCI's Core Genotyping Facility and chief of the Laboratory of Translational Genomics in the Division of Cancer Epidemiology and Genetics (DCEG). "The two new regions identified in our study open up great possibilities for research into novel pathways contributing to the development of breast cancer. In turn, an in-depth understanding of the biology underlying the contribution of these genetic variations could one day lead to new approaches for therapy or prevention of breast cancer."

"Breast cancer is a complex disease, and it is important to recognize that multiple genetic alterations will be involved in predicting risk and prognosis, leading to treatment. The important next step will be to take this association of risk and, through further research, link these specific genetic defects to changes in biologic function," said NCI Director John E. Niederhuber, MD. "By understanding altered genetic pathways, we will ultimately be able to turn knowledge of genetic variations and risk into novel targets for drug development, which may enhance our ability to prevent and/or control this disease."

The region identified on chromosome 1 contained the rs11249433 SNP. Although the function of this SNP is unknown, further analysis by the CGEMS team found that this region is predominately associated with estrogen receptor-positive breast cancer, the most common molecular subtype of breast cancer.

The newly identified region found on chromosome 14, which included the rs999737 SNP, is located near an interesting gene, RAD51L1, which is in a pathway previously implicated in breast cancer risk. The protein encoded by this gene interacts directly with those of other genes that are involved in DNA repair and in the exchange of material between strands of DNA.

The researchers also confirmed previous reports that six other genomic regions—located on chromosomes 2, 5, 8, 10, and 16—are associated with breast cancer risk. Further study of these regions may help to identify possible mechanisms that may contribute to the development of breast cancer.

"We've known for over a decade about a few genes that predispose women to risk of breast cancer," said Chanock. "But, through studies like CGEMS, we're increasing the catalog of regions in the genome that contribute to breast cancer risk."

In addition to Chanock, CGEMS is co-led by Joseph Fraumeni Jr., MD; Gilles Thomas, MD, PhD; and Robert Hoover, MD, ScD, also of NCI's DCEG; Daniela Gerhard, PhD, of NCI's Office of Cancer Genomics; and David Hunter, MD, ScD., from the Harvard School of Public Health, Boston, MA. The success of the CGEMS project is based on collaboration between epidemiologists, biostatisticians, and genomic scientists at NCI and at several other research institutions, funded through grants from NCI, who together have analyzed DNA from thousands of cases and controls drawn from NCI-supported studies of both breast and prostate cancer.

The CGEMS team conducted a three-stage genome-wide association study in women of European ancestry to identify SNPs that were associated with breast cancer. Data from this CGEMS study are available to researchers through the CGEMS data portal at http://cgems.cancer.gov.

Breast cancer is the second leading cause of cancer-related death in women in the United States. Women with a family history of breast cancer more often are diagnosed at a younger age than women who do not have relatives with the disease, suggesting that inherited susceptibility is important in this disease. Several genetic variations have been identified that contribute to an inherited risk of developing breast cancer, most notably in the BRCA1 and BRCA2 genes. However, these variations account for a small fraction of breast cancer, and it is believed that the combination of many common and yet-to-be-identified genetic variations may contribute to increased risk.

The CGEMS team previously released similar data on prostate cancer, the third leading cause of cancer-related death in men. Researchers have discovered multiple genetic variations associated with prostate cancer risk.

Reference

Thomas, G., Jacobs, K.B., Kraft, P., Yeager, M., Wacholder, S., Cox, D.G., et al. (2009). A multi-stage genome-wide association in breast cancer identifies two novel risk alleles at 1p11.2 and 14q24.1 (RAD51L1). Nature Genetics, 41(5), 579–584.

Find out more information about NCI's Cancer Genetic Markers of Susceptibility (CGEMS) initiative.

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

What Did You Do on DNA Day 2009? What Did You Do on DNA Day 2009?

Millie Arnold, RN, BS, OCN®, CCRC
Dallas, TX
Mildred.arnold@baylorhealth.edu


DNA Day was celebrated on April 25th. On this date in 1953, James Watson and Francis Crick published a paper describing the structure of DNA, which was published in the journal Nature.

DNA Day marks the completion of the Human Genome Project, the 13-year international effort that identified the order, or sequence, of more than three billion building blocks (bases) in human DNA. The Human Genome Project was finished in 2003.

Cancer Genetics SIG members may find the following Web sites of interest to learn more about DNA Day, the discovery of DNA's structure, and the Human Genome Project.

DNA Day 2009 (National Human Genome Research Institute)
DNA Day 2009 (European Society of Human Genetics)
The Francis Crick Papers (U.S. National Library of Medicine)
The 1953 paper by Watson and Crick (Nature)
The Human Genome Project

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

Welcome New Cancer Genetics SIG Members!Welcome New Cancer Genetics SIG Members!

The Cancer Genetics (CAG) SIG welcomes the following new members. As of April 2009, 379 members made up the CAG SIG reflecting a 1% growth! Thanks to all the new and renewed members.

Name

City, State

E-mail

 

 

 

Melody Alexander

Kansas City, MO

alexandermelody@hotmail.com

Susan Bazinet

Whispering Pines, NC

bzntb@aol.com

Lisa Brubaker

Carefree, AZ

lisacb@gene.com

Christina Dotson

Crystal Springs, MS

cdotson@nursing.umsmed.edu

Tammy Grannell

Corpus Christi, TX

tgif60@grandecom.net

Janice Hart

Midland, TX

janice.hart@usoncology.com

Natalie James

Herne Bay, Auckland

NatalieJ@adhb.govt.nz

Jeannette Kelly

Orange Park, FL

jeannettekelly07@comcast.net

Catherine Lombardi

Marlborough, CT

cjlombardi@att.net

Cynthia Lorimer

Scottsdale, AZ

cindylorimer@cox.net

Heather McDonald

Marietta, GA

copper_netspider@yahoo.com

Mark Mohr

Edmond, OK

mmohr@genomichealth.com

Aynessa Mondlak

Huntington, WV

amondlak@st-marys.org

Jennifer Painter

Smyrna, DE

jenlloydrn@hotmail.com

Kunjumol Vadalcekara      

Missouri City, TX

kdvadalcekara@mdanderson.com

Kimberly Werner

Centralia, WA

Kimberly.Werner@providence.org

Monica Arellano

Austin, TX

salaciouswatto@hotmail.com

Patricia Berger

West Des Moines, IA

bergerpm@hotmail.com

Patricia Boralsky

Stanhope, NJ

pb7129@hotmail.com

Katie Bower

Huntington, NY

bowerkj@gmail.com

Michelle Brand

Stratford, WI

michelleb@airrun.net

Tom Eichert

Lake Stevens, WA

tom_eichert@yahoo.com

Debra Ellsworth

Western Springs, IL

bdellsworth@sbcglobal.net

Beverly Mandell              

Boynton Beach, FL

bmandell@responsegenetics.com

Jessica McNamara

West Hollywood, CA

jessabeth9@yahoo.com

Linda Mikolainis

Richfield, WI

mikolainis@sbcglobal.net

Heather Mixson

Saint Petersburg, FL

hleafl@aol.com

Patricia Voltmer

Saint Joseph, MO

p_voltmer@yahoo.com

A. Fuchsia Howard

Vancouver, Canada

fuchsia@telus.net

Roberta Jones

Fairhope, AL

rjones@providencehospital.org

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

Reminder for New Members

Reminder for New MembersFor those of you who are new to the SIG, please go to the Cancer Genetics SIG Virtual Community (VC), and sign up to receive automatic e-mails of announcements and discussions. You must go to the front page to sign up for announcements and the discussion page to sign up for discussion e-mails. The newsletter will be sent to you automatically, as long as you are an active ONS member and SIG member.

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

Writing Mentorship Program Offers Even More Rewards and Eliminates Application Deadline

Writing Mentorship Program Offers Even More Rewards and Eliminates Application DeadlineNow is the time to start writing for publication. Share your knowledge with colleagues, improve patient care, and reap professional accolades and rewards—all with the help of an experienced nurse author and ONS staff…and all from the comfort of your home or office.

The Clinical Journal of Oncology Nursing (CJON) is dedicated to developing the profession’s next generation of experts and authors through the CJON Writing Mentorship Program. CJON will pair each selected fellow with a previously published author who has knowledge in the area of interest, and ONS will offer the support of a publishing staff member and librarian. The project is completed without travel over a period of nine months, and expenses are reimbursed.

The program recently eliminated its deadline in favor of year-round application, and it now offers even more rewards.

  • Get your byline published in a respected peer-reviewed publication that is read by more than 35,000 nursing colleagues, other healthcare personnel, and pharmaceutical professionals.
  • Establish yourself as an expert in a specific clinical topic.
  • Earn a scholarship to an ONS educational event.
  • Receive points toward oncology nursing certification renewal.
  • Be recognized in the ONS awards publication, at an ONS Congress reception, and in a letter to your employer.

For more information about the CJON Writing Mentorship Program, including eligibility criteria, visit the ONS Web site or contact ONS Staff Editor Keightley Amen at 412-859-6258 or kamen@ons.org.

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

ONS Connect Launches New Blog to Continue the Conversation

ONS Connect Launches New Blog to Continue the ConversationJoin the online conversation as ONS Connect’s new blog, RE:Connect, brings together a diverse group of oncology nurses talking about life at work and at home.

When ONS’s monthly news magazine, ONS Connect, was redesigned in 2007, some of the intent was to address the interests of those new to the field and provide quick news and information to busy professionals. RE:Connect offers an extension of these goals by establishing an online community for readers to talk about issues and share experiences that they deal with on a daily basis. The RE:Connect blog was launched in November in conjunction with ONS’s annual Institutes of Learning and Advanced Practice Nursing Conference.

ONS members have been tapped to initiate the dialogue by posting to the blog on a regular basis.

  • Erin Elphee, RN, MN, CON(C), primary clinic nurse for Lymphoma and Malignant Hematology Disease Site Groups at CancerCare Manitoba in Winnipeg, Canada
  • Kimberly George, MSN, RN, ACNS-BC, OCN®, adult health CNS in Wichita Falls, TX
  • Jeanine Gordon, RN, MSN, OCN®, clinical nurse specialist/nurse manager from Brooklyn, NY
  • Kari Wujcik, nursing student at Belmont University and a nurse extern in the pediatric intensive care and cardiology units at Monroe Carell Jr. Children’s Hospital at Vanderbilt University

These bloggers will share their thoughts about 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. Readers are encouraged to join in on the conversation and connect with other oncology nurse readers by posting their own stories, tips, ideas, and suggestions in the comments section at the end of each blog post.

Check out RE:Connect today, and share this link with your friends and colleagues!

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

ONS Social Media Sites of Interest

ONS Social Media Sites of InterestDo you want up-to-the-minute information about the next conference? Would you like to network with other oncology nurses? Do you want to stay in touch with other ONS members? Now, it’s easier than ever because ONS has joined social media sites that help you do all of this and more. Sign-up is free and easy, and you always can control your privacy settings. Already have an account? Share your story, and make the most of all these sites have to offer. Be sure to invite others to join as well.

ONS is now on Facebook!

  • Oncology Nursing Month is in May and ONS wants you to share your stories. As an oncology nurse, you take on the role of teacher, listener, and shoulder to lean on. You help people through some of the most trying times of their lives. Celebrate and share the work you do.

ONS is now on Twitter!

  • Twitter is a free service that lets you keep in touch with people through the exchange of quick, frequent answers to one simple question: What are you doing? Join today to start receiving ONS’s updates.
 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

ONS Connect Puts Evidence Into PracticeONS Connect Puts Evidence Into Practice

Have the ONS PEP cards changed the way you practice nursing? In the April issue of ONS Connect, read how ONS members have worked the PEP cards into their own practice.

 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

Membership Information

SIG Membership Benefits

  • Network with colleagues in an identified subspecialty area around the country.
  • Contribute articles for your SIG’s newsletter.
  • Participate in discussions with other SIG members.
  • Contribute to the future path of the SIG.
  • Share your expertise.
  • Support and/or mentor a colleague.
  • Receive information about the latest advancements in treatments, clinical trials, etc.
  • Participate in ONS leadership by running for SIG coordinator-elect or join SIG work groups.
  • Acquire information with a click of a mouse at http://ons.org/membership including
    • Educational opportunities for your subspecialty
    • Education material on practice
    • Calls to action
    • News impacting or affecting your specific SIG
    • Newsletters
    • Communiqués
    • Meeting minutes.

Join a Virtual Community

A great way to stay connected to your SIG is to join its Virtual Community. It’s easy to do so. All you will need to do is

  • Log on to the ONS Web site (http://www.ons.org/).
  • Select "Membership" from the tabs above.
  • Then, click on "ONS Chapters and Special Interest Groups."
  • Scroll down to "Visit the ONS Special Interest Groups (SIG) Virtual Community" and click.
  • Now, select "Find a SIG."
  • Locate and click on the name of your SIG from the list of all ONS SIGs displayed.
  • Once the front page of your SIG’s Virtual Community appears on screen, select "New User" from the top left. (This allows you to create log-in credentials.)
  • Type the required information into the text fields as prompted.
  • Click "Join Group" (at the bottom right of the text fields) when done.

    Special Notices


    • If you already have log-in credentials generated from the ONS Web site, use this information instead of attempting to generate new information.
    • If you created log-in credentials for the ONS Web site and wish to have different log-in information, you will not be able to use the same e-mail address to generate your new credentials. Instead, use an alternate e-mail address.

Subscribe to Your SIG’s Virtual Community Discussion Forum
Once you have your log-in credentials, you are ready to subscribe to your SIG’s Virtual Community discussion forum. To do so,

  • Select "Log In," located next to "New User," and enter your information.
  • Next, click on the "Discussion" tab on the top right of the title bar.
  • Locate and select "Subscribe to Discussion"
  • Enter e-mail address.
  • Click "Finish."
  • You are now ready to begin participating in your SIG’s discussion forum.

Participate in Your SIG’s Virtual Community Discussion Forum

  • First, log in. (This allows others to identify you and enables you to receive notification [via e-mail] each time a response or new topic is posted.)
  • Click on "Discussion" from the top title bar.
  • Click on any posted topic to view contents and post responses.

Sign Up to Receive Your SIG’s Virtual Community Announcements
As an added feature, members also are able to register to receive their SIG’s announcements by e-mail.

  • From your SIG’s Virtual Community page, locate the "Sign Up Here to Receive Your SIG’s Announcements" section.
  • Select the "Click Here" feature, which will take you to a link to subscribe.
  • Once the "For Announcement Subscription Only" page appears select how you wish to receive your announcements.
    • As individual e-mails each time a new announcement is posted
    • One e-mail per day comprised of all new daily announcements posted
    • Opt-out, indicating that you will frequently browse your SIG’s Virtual Community page for new postings
  • Enter your e-mail address.
  • Click on "Next Page."
  • Click "Finish"
  • You are now subscribed to receive announcements.
 
 
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Cancer Genetics
Special Interest Group Newsletter  June 2009
 
   

Cancer Genetics SIG Officers

Coordinator (2008-2010)
Lisa Aiello-Laws, RN, MSN, APNG, AOCNS®
North Cape May, NJ
llaws@itapartners.com

Coordinator-Elect (2009-2010)
Patricia Kelly, MS, RN, CNS, AOCN®
Dallas, TX
patriciakelly@texashealth.org

Editor
Millie Arnold, RN, OCN®, CCRC
Dallas, TX
mildreda@baylorhealth.edu

 

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

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

Know someone who would like to receive a print copy of this newsletter?
To print a copy of this newsletter from your home or office computer, click here or on the printer icon located on the SIG Newsletter front page. Print copies of each online SIG newsletter also are available through the ONS National Office. To have a copy mailed to you or another SIG member, contact Membership/Leadership Specialist Carol DeMarco at cdemarco@ons.org or 866-257-4ONS, ext. 6230.

View past newsletters.

ONS Membership/Leadership Team Contact Information

Angie Stengel, MS, CAE, Director of Membership/Leadership
astengel@ons.org
412-859-6244

Diane Scheuring, MBA, CAE, CMP, Manager of Member Services
dscheuring@ons.org
412-859-6256

Carol DeMarco, Membership/Leadership Specialist
cdemarco@ons.org
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.

Oncology Nursing Society
125 Enterprise Dr.
Pittsburgh, PA 15275-1214
866-257-4ONS
412-859-6100
www.ons.org

 
 
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