Our 24/7 cancer helpline provides information and answers for people dealing with cancer. We can connect you with trained cancer information specialists who will answer questions about a cancer diagnosis and provide guidance and a compassionate ear.
Chat live online
Select the Live Chat button at the bottom of the page
Our highly trained specialists are available 24/7 via phone and on weekdays can assist through online chat. We connect patients, caregivers, and family members with essential services and resources at every step of their cancer journey. Ask us how you can get involved and support the fight against cancer. Some of the topics we can assist with include:
- Referrals to patient-related programs or resources
- Donations, website, or event-related assistance
- Tobacco-related topics
- Volunteer opportunities
- Cancer Information
For medical questions, we encourage you to review our information with your doctor.
- Triggering Signals of BRCA1 Breast Cancer (K Kessenbrock)
- Testing Diverse Groups Finds New Breast Cancer Genes (L Teras)
- Black Women & Genetic Testing (J Palmer)
- Women 65+ & Genetic Tests for Breast Cancer Risk (L Teras)
- High-Risk Genes and Screening (A Patel)
- New Risk Calculation May Affect Breast Cancer Screening (L Teras)
- Black Men and Breast Cancer (H Sung)
- Platelets May Help Breast Cancer Spread (E Battinelli)
- Natural Killer Cells & TNBC (R. Chakrabarti)
- Improving Chemotherapy (O Sahin)
- Combo Treatment for TNBC (K Varley)
- Treatments Attack Cell Division (A Holland)
- ER+ Treatment in Mice (P Kenny)
- Blood DNA Monitors Metastasis Treatment (H P Ji)
- PTK6 Gene as Treatment Target (H Irie)
- Time-Lapse Cell Movies (S Spencer)
- 3D Mini Breast Tumors May Help ID New Cancer Treatments
- AI Tool Improves Breast Cancer Prognosis Accuracy
- Exercise & Sitting Time (E. Rees-Punia)
- Cancer Risk Factors in LGBTQ Populations (B. Charlton)
- CPS-3 Disparities Studies
- Cancer Disparities in the US (F. Islami)
- Housing Assistance and Mammograms (H Lee)
- Clinical Trial Treatment Cost App (L Hamel)
- Podcasts, TheoryLab
- Patients Health Insurance Tool (M. Politi)
- Breast Cancer Treatment in Ethiopia (A. Jemal)
- Better Survival Requires Better Insurance (J Zhao)
- Medicaid Eligibility Limits (J Zhao)
- New Treatment for Neuroblastoma (A Heczey)
- Oncogenic Fusions AML (S Meshinchi)
- Genetic Risks (L Teras)
- New Medulloblastoma Drugs (J Rodriguez-Blanco)
- Potential New Hope for MLL (J Grembecka)
- Increase in Brain Tumor Diagnosis (K Miller)
- Longer Life Expectancy for Survivors (J Yeh)
- Potential Target for New Osteosarcoma Drugs (C Benavente)
- At-Home Chemo for Children with HR ALL (L Ranney)
- Childhood Cancer Research Landscape Report
- Tumor-Infiltrating Neutrophils (R. Sumagin)
- New Epigenetic Target (K Rai)
- Extra Chromosomes (Aneuploidy) Effect on Cancer (J. Sheltzer)
- Discovery of a New Biomarker Is the First Step to New Treatment (C. Maher)
- Designer Virus Targets and Kills CRC Cells in Mice (S. Warner)
- Tiny Sensor in Mice May Find Cancer That's Trying to Spread (L. Hao)
- Targeting a Protein “Turned on” by Mistake (N. Gao)
- Spatial Map Intestines (J Hickey)
- CRC Treatment Podcasts
- Keto Molecule & Colorectal Cancer (M Levy)
- Availability of Healthy Food (L Tussing-Humphreys)
- 45 Min/Day of Physical Activity (A Minihan)
- Fewer than 10K Steps/Day (A Patel)
- Yogurt & Cheese & ER- Breast Cancer (M McCullough)
- Stage 2 Clinical Trials for New Endometrial Cancer Drug (V Bae-Jump)
- Hard-to-Starve Pancreatic Cancer Cells (N Kalaany)
- Coffee Risks for Colorectal Cancer (C Um)
- Food Parasite & Brain Cancer Risk (J Hodge)
- Exercise & Quality of Life in Older Survivors (E Rees-Punia)
- 21 Metabolites Linked with Breast Cancer (Y Wang)
- Replacing Sitting May Affect Weight (E Rees-Punia)
- CPS-3 Researchers Ask What People Eat and Check Urine Samples (Y Wang)
- Video Games Motivate Exercise? (E. Lyons)
- Food Choices and Colon Cancer Risk (P. Chandler)
- Race, Exercise & Breast Cancer (C. Dallal)
- Diet with Colorectal Cancer (M. Guinter)
- Biomarkers May Improve Prediction (Y Wang)
- Kickstart NSCLCs Clinical Trials (L. Eichner)
- Mapping Mitochondria's “Dance” (D. Shackleford)
- E-Cig Use Ages 18 to 29 (P. Bandi)
- Stopping Smoking Earlier in Life (F Islami)
- Most with Lung Cancer Smoked (A Jemal)
- Furthering Lung Cancer Screening & Equity (S Fedewa)
- Mouse Lung Organoids for Research (C Kim)
- Quality of Life for Lung Cancer Survivors (J Temel)
- Precision Therapies for NSCLC (P Jänne)
- Cancer Deaths from Smoking (F Islami)
- Lung Cancer Surgery Disparities (A Jemal)
- BRG1-Deficient Lung Cancers (C Kim)
- Yoga for Couples with Lung Cancer (K Milbury)
- Metabolic Differences as New Drug Targets (A Marcus)
- CPS-II & CPS-3 Inform About Risks of Ovarian Cancer
- Machine Learning & Glowing Nanosensors (D Heller)
- Ovarian Cancer May Start in Fallopian Tube Cells (K Lawrenson)
- New Gene Linked with Deadliest Type (C Han)
- Gene-Testing Tools May Personalize Care (A Sood)
- Chromosome-Hoarding Ovarian Cancer Cells & Treatment (J Sheltzer)
- Nanoparticles as Drug Delivery for Metastases (X Lu)
- Turning Off 2 Proteins to Slow HGSC (P Kreeger)
- Targeted Light Therapy in Mice (M Bai)
- Nanoparticles, CAR T, and CRISPR (M Stephan)
- Endometriosis & Ovarian Cancer in Mice (M Wilson)
- Ovarian Cancer Special Section
- UV Exposure, Melanoma, & Dark Skin Types (A. Adamson)
- Melanoma and Lipid Droplets (R. White)
- Zebrafish and Acral Melanoma (R. White)
- T-Cell Lymphoma and PD1 (J. Choi)
- New Drug Destroys Cancer-Causing Protein (C. Crews)
- Virus & Merkel Cell Skin Cancer (R. Wang)
- Non-Genetic Drug Resistance (S. Spencer)
- Hijacking the Body's Sugar (R. Wang)
- Telling about High Risk (P. Kanetsky)
- Brain Metastasis and Alzheimer’s (E. Hernando)
- Exhausted Melanoma "Killer" Cells (W. Cui)
New Findings About the Genetic Risks of Childhood Cancer
A large study of childhood cancer long-term survivors found new variants of cancer susceptibility genes that could inform and improve genetic counseling.
The Challenge
Treatment and supportive care for childhood cancers has greatly improved over the last decades. That means an increasing number of adults have a history of childhood cancer.
These survivors are at risk for developing several late and long-term effects from their cancer treatment, including a risk of the cancer returning and a small risk of developing another type of cancer.
One thing that contributes to both the risk of developing a childhood cancer and the risk of having late and long term effects is whether or not the child Inherited certain gene variants in cancer-susceptibility genes from one or both parents.
Most pediatric cancers have only been associated with a subset of cancer susceptibility genes. It is not known if variants in other cancer susceptibility genes, including those related to adult-onset cancers, are present in childhood cancer survivors.
The Research
To better understand the genetic causes of childhood cancers, a large group of scientists, including Ryan Diver, MSPH, and Lauren Teras, PhD, in Population Science in the American Cancer Society conducted a comprehensive analysis of 5,451 long-term cancer survivors from the Childhood Cancer Survivor Study (CCSS) who were studied for more than 30 years. For a comparison group—people without a history of childhood cancer—the scientists used data from the American Cancer Society’s Cancer Prevention Study II.
I’m a childhood cancer survivor myself, and my family was screened for genetic variants related to my cancer. However, the genes identified in this study were not considered at the time my family and I were screened. Following up on these findings with more research is key for finding the best treatment for childhood cancer patients and better genetic counseling for them and their families.”
Ryan Diver, MSPH
Population Science
American Cancer Society
The researchers identified pathogenic or likely pathogenic (P/LP) variants in cancer susceptibility genes not previously associated with pediatric cancer. They found that pediatric cancer survivors were more likely to have P/LP variants than those who hadn’t had a pediatric cancer. Additionally, the pediatric cancer survivors with more P/LP variants had worse survival than pediatric cancer survivors with fewer variants.
Inheriting Cancer Risks: Some Basic Terms
Permanent changes in the DNA sequence of a gene are called gene mutations. Some scientists think that “gene variant” is a more accurate term because changes in DNA do not always lead to disease. Sometimes “gene mutation” and “gene variant” are used as synonyms.
Genetic variants can have a large or small effect on the likelihood of developing a particular disease. The term “pathogenic” refers to something that causes a disease. When genetic variants lead to disease, they’re called pathogenic variants or pathogenic mutations.
Genes that are vulnerable to cancer-causing variants or changes are called cancer predisposition genes or cancer susceptibility genes. In some cases, a cancer predisposition gene variant is inherited, or passed along from generation to generation. Several dozen cancer-predisposition genes have been identified, and about 5 to 10% of all cancers result directly from variants in those genes that are inherited from a parent.
For example, BRCA1 and BRCA2 are inherited cancer predisposition genes. Mutations in these genes increase the risk for developing certain cancers.
The type of gene changes that get passed from parents to a child are called “germline variations.” When BRCA1 and BRCA2 mutations are passed down by parents, they’re an example of what are considered germline pathogenic variations.
Peoplewho inherit certain changed genes that make them more likely to develop cancer are said to have a genetic predisposition or a genetic susceptibility to a cancer or certain types of cancer. Sometimes this is referred to as having a family cancer syndrome.But having this doesn’t mean that person will develop cancer. And if they do develop cancer, it may not be caused by the inherited genetic mutation.
The term penetrance is used to describe how many people carrying a mutation in a cancer predisposition gene will eventually develop cancer. If everyone who inherits a mutation develops cancer, that mutation is said to have complete penetrance. If some people don’t, it’s incomplete or reduced penetrance. If most people with an inherited mutation develop cancer, that mutation has high penetrance. For example,pathogenic variations on the BRCA1 and BRCA2 genes are high-penetrance gene mutations. Other gene mutations are in categories considered to be moderate- or low-penetrance.
“This is an important study because it shows that pediatric cancer patients may have genetic variants in other cancer-related genes that they’re not aware of," says Ryan Diver, MSPH, a data analysis within ACS Population Science.
Here are two more noteworthy findings from this study.
- Many of the cancer survivors were recruited more than 10 years after their diagnosis, which suggests that these variants may continue to influence the development of late effects for much longer than shown in previous research.
- Several of the gene variants identified in the pediatric cancer survivors are typically associated with adult cancers but not childhood cancers, such as BRCA2 in breast cancer.
Why it Matters
This large pediatric cancer study identified that pediatric cancer patients are more likely to have variants in cancer-susceptibility genes that have not previously been associated with the type of cancer they had.
Further characterization of variants in these genes is necessary to provide the most helpful genetic counseling for childhood cancer patients and their families. For patients, identification of additional gene variants could change treatment options and follow-up procedures. For older childhood cancer survivors, this new information may influence changes to the guidelines for genetic screening to improve the prevention of late effects, like the recurrence of the cancer or development of a second type of cancer.