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Carrie House, PhD

Carrie House, PhD

Carrie House, PhDSan Diego State University Research FoundationSan Diego, CA Role of Macrophages in the Development of Drug-Resistant Ovarian Cancer Stem Cells Following Chemotherapy Ovarian cancer is the deadliest gynecological cancer in the United States and is associated with a high rate of recurrence. Unfortunately, tumors that grow back stop responding to chemotherapy and become […]

Lori Brotto, PhD

Lori Brotto

Lori Brotto, PhDThe University of British Columbia2022 Maxine & Julie Eisen Pilot Study Award eSense Cancer: Adapting an online intervention for sexual health concerns to ovarian cancer Sexual health concerns are common after treatment of ovarian cancer, yet effective and accessible treatments to manage those concerns are not available. Dr. Brotto’s team has developed an […]

Priyanka Verma, PhD

Priyanka Verma

Priyanka Verma, PhDWashington University, St. Louis2022 MCM Pilot Study Award Targeting drug resistance in BRCA-mutant ovarian cancers by exploiting endogenous base damage Many ovarian cancers are caused by mutations in proteins that usually function to repair DNA damage. These cancer cells with accumulated DNA damage are targeted by PARP inhibitor therapies. Despite ovarian tumors showing […]

Hector Franco, PhD

Hector Franco

Hector Franco, PhDUniversity of North Carolina, Chapel Hill2022 Lester and Bernice Smith Pilot Study Award Identifying Drivers of Therapeutic Resistance in Ovarian Cancer at Single-Cell Resolution Ovarian cancer is one of the deadliest cancers among women worldwide. Most women respond well to the standard treatment; however, up to 75% of these patients experience a recurrence […]

Toni Antalis, PhD

Toni Antalis

Toni Antalis, PhDUniversity of Maryland, Baltimore2022 Rosser Family Pilot Study Award Emerging roles of MASP activation in ovarian cancer metastasis and acquired chemoresistance While ovarian cancer responds well to initial treatments, it frequently returns due to acquired chemotherapy resistance. Although chemotherapies aim slow or stop tumor growth, cancer cells continue to evolve between chemotherapy cycles. […]

Sneha Saxena, PhD

Sneha Saxena

Sneha Saxena, PhDMassachusetts General Hospital2022 James A. Harting Scientific Scholar Award Targeting ovarian cancer by exploiting a novel type of replication stress induced by unprocessed uracil in DNA Despite decades of work to develop new treatments, the five-year survival of patients with advanced ovarian cancer is between 10-30 percent. Hence, there is a pressing need […]

Sarah Gitto, PhD

Sarah Gitto

Sarah Gitto, PhDUniversity of Pennsylania2022 Pape Family Scientific Scholar Award Transcriptomic and proteomic analysis of tumor-specific TILs to enhance immunotherapy in ovarian cancer Immunotherapies aim to enhance the immune system’s capability of eliminating disease within the body. Often, immunotherapy for cancer targets a type of immune cell called T cells to activate their ability to […]

Z. Ping Lin, PhD

headshot-of-dr-lin

Targeting STAT3 Signaling for Immune Checkpoint Blockade to Augment PARP Inhibitor Therapy in BRCA-Mutated Ovarian Cancer  PARP inhibitors and immune checkpoint inhibitors are two promising new therapies for ovarian cancer patients who have mutations in the BRCA gene. BRCA-mutated ovarian cancer cells produce a protein called PD-L1 to avoid being recognized and killed by immune […]

Weei-Chin Lin, MD, PhD

Novel approaches to target MYC in ovarian cancer Many ovarian cancers express the cancer-causing MYC protein at unusually high levels. The activation of MYC is a hallmark of cancer initiation, progression, and resistance to therapy. Unfortunately, MYC is one of the most difficult proteins to target therapeutically. Development of an effective therapy against MYC activity […]

David George Huntsman, MD

Combining MEK inhibition with oncolytic viral therapy as a novel treatment for low grade serous ovarian carcinoma Low grade serous ovarian cancer (LGSC) is a rare form of ovarian cancer accounting for about 5% of ovarian cancer cases. While LGSC grows relatively slowly, it is stubbornly resistant to almost all therapeutics. As a result, outcomes […]


Talk to your Family

Talking to your family and identifying cancer in your family tree can be a good indicator of your health risks. Download our Family Tree Worksheet here.  Be sure to include yourself, children, parents, siblings, aunts, uncles, and grandparents.

Get Educated

Know your body and be proactive about your health. Learn about your breast and ovarian health. Learn about the risk factors and signs & symptoms for breast and ovarian cancer.

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Having a relationship with a health care provider you know and trust is one of the most important decisions you’ll make about your health care. Click here to find a provider

Higher Risk in the Ashkenazi Jewish Population

In the general population, around 1 in 400 people carry a BRCA1 or BRCA2 mutation. People of Ashkenazi Jewish ancestry have a 1 in 40 chance of carrying a BRCA mutation, making them 10 times as likely to carry a BRCA mutation as someone in the general population. Whether you’re a man or a woman, if you have a BRCA mutation then there is a 50% chance of passing the mutation on to your children, whether they are boys or girls. It’s important to note that these mutations significantly increase risk, but are not a guarantee a person will get cancer.

Why is the Ashkenazi Jewish population at higher risk?

Over 90% of the BRCA mutations found in the Jewish community are one of three “founder mutations”. A founder mutation is a specific gene mutation in a population that was founded by a small group of ancestors that were geographically or culturally isolated. Because the population was isolated, the rate of founder mutations in descendants is much higher than it would be if the population were larger and co-mingling with more genetically diverse populations. A large expansion in the population caused the current high frequency of the mutations in the Ashkenazi Jewish population. If you are of Ashkenazi Jewish ancestry, the chance of carrying a BRCA gene mutation compared to the general population is increased tenfold. BRCA mutations can be passed down from either your mother’s or father’s side, and may be associated with any of the following cancers:
  • Breast cancer
  • Ovarian cancer, fallopian tube, peritoneal cancer
  • Male breast cancer
  • Prostate cancer
  • Pancreatic cancer
  • Colon Cancer

Ready to take action? Knowledge is power. Take this short quiz to be proactive about your health.

Genes 101

Our bodies are made of many tiny building blocks called cells. Our cells contain a copy of our genome – all of the DNA genetic code we inherited from our parents. Our genome is organized into 46 chromosomes, 23 inherited from mom and 23 from dad. Each chromosome has hundreds or thousands of genes. Each gene has the instructions to make a protein that may control the structure or function of cells, can determine many things including how tall we are or the color of our eyes. Genes also contain instructions for many things inside of us that we cannot see, such as how our bones are formed or how our heart works. Each gene is made up of molecules called nucleic acids (A, T, C, and G). The specific sequence of the nucleic acids holds the instructions that control all the components and their functions in cells.

If the DNA sequence is changed, like a spelling mistake, the instructions may not make sense. The technical term for this change is “mutation,” meaning there is a change to the usual genetic code that may change the instructions stored in the gene. A mutation in a gene that repairs DNA damage or controls cell growth can increase the risk of developing cancer.

Sporadic vs Hereditary Cancers:

Ovarian and breast cancer can be either sporadic or hereditary. Sporadic cancers make up the vast majority (85-90%) of ovarian and breast cancers and are not associated with family history of either cancer or inherited cancer-associated mutations. Sporadic cancers arise from genetic mutations acquired in some cells of the body by events part of normal metabolism and environmental factors. This type of cancer can happen to anyone. Most acquired gene mutations are not shared among relatives or passed on to children.

Hereditary (also known as inherited, or familial) cancers are those that occur due to genetic mutations that are inherited from mom or dad. Other blood relatives may also share these same gene mutations. Parents give one copy of each gene to their children. If a parent has a genetic mutation in a gene, each of their children have a 50% chance of inheriting that mutation. Therefore, even in families with hereditary cancer, not all family members inherit the mutation that is causing cancer, and their risk of cancer is similar to the average person in the general population. Individuals who are suspected to have a family history with high incidence of ovarian, breast, and other cancers may be offered genetic testing to try to find the specific genetic mutation that may put them at risk. Importantly, individuals who do not have a known genetic mutation but have high incidence of ovarian, breast, or other cancers in their families are still considered at higher risk for developing those cancers.

Hereditary cancers often occur at an earlier age than the sporadic form of the same cancer, so experts often recommend starting cancer screening at a younger age for individuals at high risk for hereditary cancer. Hereditary cancers can also be more aggressive than the sporadic form of the same cancer. Individuals who have inherited a gene mutation may be at a higher risk for more than one type of cancer.

BRCA 1 and BRCA 2: Most Common hereditary breast and ovarian cancer

The genes that are most commonly involved in hereditary breast and ovarian cancer (HBOC) are BRCA1 and BRCA2. These genes are named for their link to breast (BR) cancer (CA), but they are also linked to ovarian cancer risk as well as other cancers. Both women and men can inherit mutations in these HBOC genes. BRCA1 and BRCA2 are tumor suppressor genes that have a usual role in our body of providing instructions on repairing DNA damage and preventing cancer. When a family has an inherited mutation in BRCA1 or BRCA2, this leads to an increase in cancer risk. Not every man or woman who has inherited a mutation in the BRCA1 or BRCA2 gene will develop cancer, but people who have a mutation do have a significanlty increased chance of developing cancer, particularly cancer of the breasts or ovaries.

While breast and ovarian cancers are the most common cancers diagnosed in people with BRCA1 and BRCA2 mutations, the risk of some other cancers is also increased. Men with BRCA1 and BRCA2 mutations have a higher risk of early-onset prostate cancer than men without mutations in either gene. Other cancers seen at increased rates, particularly in individuals with BRCA2 mutations, include pancreatic cancer and melanoma. Researchers are continuing to find new genes that are involved in hereditary breast and/or ovarian cancer so it is important to follow up with a genetic counselor on a regular basis if hereditary breast and ovarian cancer is likely in your family.

Talk to your family about your health history and take the Assess Your Risk quiz here

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