The American Cancer Society estimates health care providers will diagnose 232,670 new cases of invasive breast cancer and 62,570 incidences of ductal carcinoma in U.S. women during 2014. Mortality peaked at a rate of 33 deaths for every 100,000 women in 1989 and 1990. Thanks to increased awareness, early detection and innovative prediction, diagnostic and treatment methods, breast cancer death rates have declined steadily since then.
Mole Count Raises Breast Cancer Risk
Most adults have 10 to 40 cutaneous nevi, or skin moles, on areas above their waists that receive sun exposure. Because research has linked 50 or more moles to increased melanoma risk, researchers tested their relationship to breast cancer. In America, investigators analyzed data from the Nurses’ Health Study that tracked 74,523 women for 24 years. Meanwhile in France, another research team evaluated the E3N Teachers’ Study Cohort that monitored 89,902 women for 18 years. These of mostly white women found that a higher mole count on their left arms may be a marker for breast cancer risk. In the nurse study, women with 15 or more moles were 35 percent more likely to develop breast cancer than those without moles. The absolute risk was 11.4 percent for women with moles and 8.48 percent for those without. Postmenopausal women with six or more moles had higher estrogen and testosterone blood levels than those without moles. The association between moles and breast cancer risk disappeared after researchers adjusted for hormone levels. This study concluded that sex hormones, which may contribute to breast cancer, also affect moles. The teacher study classified participants as having very many, many, a few or no moles. Women in the highest category had a 13 percent higher breast cancer risk than those in the lowest. The association was no longer significant after researchers adjusted for breast cancer risk factors, especially benign breast disease and breast cancer family history, which correlated with higher mole numbers. Researchers determined that genes affect both mole and breast cancer risks.
Previously, doctors classified cancers only on where they originated in your body and how they looked under a microscope. But one treatment didn’t always fit everyone. Research discovered that mutations in driver genes change how cancers behave and respond to treatment. A University of Washington team developed , a multiplexed gene-sequencing panel, to detect actionable mutations in 194 driver genes from tumor tissue. It includes genes related to cancer diagnosis, treatment and prognosis. Thanks to this precision medicine approach, your mutation profile will indicate how your cancer is likely to behave and which specific treatments from many therapeutic options will be most effective for your unique situation. Classifying your cancer and targeting your therapy this exclusively represent a paradigm shift in personalized cancer care that will improve your treatment and survival rate.
Revolutionary Treatment Delivery Method Triggers Cancer Cell Death
Biomedical engineering researchers developed a fast way to introduce a drug and its release mechanism into a cancer cell. Nanoscale lipid-based capsules, or liposomes, deliver both components. One set contains doxorubicin (Dox), an anti-cancer drug embedded in a complex of DNA molecules. The adenosine-5′-triphosphate (ATP), or energy molecule, in the second set of liposomes triggers the cancer drug’s release. Researchers likened this method to keeping a cancer-killing bomb and its detonator separate until both infiltrate a cancer cell where they combine to destroy it. When the DNA molecules encounter high ATP levels, they unfold and release the Dox. Positively charged lipids or peptides integrate the surface of the liposomes. They act as corkscrews to introduce the liposomes into the cancer cell. As the cancer cell absorbs the liposomes, an endosome seals them off from the rest of the cell. This compartment walls off all foreign material that gets into a cell. The environment inside the endosome is acidic, which causes the Dox and ATP liposomes to fuse together as well as to the endosome wall. Meanwhile, two other things happen simultaneously. First, the ATP liposomes spill their contents into the Dox liposomes, releasing the drug from its DNA cage. Second, the walls of the Dox liposomes create an opening in the endosome, spilling their Dox-rich contents into the surrounding cell, leading to cell death. Researchers found that the new technique killed breast cancer cells and decreased tumor size significantly in mice, compared to Dox treatment without liposomes.
Early Detection and Treatment Save Lives
The American Cancer Society’s recommended screening schedule helps detect breast cancer before it starts to cause symptoms. Breast self-exams should start in your 20s. Clinical breast exams should occur about every three years in your 20s and 30s and every year when you’re 40 and over. Annual mammograms should start at 40. Due to family history, genetic tendencies and other factors, some women should undergo both MRI and mammogram screenings. You should know how your breasts look and feel normally and report any changes to your doctor promptly. Early detection tests save thousands of lives each year. At early states, breast cancer is more likely to be smaller and confined to your breast. Depending on your condition, you may be able to take a prescription medication like Capecitabine at home instead of undergoing surgery, chemotherapy or radiation. After successful treatment, you can join the growing throng of America’s 2.8 million plus breast cancer survivors.