Monday, March 18, 2019
Experimental Drug Boosts Ovarian Cancer Survival Rates
Hematologist and oncologist Kenneth D. Nahum, DO, practices at Regional Cancer Care Associates, LLC, in Howell, New Jersey. With more than three decades of medical experience, he has skillfully divided his time between clinical practice and medical research. Over the years, Dr. Kenneth D. Nahum has studied numerous conditions, including ovarian cancer.
A deadly form of cancer, ovarian cancer has nearly a 70 percent recurrence rate. The reason for this high rate of recurrence relates to the continued presence of stem-like cells in the body once ovarian cancer is treated. Upon diagnosis, patients usually go through a round of chemotherapy or other treatments. These kill 90 to 99 percent of ovarian cancer cells, thus effectively sending the condition into remission.
However, routine ovarian cancer treatment does not kill stem-like ovarian cancer cells. These cells behave similarly to a plant and can take root in the body after ovarian cancer is destroyed. Over time, the cells grow into a new tumor, a process that can be enabled when as few 11 stem-like cells are left behind.
To address this issue, researchers from the University of Pittsburgh, Magee-Womens Research Institute (MWRI), and UPMC Hillman Cancer Center examined the efficacy of a new drug that targets these stem-like cells. An experimental drug known as 673A was discovered by these researchers and tested in mice with ovarian cancer cells. When used in combination with chemotherapy, this drug significantly improves survival rates among mice with ovarian cancer.
673A works by targeting the ALDH pathway in the body. This pathway clears the toxins produced by stem-like cells, thus allowing them to multiply so quickly. While 673A only kills 3 to 5 percent of stem-like cells, the impact was significant and allowed roughly 60 percent of mice treated with chemotherapy and the drug to survive past the six-month point. Only 10 percent of mice treated with just chemotherapy survived to this point.
Thursday, March 7, 2019
Researchers Discover and Block Activating Protein Related to Melanoma
For more than four decades, Kenneth D. Nahum, MD, has been working as a physician. A hematologist and oncologist practicing at Regional Cancer Care Associates (RCCA), he treats patients with cancer or blood disorders. Dr. Kenneth D. Nahum routinely conducts research on numerous conditions, including melanoma.
It’s predicted that roughly 96,000 new cases of melanoma will be diagnosed in the United States in 2019 and over 7,000 Americans will die of the disease. However, researchers recently discovered a possible way to manage melanomas and other cancers.
Researchers focused on NRAS, a gene responsible for instructing cells to produce an NRAS protein. Mutations in this gene have previously been linked to roughly 25 percent of skin cancers.
However, for NRAS to trigger the development of cancer, it must be activated by another protein. Researchers tested several proteins to determine how they affect NRAS activity and discovered that STK19 appears to be the primary activating protein.
While NRAS activity cannot be disabled, STK19 gene activity can be disabled with a new drug compound. When STK19 was blocked from activating NRAS in animal models and skin cells, it kept melanoma from developing. More research is needed, but researchers hope this discovery will pave the way for new treatments for difficult-to-cure cancer via the identification and blocking of activating proteins.
It’s predicted that roughly 96,000 new cases of melanoma will be diagnosed in the United States in 2019 and over 7,000 Americans will die of the disease. However, researchers recently discovered a possible way to manage melanomas and other cancers.
Researchers focused on NRAS, a gene responsible for instructing cells to produce an NRAS protein. Mutations in this gene have previously been linked to roughly 25 percent of skin cancers.
However, for NRAS to trigger the development of cancer, it must be activated by another protein. Researchers tested several proteins to determine how they affect NRAS activity and discovered that STK19 appears to be the primary activating protein.
While NRAS activity cannot be disabled, STK19 gene activity can be disabled with a new drug compound. When STK19 was blocked from activating NRAS in animal models and skin cells, it kept melanoma from developing. More research is needed, but researchers hope this discovery will pave the way for new treatments for difficult-to-cure cancer via the identification and blocking of activating proteins.
Monday, February 25, 2019
Iron Deficiency Anemia Higher among Adolescent Female Blood Donors
An oncologist and hematologist, Dr. Kenneth D. Nahum has been practicing medicine for upwards of 35 years. Through both his clinical and research experience, Dr. Kenneth D. Nahum has experience treating dozens of conditions, including iron deficiency anemia.
According to recent research from the Johns Hopkins University School of Medicine, adolescent females have an increased risk of iron deficiency anemia and other adverse effects, such as fainting, after they donate blood. This is believed to occur because adolescent girls typically have a lower blood volume and higher iron levels than their adult peers. Because of this, adolescent donors lose more iron than adult donors, despite giving the same amount of blood.
Rather than discouraging adolescent donors from giving blood, this information should encourage adolescent females to prepare for their blood donation by taking iron tablets and eating green vegetables and other iron-rich foods. Further, adolescent females should limit the number of times they donate.
In the United States, this age group can donate blood every eight weeks as long as they meet weight requirements. However, additional policies to protect this group from adverse health reactions is advised by researchers.
Sunday, February 17, 2019
Jersey Shore University Medical Center Offers Collaborative Care
A hematologist and an oncologist at Regional Cancer Care Associates, LLC, in New Jersey, Kenneth D. Nahum, DO, has received New Jersey Monthly Magazine’s Top Doctors award four times. Frequently offering his support to health-related charities, Dr. Kenneth D. Nahum served for six years as a co-chair of the Sweetheart Ball fundraiser benefiting the cancer program at Jersey Shore University Medical Center.
Jersey Shore cancer treatment is built around a collaborative care model. Each patient is assigned a comprehensive care team that includes a radiation oncologist, medical oncologist, radiation therapist, diagnosing and treating surgeon, and primary care physician. For patients with aggressive cancers who may benefit from emerging treatments, Jersey Shore participates in clinical trials run by The Cancer Institute of New Jersey and the Radiation Therapy Oncology Group.
The Center also features a unique patient-centered program known as Nurse Navigation, where registered nurses provide patients with logistical and emotional support throughout the treatment process, including with social service and insurance paperwork. Aside from cancer treatments, Jersey Shore offers patients rehabilitation services, nutrition counseling, support groups, and genetic testing to support whole patient care from initial testing through recovery.
Sunday, February 3, 2019
Possible Causes of Neuroblastoma
New Jersey-based physician Kenneth D. Nahum, DO, practices as a hematologist and an oncologist at Regional Cancer Care Associates, LLC, in Howell. With more than three decades of experience in the field, Dr. Kenneth D. Nahum has cared for thousands of patients with various cancers and blood disorders.
Although cancer is most often thought of as an adult condition, it can occur in infants and children, as is the case with neuroblastomas. The most common type of cancer affecting infants, this rare form of cancer is normally found in children aged 5 or younger. It occurs when a solid tumor grows from immature nerve cells, or neuroblasts, in the body.
As a fetus develops, its neuroblasts should turn into nerve cells, fibers, and other cells that make up the adrenal glands. In most cases, the neuroblasts mature by the time a fetus is born, but they can occasionally mature after birth, as well. These immature cells will continue to mature after birth; however, sometimes they start growing uncontrollably and form a tumor, or neuroblastoma, instead.
Scientists aren’t sure exactly what causes the neuroblasts to become cancerous in some patients, though they have linked the condition to genetics. DNA changes that turn on oncogenes, which help cells grow and divide, increase the risk of neuroblastomas. The same is true of changes that turn off tumor suppressor genes that are responsible for controlling cell death.
Specific chromosome changes, including mutations to the ALK oncogene and PHOX2B gene, the latter of which helps nerve cells mature, have also been linked to the development of neuroblastomas. These specific changes are inherited by parents. Oncogene and tumor suppressor gene changes may also be inherited by parents, but some patients do experience these changes naturally over time.
Despite the genetic link, and the fact that infants have a higher chance of developing neuroblastoma if there is a family history of the condition, most neuroblastomas form spontaneously.
Although cancer is most often thought of as an adult condition, it can occur in infants and children, as is the case with neuroblastomas. The most common type of cancer affecting infants, this rare form of cancer is normally found in children aged 5 or younger. It occurs when a solid tumor grows from immature nerve cells, or neuroblasts, in the body.
As a fetus develops, its neuroblasts should turn into nerve cells, fibers, and other cells that make up the adrenal glands. In most cases, the neuroblasts mature by the time a fetus is born, but they can occasionally mature after birth, as well. These immature cells will continue to mature after birth; however, sometimes they start growing uncontrollably and form a tumor, or neuroblastoma, instead.
Scientists aren’t sure exactly what causes the neuroblasts to become cancerous in some patients, though they have linked the condition to genetics. DNA changes that turn on oncogenes, which help cells grow and divide, increase the risk of neuroblastomas. The same is true of changes that turn off tumor suppressor genes that are responsible for controlling cell death.
Specific chromosome changes, including mutations to the ALK oncogene and PHOX2B gene, the latter of which helps nerve cells mature, have also been linked to the development of neuroblastomas. These specific changes are inherited by parents. Oncogene and tumor suppressor gene changes may also be inherited by parents, but some patients do experience these changes naturally over time.
Despite the genetic link, and the fact that infants have a higher chance of developing neuroblastoma if there is a family history of the condition, most neuroblastomas form spontaneously.
Tuesday, January 22, 2019
Medical Journal Reports Possible New Treatment for Cold Agglutinin
Responsible for treating thousands of hematology and oncology patients over the past 30 years, Kenneth D. Nahum, DO, works at Regional Cancer Care Associates, LLC, in Howell, New Jersey. Active in his professional community, Dr. Kenneth D. Nahum maintains membership with the American Society of Hematology (ASH).
ASH’s medical journal, Blood, recently reported exciting news about the effort to develop a treatment for cold agglutinin disease, a rare blood disorder with no approved treatment at present. Affecting about 10,000 people in the United States and Europe, cold agglutinin is an immune system malfunction that mistakenly causes antibodies to target and destroy red blood cells faster than the bone marrow can replace them.
As reported in Blood, the first clinical trial with 10 humans showed the investigational drug sutimlimab may be an effective treatment for cold agglutinin disease. Sutimlimab, which is a specific C1s inhibitor, showed the ability to prevent red blood cell destruction and increase hemoglobin levels in seven of the 10 patients. The patients who responded well to the new drug therapy no longer had the need for transfusions.
Wednesday, January 16, 2019
Study Finds Link between Persistent VMS and Breast Cancer Risk
New Jersey-based oncologist and hematologist Kenneth D. Nahum, MD, treats patients with blood disorders and cancers at Regional Cancer Care Associates (RCCA). With more than 30 years of medical and clinical research experience, Dr. Kenneth D. Nahum has treated many instances of breast cancer.
A recent study published in the journal of the North American Menopause Society (NAMS), revealed a link between breast cancer and vasomotor symptoms (VMS). Researchers looked at more than 25,000 women over the course of nearly 18 years.
In this period, 1,399 cases of new breast cancer were diagnosed among participants. Many of the women with breast cancer had experienced persistent VMS symptoms, such as night sweats and hot flashes, that lasted for at least 10 years. Breast cancer rates were lower among women who had not experienced persistent VMS.
Researchers also looked at the survival rates of women with and without persistent VMS after they were diagnosed with breast cancer. While a small difference was seen, it was not statistically significant, which suggests that persistent VMS did not affect survival rates of women with breast cancer.
Saturday, January 12, 2019
Common Types of Hemophilia
Dr. Kenneth D. Nahum, an experienced clinical researcher, has served as an investigator in more than 70 drug studies over the course of 20 years. In addition, Kenneth D. Nahum, MD, serves as an oncologist (a doctor who specializes in the diagnosis and treatment of cancer) and a hematologist (a doctor who specializes in diseases related to blood).
Hemophilia is an inherited condition in which the blood lacks the protein it needs to properly clot. Hemophilia is usually seen as one of two types: A or B.
Hemophilia A, which accounts for roughly 80 percent of all hemophilia cases, is caused by defective or missing Factor VIII, an essential blood-clotting protein. People with defective or missing Factor VIII develop mild, moderate, or severe hemophilia A.
In most situations, hemophilia A is inherited on the X chromosome. However, the condition may develop because of a spontaneous genetic mutation, which accounts for roughly a third of all hemophilia A cases.
Meanwhile, hemophilia B is caused by a deficiency in Factor IX. In most ways, hemophilia B functions the same as hemophilia A. B is inherited on the X chromosome, but it can develop from a spontaneous mutation. Despite these similarities, the chance of developing hemophilia B is about four times lower than the chance of developing hemophilia A.
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