Have you ever known of anyone that had tumors removed from their heart? If you haven't it is because it is not very common.
Human heart cancer
health care medicine concept with the inner human organ and red cancer
cells forming tumors spreading in the body as a malignant disease that
needs chemotherapy or heart surgery.
Classification and external resources
Heart cancer is an extremely rare form of cancer that is divided into primary tumors of the heart and secondary tumors of the heart.
Most heart tumors are benign myxomas, fibromas, rhabdomyomas, and hamartomas, although malignant sarcomas (such as angiosarcoma or cardiac sarcoma)
have been known to occur. In a study of 12,487 autopsies performed in
Hong Kong seven cardiac tumors were found, most of which were benign. According to Mayo Clinic: "At Mayo Clinic, on average only one case of heart cancer is seen each year."
Video of a removal of a cardiac tumor.
For more information go to www.mayoclinic.com or
http://en.wikipedia.org/wiki/Heart_cancer
Phase 2 study has been completed for the drug , blinatumomab (AMG 103. The success for this drug of patients with relapsed lymphoblastic leukemia and refractory B-precursor acute lyphoblastic leukemia was phenomenal.
AMG 103) helped achieve a high-rate of complete response (CR) in 72
percent of adult patients with relapsed or refractory B-precursor acute
lymphoblastic leukemia (ALL) treated in the study. Blinatumomab is the
first of a new class of agents called bi-specific T cell engagers
(BiTE®) antibodies, designed to harness the body's cell-destroying T
cells to kill cancer cells. Blinatumomab targets cells expressing CD19,
a protein found on the surface of B-cell derived leukemias and
lymphomas, such as ALL. Full results of the study will be presented
during an oral abstract session at the 48th Annual Meeting of the
American Society of Clinical Oncology (ASCO) on June 4 (Abstract Number
6500, 8:00 a.m. - 8:15 a.m. CDT, E354a).
In this Phase 2 single-arm dose-ranging trial, 26 of the 36 patients
treated with blinatumomab across all of the tested doses and schedules
achieved a CR with partial hematologic recovery (CRh*). All but two
patients achieved a molecular response, meaning there was no evidence of
leukemic cells by polymerase chain reaction. No treatment related
deaths or serious adverse events (AEs) were reported in the study.
"For these patients with limited treatment options, the remission rate
observed in the trial is a vast improvement over the current standard of
care," said Professor Max Topp, Department of Internal Medicine II,
University of Wuerzburg and chair of the study. "These results also
represent significant progress in our research of immunotherapies; a new
approach to fighting cancer that we believe could make a real
difference for patients."
Explanation of Immunotherapy for Fighting Cancer
Phase 2 Study DesignThis Phase 2 dose-ranging study evaluated the
efficacy, safety and tolerability of blinatumomab in adult patients with
B-precursor ALL who had relapsed following treatment with standard
front-line chemotherapy or allogeneic stem cell transplant. Patients
received blinatumomab for 28 days followed by two weeks off therapy over
a six week treatment cycle, for up to five treatment cycles. Patients
received a continuous intravenous infusion of blinatumomab at an initial
dose of five or 15 micrograms per meter squared per day, ranging up to
30 micrograms for the remainder of the treatment. The primary endpoint
of the study was the rate of CR/CRh*. Secondary endpoints included
molecular response rate, duration of response and overall survival. As
of April 13, 2012, all 36 patients were evaluable for efficacy and
safety.
About BlinatumomabBlinatumomab (AMG 103) is a bispecific T cell engager
(BiTE®) antibody designed to direct the body's cell-destroying T cells
against target cells expressing CD19, a protein found on the surface of
B-cell derived leukemias and lymphomas. The modified antibodies are
designed to engage two different targets simultaneously, thereby
juxtaposing T cells to cancer cells. Blinatumomab is the first of the
BiTE antibodies and Amgen has received orphan drug designation from the
U.S. Food and Drug Administration for the treatment of ALL, chronic
lymphocytic leukemia (CLL), hairy cell leukemia, prolymphocytic leukemia
and indolent B cell lymphoma and from the European Medicines Agency for
the treatment of indolent B cell lymphoma, ALL, CLL and mantle cell
leukemia (MCL).
About ALLAcute lymphoblastic leukemia (ALL) is an aggressive cancer of
the blood and bone marrow -- the spongy tissue inside bones where blood
cells are made. The disease progresses rapidly and affects immature
blood cells, rather than mature ones.(1) Worldwide, ALL accounts for
more than 12 percent of leukemia. Of the 42,000 people diagnosed
worldwide, 31,000 will die from the disease.(2) Patients with ALL have
abnormal white blood cells (lymphocytes) that crowd out healthy white
blood cells, red blood cells and platelets, leading to infection, anemia
(fatigue), easy bleeding and serious side effects.(3,4)
ww.marketwatch.com/story/amgens-bite-antibody-blinatumomab-amg-103-achieved-high-rate-of-complete-response-in-adult-patients-with-relapsed-or-refractory-acute-lymphoblastic-leukemia-2012-05-16
cute
lymphoblastic leukemia (ALL) is an aggressive cancer of the blood and
bone marrow — the spongy tissue inside bones where blood cells are made.
The disease progresses rapidly and affects immature blood cells, rather
than mature ones.(1) Worldwide, ALL accounts for more than 12 percent
of leukemia. Of the 42,000 people diagnosed worldwide, 31,000 will die
from the disease.(2) Patients with ALL have abnormal white blood cells
(lymphocytes) that crowd out healthy white blood cells, red blood cells
and platelets, leading to infection, anemia (fatigue), easy bleeding and
serious side effects.(3,4)
cute
lymphoblastic leukemia (ALL) is an aggressive cancer of the blood and
bone marrow — the spongy tissue inside bones where blood cells are made.
The disease progresses rapidly and affects immature blood cells, rather
than mature ones.(1) Worldwide, ALL accounts for more than 12 percent
of leukemia. Of the 42,000 people diagnosed worldwide, 31,000 will die
from the disease.(2) Patients with ALL have abnormal white blood cells
(lymphocytes) that crowd out healthy white blood cells, red blood cells
and platelets, leading to infection, anemia (fatigue), easy bleeding and
serious side effects.(3,4)
Acute
lymphoblastic leukemia (ALL) is an aggressive cancer of the blood and
bone marrow — the spongy tissue inside bones where blood cells are made.
The disease progresses rapidly and affects immature blood cells, rather
than mature ones.(1) Worldwide, ALL accounts for more than 12 percent
of leukemia. Of the 42,000 people diagnosed worldwide, 31,000 will die
from the disease.(2) Patients with ALL have abnormal white blood cells
(lymphocytes) that crowd out healthy white blood cells, red blood cells
and platelets, leading to infection, anemia (fatigue), easy bleeding and
serious side effects.(3,4)
Acute
lymphoblastic leukemia (ALL) is an aggressive cancer of the blood and
bone marrow — the spongy tissue inside bones where blood cells are made.
The disease progresses rapidly and affects immature blood cells, rather
than mature ones.(1) Worldwide, ALL accounts for more than 12 percent
of leukemia. Of the 42,000 people diagnosed worldwide, 31,000 will die
from the disease.(2) Patients with ALL have abnormal white blood cells
(lymphocytes) that crowd out healthy white blood cells, red blood cells
and platelets, leading to infection, anemia (fatigue), easy bleeding and
serious side effects.(3,4)
You may be asking yourself the question as to why a government panel would reject a prostate screening test that could save a life. This news is getting posted on many medical websites.
The panel decided that the harm of the screening test outweighs the benefit for preventing prostate cancer.
The following is an article from a Boston publication.
The US Preventive Services Task Force determined that based on evidence
from two large randomized trials, the lifesaving benefits of screening
were “at best very small” and were offset by overdiagnosis and
overtreatment of non-lethal cancers.
.“Our most optimistic estimate is that 1 out of 1,000 men screened will
avoid dying from prostate cancer” because of early detection via the PSA
test, said Dr. Michael LeFevre, co-vice chair of the task force. “We’re
not saying it’s zero. We’re leaving the window open for at least a
small benefit.”
“It’s hard to understand where they’re coming from,” said Dr. Anthony
D’Amico, chief of genitourinary radiation oncology at Brigham and
Women’s Hospital, in an interview.
D’Amico argued that the task force relied too heavily on data from a
flawed study and failed to consider making separate recommendations for
men in high-risk groups, such as those with a family history of prostate
cancer and African Americans, who have a two to three times greater
risk of dying of the cancer than white men.
The task force, which is comprised of 16 primary care physicians and
public health experts with no financial interests in tests or
treatments, issues screening and other preventive health recommendations
that tend to be more conservative than those of medical societies --
composed mostly of specialists who treat diseases detected through
screening -- or patient advocacy groups.
Former New England Patriots player Mike Haynes, a paid spokesperson for
the urological association, said in an interview that he was diagnosed
with prostate cancer in 2008, at age 55, after getting a free screening
PSA test at an NFL event for retired players, sponsored by the
urological association. He said he wasn’t told about any of the risks of
the tests such as false positive results, unnecessary biopsies, and
overtreatment of slow-growing cancers. His elevated PSA and subsequent
biopsy revealed a stage 1, slow-growing cancer, and he said, “one of my
options was watchful waiting, but my immediate reaction was let’s get it
out of my system.”
He considers himself lucky, however, in that the only side effect he had
from his surgery was a few months of urinary incontinence that has
since resolved.
A wonderful explanation for us to understand 'triple negative breast cancer' is found at breastcancer.org.
To understand triple-negative breast cancer, it’s important to understand receptors, which are proteins found inside and on the surface of cells. These receptor proteins are the “eyes” and “ears” of the cells, receiving messages from substances in the bloodstream and then telling the cells what to do.
Hormone receptors inside and on the surface of healthy breast cells receive messages from the hormones estrogen and progesterone. The hormones attach to the receptors and provide instructions that help the cells continue to grow and function well. Most, but not all, breast cancer cells also have these hormone receptors. Roughly 2 out of 3 women have breast cancer that tests positive for hormone receptors. (For a more complete explanation, see the previous section on Hormone Receptor Status.)
A smaller percentage of breast cancers — about 20-30% — have too many HER2 receptors. In normal, healthy breast cells, HER2 receptors receive signals that stimulate their growth. With too many HER2 receptors, however, breast cancer cells grow and divide too quickly. (For a more complete explanation, see the previous section on HER2 Status.)
Hormonal therapies and HER2-targeted therapies work to interfere with the effects of hormones and HER2 on breast cancer, which can help slow or even stop the growth of breast cancer cells.
About 10-20% of breast cancers test negative for both hormone receptors and HER2 in the lab, which means they are triple-negative. Since hormones are not supporting its growth, the cancer is unlikely to respond to hormonal therapies, including tamoxifen, Arimidex (chemical name: anastrozole), Aromasin (chemical name: exemestane), Femara (chemical name: letrozole), and Faslodex (chemical name: fulvestrant). Triple-negative breast cancer also is unlikely to respond to medications that target HER2, such as Herceptin (chemical name: trastuzumab) or Tykerb (chemical name: lapatinib)
The Biology of Triple Negative Breast Cancer
In addition, triple-negative breast cancer
Tends to be more aggressive than other types of breast cancer. Studies have shown that triple-negative breast cancer is more likely to spread beyond the breast and more likely to recur (come back) after treatment. These risks appear to be greatest in the first few years after treatment. For example, a study of more than 1,600 women in Canada published in 2007 found that women with triple-negative breast cancer were at higher risk of having the cancer recur outside the breast — but only for the first 3 years. Other studies have reached similar conclusions. As years go by, the risks of the triple-negative breast cancer recurring become similar to those risk levels for other types of breast cancer.
Tends to be higher grade than other types of breast cancer.The higher the grade, the less the cancer cells resemble normal, healthy breast cells in their appearance and growth patterns. On a scale of 1 to 3, triple-negative breast cancer often is grade 3.
Usually is a cell type called “basal-like.”“Basal-like” means that the cells resemble the basal cells that line the breast ducts. This is a new subtype of breast cancer that researchers have identified using gene analysis technology. Like other types of breast cancer, basal-like cancers can be linked to family history, or they can happen without any apparent family link. Basal-like cancers tend to be more aggressive, higher grade cancers — just like triple-negative breast cancers. It’s believed that most triple-negative breast cancers are of the basal-like cell type.
The following video is very informational about when genetic testing should be done pertaining to cancer. This question and answer time is with a panel of oncolgists at MD Anderson Cancer Center which is one of the leading cancer centers in the United States. If you have cancer in your family then you must view this video!
How
often you should get tested for breast cancer depends on your chances
for getting the disease. If you are at increased risk for breast
cancer, you may need to start screening exams at an earlier age, get
additional tests or be tested more often.
Learn when genetic testing makes sense for you.
Dr.
Banu Arun, Professor of Breast Medical Oncology and Co-Director of
Clinical Cancer Genetics at The University of Texas MD Anderson Cancer
Center and Diana Turco, Certified Genetic Counselor in Clinical Cancer
Genetics, answer common questions regarding hereditary risk factors for
breast cancer. Dr. Jennifer Litton, Assistant Professor of Breast
Medical Oncology, at The University of Texas MD Anderson Cancer Center
moderates the discussion.
I hope that this video was very helpful and please share this with others that are concerned about their family history of cancer.
Primitive neuroectodermal tumors or PNET are very rare group of tumors that are highly malignant. In clinical manifestation these tumors exhibit great diversity. They manifest in the bone and soft tissue. Pathologist find them very difficult to distinguish because they have similarities to other small, round tumors.
PNET tumors under a microscan
PNET tumors are classified into three groups.
I. CNS primitive neuroectodermal tumors (PNETs) - Tumors derived from the central nervous system
II. Neuroblastoma - Tumors derived from the autonomic nervous system
III.Peripheral primitive neuroectodermal tumors (pPNETs) - Tumors derived
from tissues outside the central and autonomic nervous system
This cancer is usually seen in children and adolescents and is very fast growing and can quickly metastasize to other organs.
Peripheral primitive neuroectodermal tumors (pPNETs) are also classified
as part of the Ewing family of tumors (EFTs); peripheral primitive
neuroectodermal tumors (pPNETs) and Ewing family of tumors (EFTs) are
often referred to interchangeably in the literature. Generally, Ewing
family of tumors (EFTs) and peripheral primitive neuroectodermal tumors
(pPNETs) represent different manifestations of the same tumor and have
similar genetic alterations. Ewing sarcoma, however, is more common in
bone, while peripheral primitive neuroectodermal tumors (pPNETs) are
more common in soft tissues. Immunohistochemical and cytogenetic studies
suggest that these tumors all have a common origin.
Tissue biopsy with cytogenetic and immunohistochemical studies is
paramount in diagnosing peripheral primitive neuroectodermal tumors
(pPNETs). Radiologic studies such as CT scans and MRI are essential in
determining the limits of tumor involvement and ruling out metastatic
disease. On CT scans, peripheral primitive neuroectodermal tumors
(pPNETs) appear as heterogeneous masses, often invading surrounding
tissues, including bone. MRI reveals a mass isointense to muscle on
T1-weighted images, while hyperintense on T2-weighted image
Chemotherapy and radiation are necessary adjuncts in the treatment of
primitive neuroectodermal tumors (PNETs). Chemotherapy regimens have
significantly improved outcomes in patients with peripheral primitive
neuroectodermal tumors (pPNETs). The treatment paradigms differ based on
whether the disease is localized or metastatic. As would be expected,
the treatments for peripheral primitive neuroectodermal tumors (pPNETs)
and Ewing family of tumors (EFTs) are similar in terms of
chemotherapeutic regimens.
Current recommendations advocate
complete surgical resection whenever possible, adjuvant versus
neoadjuvant chemotherapy, and radiotherapy. Multimodality treatment is
advocated to prevent metastatic disease, recurrent disease, and to treat
residual tumor after resection. Carvajal and Meyers, in a comprehensive
review of the chemotherapeutic regimens in the treatment of PNETs and
Ewing family of
tumors (EFTs), recommend a regimen that includes
vincristine, doxorubicin, and cyclophosphamide with ifosfamide and
etoposide.
For more specific information: http://emedicine.medscape.com/article/855644-overview#aw2aab6b8
Researcher finds problems with the fact that all women with ovarian cancer do not have access to top quality care to boost survival. Dr. Robert Bristow believes a decidedly low-tech approach could
significantly enhance the survival rate for ovarian cancer, even though
it’s the deadliest women’s reproductive cancer, claiming 15,000 lives
each year; it has no reliable screening or prevention methods; and its
research funding is about one-sixth the amount for breast cancer. According to CancerCenter.com recent study and interview there only need to be excellent care for all women concerning ovarian cancer.
“We don’t have to redesign a molecule to improve the outcome for women
with ovarian cancer,” says Bristow, the Philip J. DiSaia Chair in Gynecologic Oncology
and director of UC Irvine’s Division of Gynecologic Oncology. “Recent
research has shown that the most profound impact on survivorship occurs
when women get proper care from surgeons trained in the latest
techniques for treating ovarian cancer.”
The sad news is that it was discovered that women with low income and black women did not receive the excellent care as white women or affluent women. This study was done in March of 2012. Our health plans have got to change.
“Not all women are benefiting equally from improvements in ovarian cancer care,” Bristow says. “The reasons behind these disparities are not entirely clear, which is why we need additional research.”
For the women who did not receive excellent care due to race and social standing they also extended the research to see if when they were treated for ovarian cancer if the they followed the National Comprehensive Cancer Network treatment guidelines.
Bristow and colleagues found that five-year survival rates
varied significantly. (Improvement in ovarian cancer care is measured
in length of survival after diagnosis rather than a “cure” rate.)
Among those whose care met NCCN standards, the rate for white women
was 41.4 percent, compared with 33.3 percent for African American women.
Among those whose care did not meet NCCN standards, the rate for white
women was 37.8 percent, compared with 22.5 percent for African American
women. Those on Medicaid or without insurance faced a 30 percent
increased risk of death. Poor women – defined as having an annual
household income of less than $35,000 – had worse survival rates
regardless of race.
