Friday, October 22, 2010

A Further Study on the Regulation of Cyclic Nucleotide Phosphodiesterase Activity in Neuroblastoma Cells: Effect of Growth

Adenosine 3',5'-cyclic monophosphate (cyclic AMP) phosphodiesterase activity in mouse neuroblastoma cells in culture markedly increased during exponential growth and reached a maximal level at confluency; whereas guanosine 3',5'-cyclic monophosphate (cyclic GMP) phosphodiesterase activity only slightly but significantly increased under a similar experimental condition. The increase in cyclic AMP phosphodiesterase activity was blocked by both cycloheximide and dactinomycin, whereas the increase in cyclic GMP phosphodiesterase was blocked by only cycloheximide. When the confluent cells were replated at low density, the cyclic nucleotide phosphodiesterase activity decreased; however, when they were plated at high cell density which equaled confluency, the enzyme activity did not decrease. Unlike cyclic AMP phosphodiesterase activity, cyclic GMP phosphodiesterase activity did not change significantly in prostaglandin cells, but decreased in cells treated with the inhibitor of phosphodiesterase. Like cyclic AMP phosphodiesterase activity, cyclic GMP phosphodiesterase activity also did not change in cells treated with serum-free medium, X-irradiation, sodium butyrate and 6-thioguanine.


Once again I will email you a copy if you would like is my email

Monday, October 18, 2010

Perinatal Risk Factors for Neuroblastoma

Neuroblastoma is the most common cancer among infants, suggesting an etiologic role for prenatal factors. In this case-cohort study, neuroblastoma cases (n = 529) diagnosed between 1985 and 2001 were identified from the New York State Cancer Registry and were matched to the electronic birth records for 1983–2001 from New York State and New York City. Controls (n = 12,010) were selected from the same birth cohorts. Analysis was stratified by age at diagnosis, with one to six months (younger infants), seven to 18 months (older infants), and older than 18 months (older children) analyzed separately. Perinatal exposure data was obtained from the birth certificates. No risk factors were identified to be consistently associated with risk across all three age groups. Generally, more risk factors were identified as associated with neuroblastoma among younger infants relative to older ages, including high birth weight, heavier maternal gestational weight gain, maternal hypertension, older maternal age, ultrasound, and respiratory distress. Among older infants, low birth weight was associated with increased risk while heavier maternal gestational weight gain was protective. In the oldest age group, first born status, primary cesarean delivery, prolonged labor and premature rupture of the membranes were associated with increased risk.

If you want a copy, I will email it to you, email me at, thank you.


Sunday, October 17, 2010

More about why I made this site

This is the reason I want to raise awareness of neuroblastoma in children and find a cure for this nasty disease. The kid's been through so much as have others and we need to put an end to this nonsense. Neuroblastoma in children is one of the most searched terms on google and all you usually get is wikipedia. I want all the information on the web about neuroblastoma in children, symptons, treatment, ongoing clinical trials, stages of neuroblastoma and neuroblastoma cancer in general in one easy to find place for all parents and people alike. Now if your looking for a post, just look on the right to the blog archive and you should find what you are looking for and if you want me to add something, I would be willing to. Thank you and raise the awareness in fighting neuroblastoma in children.

Wednesday, October 13, 2010


I surpassed my goal of getting 30 visitors to and got 8 more then my goal was! Keep it up! My next goal is for 50 a day! Today we've only had 3 but I posted in the post below information about neuroblastoma and pesticides effects. It is a journal article so you may need a membership or I can email you a copy of it.

God bless all those with, fighting or who have lost their battle with neuroblastoma

Histology and Cytogenetics

N-myc amplification. N-myc is an oncogene, or a gene (DNA sequence) that turns on cell growth. Amplification means that more than one copy is found in the cell.

Hyperploidy. A normal cell has 46 chromosomes. Cancer cells often have extra chromosomes, and this is termed "hyperploidy".

VMA/HVA ratio. This is the ratio of catecholamine metabolites found in the urine.

NSE. Neuron-specific enolase, a serum marker. This is an enzyme specific to the sympathetic nervous cells from which the neuroblastoma derives.

Serum ferritin. An accurate estimate of the body's iron stores; a serum marker.

LDH. Lactate dehydrogenase (LDH) is a group of enzymes that have a similar biological activity; a serum marker.

Gd2. Presence of this serum marker (a sialic acid-containing glycosphingolipid) may play a role in faster tumour progression.

CD44 antigen. The presence of this antigen indicates a particular developmental stage of the neuroblastoma cells.

TRK-A protooncogene. Again, oncogenes turn on cell growth.

1p deletion. Deletion on chromosome 1.


Residential Pesticides and Neuroblastoma

Neuroblastoma is the most common neoplasm in children under 1 year of age. We examined the relation between residential exposure to pesticides and neuroblastoma, using data from a case-control study of risk factors for neuroblastoma. Incident cases of neuroblastoma (N = 538) were identified through the Pediatric Oncology Group and the Children's Cancer Group. One age-matched control was identified for each case by random digit dialing. Telephone interviews with each parent collected information on residential exposure to pesticides. Pesticide use in both the home and garden were modestly associated with neuroblastoma [odds ratio (OR) = 1.6 (95% confidence interval [95% CI] = 1.0-2.3, and OR = 1.7 (95% CI = 0.9-2.1), respectively]. Compared with infants [OR = 1.0 (95% CI = 0.6-2.0)], stronger associations were found for garden pesticides in children diagnosed after 1 year of age [OR = 2.2 (95% CI = 1.3-3.6)], which suggests that pesticides may act through a mechanism more common for neuroblastomas in older children. There was no evidence of differential pesticide effects in subgroups of neuroblastoma defined by MYCN oncogene amplification or tumor stage.


Youll need to have an account to read or be a macomb student, i'm aware it should be somewhere else on the web as well.

Tuesday, October 12, 2010


This site has had 21 visitors, 9 more away from my goal of 30 a day! Keep it up! Raise awareness of neuroblastoma!

Results of the phase II, Hu CH14:18 +IL2 trial published. (not a new trial).

PURPOSE The hu14.18-IL2 fusion protein consists of interleukin-2 molecularly linked to a humanized monoclonal antibody that recognizes the GD2 disialoganglioside expressed on neuroblastoma cells. This phase II study assessed the antitumor activity of hu14.18-IL2 in two strata of patients with recurrent or refractory neuroblastoma. PATIENTS AND METHODS Hu14.18-IL2 was given intravenously (12 mg/m(2)/daily) for 3 days every 4 weeks for patients with disease measurable by standard radiographic criteria (stratum 1) and for patients with disease evaluable only by [(123)I]metaiodobenzylguanidine (MIBG) scintigraphy and/or bone marrow (BM) histology (stratum 2). Response was established by independent radiology review as well as BM histology and immunocytology, and durability was assessed by repeat evaluation after more than 3 weeks. Results Thirty-nine patients were enrolled (36 evaluable). No responses were seen in stratum 1 (n = 13). Of 23 evaluable patients in stratum 2, five patients (21.7%) responded; all had a complete response (CR) of 9, 13, 20, 30, and 35+ months duration. Grade 3 and 4 nonhematologic toxicities included capillary leak, hypoxia, pain, rash, allergic reaction, elevated transaminases, and hyperbilirubinemia. Two patients required dopamine for hypotension, and one patient required ventilatory support for hypoxia. Most toxicities were reversible within a few days of completing a treatment course and were expected based on phase I results. CONCLUSION Patients with disease evaluable only by MIBG and/or BM histology had a 21.7% CR rate to hu14.8-IL2, whereas patients with bulky disease did not respond. Hu14.18-IL2 warrants further testing in children with nonbulky high-risk neuroblastoma.

the full text is for paying customers only.

Monday, October 11, 2010


1. What is the theory behind antibody therapy?
A person's immune system makes antibodies to attack germs such as bacteria or viruses, but it will not attack neuroblastoma because the tumor is part of our own bodies. An antibody that attaches to neuroblastoma can be made in a laboratory and then given intravenously to a patient. This antibody will circulate in the bloodstream until it finds and attaches to a neuroblastoma cell. And then the patient's own immune system will attack and kill that neuroblastoma cell.

2. What is 3F8?
3F8 is the name of a substance called a monoclonal antibody. It attaches to GD2, which is a marker on the surface of neuroblastoma cells. 3F8 was produced by white blood cells of mice, and it must be carefully prepared for human use. 3F8 is part of our standard treatment for high-risk neuroblastoma.

3. How does 3F8 work?
When 3F8 is injected into the bloodstream, it travels through the body until it attaches to the marker GD2 that is present on all neuroblastoma cells. The attachment of 3F8 to a neuroblastoma cell signals the patient's own immune system (e.g. the white blood cells) to treat neuroblastoma cells as foreign. In other words, the 3F8 directs the patient's immune system, which ordinarily acts only to control infections, to attack neuroblastoma cells and kill them. The treatment is effective even when a patient's immune system has been weakened by chemotherapy treatments because chemotherapy does not affect the part of the immune system that responds to 3F8 antibodies. Over time, as the body's immune system becomes stronger, 3F8 treatments may help the body learn to fight tumors on its own.

4. How do we know 3F8 has reached neuroblastoma cells in patients?
When 3F8 is injected into the body, we attach a radioactive isotope called 131-iodine (131I) or 124-iodine (124I). A gamma camera or a PET scanner is then used to scan the patient's body, allowing us to see radioactivity (from the radioactive iodine) in areas with neuroblastoma, but not in parts of the body in which neuroblastoma cells are not present.

5. How long have 3F8 treatments been available?
Since 1987, over 30,000 infusions of 3F8 have been safely used in more than 500 patients. During this time, we have continued to make improvements to the effectiveness of 3F8 in killing neuroblastoma.

6. What types of 3F8 treatment are available?
We have a number of different 3F8 protocols available at any given time, each of which is the subject of a clinical trial. Patients are recruited for clinical trials every one to three months. Availability of particular protocols will depend in part on when the patient is ready to begin treatment.

As of early 2008, we are offering three primary protocols:

For patients who are in near-complete or complete remission after induction therapy, 3F8 treatment is combined with GM-CSF (a protein that enhances the functioning of 3F8). This is a phase II trial that builds on previous trials that have shown promise. See Protocol 03-077 for more details.

For patients who have disease present after induction therapy but no progression, protocol 03-077 and other protocols described below may be appropriate, depending on the particular circumstances of the patient.

For patients who do not show sufficient improvement after induction therapy or whose neuroblastoma has recurred or progressed, there are phase I trials that may be appropriate.

The first protocol, sometimes referred to as "dose escalated" 3F8, combines 3F8 with GM-CSF. This trial seeks to maximize the efficacy of 3F8 by determining the highest dose of 3F8 that can be given safely to patients.

The second protocol, often referred to as hot antibodies, couples 3F8 and radioactive iodine. This treatment uses 3F8 to seek out and attach to tumor cells and then to deliver radiation directly to kill the cells without damaging normal tissues.

7. Which patients are eligible for treatment with 3F8?
We have a number of 3F8 protocols for patients with high-risk neuroblastoma, including patients with bone marrow disease, bone disease, bulky disease (i.e., solid tumors), and relapsed and refractory disease. See the previous Q&A for an overview of the protocols and eligibility. Our clinical trial database also has information about specific protocols, including eligibility. The brief descriptions provided in the Q&A above and in the online clinical trial database are very general. Each patient must be evaluated to determine which protocol would likely be most effective for him or her. When necessary, we can customize a treatment regimen for individual patients, calling on many modalities, including chemotherapy, surgery, and radiation, to optimize the 3F8 treatment.

8. How is 3F8 administered?
3F8 is given intravenously through a Broviac, Hickman, MediPort, or peripheral line (all means of injecting substances into the bloodstream) on an outpatient basis. When being treated with 3F8, patients usually need to be in the clinic for about three hours. This includes time for giving medicines to prevent possible side effects, the 30-minute 3F8 treatment, and one to two hours to monitor the patient for side effects. 3F8 treatment is provided in one- or two-week cycles.

9. How long will a patient need to be treated with 3F8?
3F8 treatment is provided in what are referred to as rounds or cycles of one- or two-week periods of daily infusions (except weekends), approximately three weeks off in between rounds. The number of rounds of 3F8 treatment will vary depending upon the protocol, but typically patients will receive at least two to four rounds. The primary consideration in determining the length of 3F8 treatment is that we want patients to receive at least 400 mg/m2 of 3F8 before developing human anti-mouse antibodies (HAMA) to the 3F8. See below for more information about HAMA.

10. What are the common side effects of 3F8?
Pain is the main side effect. All patients have pain. The second most common side effect is rash (hives with itching), which is an allergic reaction. Pain can lead to a fast pulse (rapid heart rate) and sometimes causes high blood pressure for a short period. Less-common side effects include fever, vomiting, and diarrhea. These problems can usually be taken care of in the outpatient clinic, but sometimes a patient needs to be admitted to the hospital for an overnight stay. In the neuroblastoma outpatient clinic at Memorial Sloan-Kettering, we routinely treat 10 to 12 patients a day with 3F8, and manage side effects of the treatment without much difficulty.

11. Why does 3F8 cause pain?
3F8 attaches to GD2, which is present on some nerve cells as well as on neuroblastoma cells. When 3F8 attaches to a nerve cell, a message is sent to the brain, and the patient feels pain. The pain usually starts toward the middle or end of the daily 3F8 treatment and lasts a short time (usually from a few minutes up to an hour). Sometimes discomfort or minimal pain continues during the hours after the treatment. Medicines are used to prevent or control the pain (usually morphine or Dilaudid) and the allergic reactions (usually Benadryl or Vistaril). Ativan and Zofran are other medicines that can help. Patients who were treated with 3F8 beginning in 1986 have been followed, and to date, no permanent side effects on their nerves have appeared.

12. What is HAMA?
HAMA stands for "human anti-mouse antibodies." HAMA measures how strongly the body's immune system is reacting to 3F8. 3F8, like most monoclonal antibodies, comes from the white blood cells of a mouse. This means that 3F8 looks different from a human antibody, and thus patients will eventually form antibodies (HAMA) against 3F8. Once a patient has developed HAMA, 3F8 treatments no longer effective because the HAMA blocks the 3F8 from getting to neuroblastoma cells. If the patient has received the desired amount of 3F8 (see next question for further information) by the time HAMA has developed, then treatment with 3F8 will be discontinued. However, if the patient has not yet received the desired amount, it is possible that HAMA may recede, and in that case we can resume 3F8 treatments. We conduct a blood test for HAMA usually one to two weeks after each round of 3F8 infusions. Patients with HAMA usually do not have pain or other side effects from 3F8 treatment.

13. Is HAMA good or bad?
HAMA is a positive sign in that it may mean the patient is developing an immune response against the neuroblastoma. However, when HAMA develops before the patient has received the usual 400 mg/m2 of 3F8 (two to four cycles), it may interrupt treatment. (As noted above, once HAMA is present, the 3F8 treatment is no longer effective.) Once HAMA has receded, treatment can resume. Most patients who have received chemotherapy only a short time before 3F8 treatment do not produce HAMA because part of their immune system is too suppressed. In these cases, 3F8 treatment will usually continue for up to two years. The aim of our protocols is to give repeated treatments with 3F8 until HAMA is made, because we believe that approach yields the best chances for cure. We continue to study HAMA to get a better understanding of how it may hurt or benefit patients in the long term.

14. Is 3F8 made at Memorial Sloan-Kettering?
No. An outside company produces it for us under GMP (good manufacturing practice) conditions. Private funding from foundations and philanthropic benefactors has been critical in paying for the production of 3F8 and for carrying out tests to meet the many governmental safety requirements. We do not charge our patients for 3F8. While we have been successful in getting government funding for much of our laboratory science, the government does not support the manufacturing process for 3F8. It is our hope that 3F8 will soon become a licensed drug.

15. Is 3F8 treatment available to patients who received initial treatment at hospitals other than Memorial Sloan-Kettering?
Yes, as long as they meet the eligibility requirements of the individual treatment protocols.

16. Are there other treatment options for neuroblastoma at Memorial Sloan-Kettering aside from 3F8?
There are a number of phase I and phase II studies, as well as state-of-the-art chemotherapy currently being offered at Memorial Sloan-Kettering. Several promising approaches are in the pipeline waiting to be introduced into the clinic. See our clinical trial database for current information.


Stages of Neuroblastoma

After neuroblastoma has been diagnosed, tests are done to find out if cancer has spread from where it started to other parts of the body.

The process used to find out the extent or spread of cancer is called staging. The information gathered from the staging process helps determine the stage of the disease. For neuroblastoma, stage is one of the factors used to plan treatment. The following tests and procedures may be used to determine the stage:

Bone marrow aspiration and biopsy: The removal of bone marrow, blood, and a small piece of bone by inserting a hollow needle into the hipbone or breastbone. A pathologist views the bone marrow, blood, and bone under a microscope to look for signs of cancer.
Lymph nodebiopsy: The removal of all or part of a lymph node. A pathologist views the tissue under a microscope to look for cancer cells. One of the following types of biopsies may be done:
Excisional biopsy: The removal of an entire lymph node.
Incisional biopsy: The removal of part of a lymph node.
Core biopsy: The removal of tissue from a lymph node using a wide needle.
Fine-needle aspiration (FNA) biopsy: The removal of tissue or fluid from a lymph node using a thin needle.
CT scan (CAT scan): A procedure that makes a series of detailed pictures of areas inside the body, taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerized tomography, or computerized axial tomography.
MRI (magnetic resonance imaging): A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the body. This procedure is also called nuclear magnetic resonance imaging (NMRI).
X-rays of the chest, bones, and abdomen: An x-ray is a type of energy beam that can go through the body and onto film, making a picture of areas inside the body.
Ultrasound exam: A procedure in which high-energy sound waves (ultrasound) are bounced off internal tissues or organs and make echoes. The echoes form a picture of body tissues called a sonogram. The picture can be printed to be looked at later.
Radionuclide scan: A procedure to find areas in the body where cells, such as cancer cells, are dividing rapidly. A very small amount of radioactive material is swallowed or injected into a vein and travels through the bloodstream. The radioactive material collects in the bones or other tissues and is detected by a radiation-measuring device.
There are three ways that cancer spreads in the body.

Through tissue. Cancer invades the surrounding normal tissue.
Through the lymph system. Cancer invades the lymph system and travels through the lymph vessels to other places in the body.
Through the blood. Cancer invades the veins and capillaries and travels through the blood to other places in the body.
When cancer cells break away from the primary (original) tumor and travel through the lymph or blood to other places in the body, another (secondary) tumor may form. This process is called metastasis. The secondary (metastatic) tumor is the same type of cancer as the primary tumor. For example, if breast cancer spreads to the bones, the cancer cells in the bones are actually breast cancer cells. The disease is metastatic breast cancer, not bone cancer.

The following stages are used for neuroblastoma:

Stage 1

In stage 1, the tumor is in only one area and all of the tumor that can be seen is completely removed during surgery.

Stage 2

Stage 2 is divided into stage 2A and 2B.

Stage 2A: The tumor is in only one area and all of the tumor that can be seen cannot be completely removed during surgery.
Stage 2B: The tumor is in only one area and all of the tumor that can be seen may be completely removed during surgery. Cancercells are found in the lymph nodes near the tumor.
Stage 3

In stage 3, one of the following is true:

the tumor cannot be completely removed during surgery and has spread from one side of the body to the other side and may also have spread to nearby lymph nodes; or
the tumor is in only one area, on one side of the body, but has spread to lymph nodes on the other side of the body; or
the tumor is in the middle of the body and has spread to tissues or lymph nodes on both sides of the body, and the tumor cannot be removed by surgery.
Stage 4

Stage 4 is divided into stage 4 and stage 4S.

In stage 4, the tumor has spread to distant lymph nodes, the skin, or other parts of the body.
In stage 4S, the following are true:
the child is younger than 1 year; and
the cancer has spread to the skin, liver, and/or bone marrow; and
the tumor is in only one area and all of the tumor that can be seen may be completely removed during surgery; and/or
cancer cells may be found in the lymph nodes near the tumor.
Treatment of neuroblastoma is based on risk groups.

For many types of cancer, stages are used to plan treatment. For neuroblastoma, treatment depends on risk groups. The stage of neuroblastoma is one factor used to determine risk group. Other factors are the age of the child, tumor histology, and tumor biology.

There are 3 risk groups: low risk, intermediate risk, and high risk.

Low-risk and intermediate-risk neuroblastoma have a good chance of being cured.
High-risk neuroblastoma may be difficult to cure.


Sunday, October 10, 2010

Less-Intense Chemo Effective in Children with Intermediate-Risk Neuroblastoma

Infants and children with intermediate-risk neuroblastoma who received a less-intensive chemotherapy regimen had three-year overall survival rates as good as those patients in an earlier trial who received treatment that was more intensive and more toxic


Neuroblastoma, the fourth most common solid tumor in children under the age of 16, begins in immature nerve cells, most often in the adrenal gland, neck, chest, or spinal cord. Neuroblastoma is classified as low, intermediate, or high risk of disease recurrence after treatment, based on factors such as the patient’s age, how far the disease has spread (metastasized), and what genetic mutations are found in the tumor.

For neuroblastoma tumors that have already spread within a limited region at the time of diagnosis, doctors can use a combination of surgery and chemotherapy to kill both the original tumor and cancer cells elsewhere. For children with intermediate-risk neuroblastoma, this treatment approach is very effective at preventing the cancer from returning and also increases survival.

However, while effective, this approach requires many months to complete and causes potentially serious side effects, including damage to the kidneys, heart, and hearing as well as a temporary decrease in white blood cells that can expose the patient to dangerous infections.

The clinical trial described below examined whether a shorter, less-intense course of chemotherapy could be as effective in preventing disease recurrence and extending survival as more-intense regimens in children with intermediate-risk neuroblastoma.
The Study

Between March 1997 and May 2005, this single-arm phase III clinical trial (called A3961) enrolled 467 eligible patients with intermediate-risk neuroblastoma from participating hospitals in Australia, New Zealand, and North America. The study used historical patient controls. That is, the investigators compared the results from the A3961 trial to an earlier study (called CCG 3881) performed by the Children’s Cancer Group among a similar population of neuroblastoma patients who had received a more-intense chemotherapy regimen between 1989 and 1996.

All participants in the A3961 trial underwent initial surgery, and were divided into two groups based on the relative likelihood of tumor recurrence—a ‘favorable’ prognosis group and an ‘unfavorable’ prognosis group.

Infants and children in the favorable-prognosis group were scheduled to receive four cycles of chemotherapy, and those in the unfavorable-prognosis group were scheduled to receive eight cycles. If a patient in the favorable-prognosis group did not experience a satisfactory tumor response to the initial treatment, the patient could receive the full eight cycles of chemotherapy. The cycles consisted of different combinations of the drugs carboplatin, etoposide, cyclophosphamide, and doxorubicin.

Based on the results from the earlier CCG-3881 study, investigators determined that the less-intense regimen would be effective if more than 90 percent of A3961 participants were alive after three years of follow up.

The trial was organized by the Children’s Oncology Group. The lead author of the study is David L. Baker, M.B.B.S., director of the pediatric and adolescent hematology-oncology program at Princess Margaret Hospital for Children, Perth, Australia.

Of the 467 eligible patients, 362 were infants (under 1 year of age) and 105 were children. Seventy-one percent (330) of all patients had a favorable prognosis, and 29 percent (137) had an unfavorable prognosis. A total of 192 patients received only four cycles of chemotherapy. The other 275 received eight cycles (including 42 percent of those in the favorable prognosis group).

At three years of follow up, 96 percent of patients remained alive and 88 percent had no progression of their cancer, an outcome indicating that the treatment was indeed effective. What’s more, the patients’ overall length of treatment and the actual number of treatment days were much less compared to the CCG-3881 historical controls.

In the earlier study using a higher-intensity regimen, patients received 71 days of treatment over the course of 268 days. In the A3961 lower-intensity study, patients with an unfavorable prognosis received 18 days of treatment (a 75 percent reduction) over the course of 168 days (a 40 percent reduction). Patients in the favorable group received 10 days of treatment (an 85 percent reduction) over the course of 84 days (a 70 percent reduction).

Damage to the kidneys, heart, and hearing each occurred in less than 2 percent of patients. Almost 70 percent of patients experienced a reduction in their number of white blood cells, but this side effect went away after treatment ended. Four of the 467 patients died from treatment-related infections during the trial. Two patients developed a second cancer - acute myeloid leukemia.

While the overall side effects were acceptable after three years of follow up, “the long-term toxicity is unknown,” said pediatric oncologist Andrew Pearson from the Royal Marsden Hospital, Surrey, United Kingdom, in a discussion at the ASCO meeting. Because patients in the unfavorable prognosis group still received a substantial dose of doxorubicin (which can permanently damage the heart), and because several cases of second cancers have already been observed, he explained, “we must aim to reduce therapy even more in this group of patients.”

Even with further room for improvement in toxicity reduction, “Without question, this is a major success,” said Pearson.

“Their goal was to have an equivalent survival outcome while using much less treatment [compared to the historical control group], and they were able to do that. It’s significant that they were able to get that same outcome with about half the number of cycles of chemotherapy,” agreed Barry Anderson, M.D., Ph.D., of the National Cancer Institute’s Cancer Therapy Evaluation Program.


Neuroblastoma Treatment..

A link to a list of current clinical trials is included for each treatment section. For some types or stages of cancer, there may not be any trials listed. Check with your doctor for clinical trials that are not listed here but may be right for you.
Low-Risk Neuroblastoma

Treatment of low-risk neuroblastoma may include the following:

* Watchful waiting alone for certain infants.
* Surgery followed by watchful waiting.
* Surgery followed by combination chemotherapy, when serious health problems occur.
* Radiation therapy to treat tumors that are causing serious health problems and do not respond quickly to chemotherapy.
* A clinical trial of surgery followed by chemotherapy. Radiation therapy is given to treat tumors that are causing serious health problems and do not respond quickly to surgery and chemotherapy.

Intermediate-Risk Neuroblastoma

Treatment of intermediate-risk neuroblastoma may include the following:

* Surgery alone.
* Surgery followed by chemotherapy. Sometimes a second surgery is needed.
* Surgery followed by chemotherapy. Radiation therapy may given to treat tumors that are causing serious health problems and do not respond quickly to surgery and chemotherapy.
* Chemotherapy followed by surgery.
* Radiation therapy to treat tumors that are causing serious problems and do not respond quickly to chemotherapy.
* A clinical trial of lower doses of chemotherapy.

High-Risk Neuroblastoma

Treatment of high-risk neuroblastoma may include the following:

* Combination chemotherapy followed by surgery to remove as much of the tumor as possible, followed by high-dose chemotherapy and stem cell transplant.
* Radiation therapy to the tumor site and, sometimes, if needed, to other parts of the body with cancer.
* 13-cis retinoic acid after recovery from previous treatment.
* A clinical trial of new regimens of chemotherapy and radiation therapy with stem cell transplant.
* A clinical trial of monoclonal antibody therapy, biologic therapy, and 13-cis retinoic acid after chemotherapy.
* A clinical trial of radiation therapy with radioactive iodine and chemotherapy before stem cell transplant.

Progressive/Recurrent Neuroblastoma

Patients First Treated for Low-Risk Neuroblastoma

Treatment for recurrent neuroblastoma that is found in one place in the body may include the following:

* Surgery followed by watchful waiting or chemotherapy.
* High-dose chemotherapy, stem cell transplant, and 13-cis retinoic acid.
* A clinical trial of surgery and if needed, chemotherapy and another surgery.

Treatment for recurrent neuroblastoma that has spread to other parts of the body may include the following:

* Watchful waiting.
* Surgery followed by chemotherapy.
* High-dose chemotherapy, stem cell transplant, and 13-cis retinoic acid.
* A clinical trial of a new treatment.

Patients First Treated for Intermediate-Risk Neuroblastoma

Treatment for recurrent neuroblastoma that is found in one place in the body may include the following:

* Surgery, with or without chemotherapy.
* A clinical trial of surgery and more courses of chemotherapy.
* A clinical trial of a new treatment.

For recurrent neuroblastoma that has spread to other parts of the body, treatment is usually high-dose chemotherapy, stem cell transplant, and 13-cis retinoic acid.

Patients First Treated for High-Risk Neuroblastoma

There is no standard treatment for recurrent neuroblastoma in patients first treated for high-risk neuroblastoma. Patients may want to consider a clinical trial. For information about clinical trials, please see the NCI Web site.

Check for U.S. clinical trials from NCI's PDQ Cancer Clinical Trials Registry that are now accepting patients with neuroblastoma. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. General information about clinical trials is available from the NCI Web site.


Saturday, October 9, 2010

What Causes Neuroblastoma?

The etiology of neuroblastoma is not well understood. Certain cases however do run in families and have been linked to genetics. Familial neuroblastoma is cased by a very rare germline mutations in the anaplastic lymphoma kinase (ALK) gene.

Several risk factors have been proposed and are the subject of ongoing research.

Due to characteristic early onset many studies have focused on parental factors around conception and during gestation. Factors investigated have included occupation (i.e. exposure to chemicals in specific industries), smoking, alcohol consumption, use of medicinal drugs during pregnancy and birth factors; however, results have been inconclusive.

Other studies have examined possible links with atopy and exposure to infection early in life, use of hormones and fertility drugs, and maternal use of hair dye.


What is Neuroblastoma?

Neuroblastoma is the most common extracranial solid cancer in childhood and the most common cancer in infancy, with an annual incidence of about 650 new cases per year in the US.[1] Close to 50 percent of neuroblastoma cases occur in children younger than two years old.[2] It is a neuroendocrine tumor, arising from any neural crest element of the sympathetic nervous system or SNS. It most frequently originates in one of the adrenal glands, but can also develop in nerve tissues in the neck, chest, abdomen, or pelvis.

Neuroblastoma is one of the few human malignancies known to demonstrate spontaneous regression from an undifferentiated state to a completely benign cellular appearance.[3] It is a disease exhibiting extreme heterogeneity, and is stratified into three risk categories: low, intermediate, and high risk. Low-risk disease is most common in infants and good outcomes are common with observation only or surgery, whereas high-risk disease is difficult to treat successfully even with the most intensive multi-modal therapies available.[4]



The purpose of this blog/site is to raise the awareness of Neuroblastoma. My good friend and neighbors son Noah was diagnosed with this horrible cancer a few years ago and recently relapsed but with treatment is doing much better. My goal for this site is to get at least 30 people a day to view and read about Neuroblastoma and help me raise awareness for this horrible disease.