Posts Tagged ‘Radiation’

Treatment for Endocrine Tumors and Side Effects

Reporter and Curator: Dr. Sudipta Saha, Ph.D.


The purpose of surgery is typically to remove the entire tumor, along with some of the healthy tissue around it, called the margin. If the tumor cannot be removed entirely, “debulking” surgery may be performed. Debulking surgery is a procedure in which the goal is to remove as much of the tumor as possible. Side effects of surgery include weakness, fatigue, and pain for the first few days following the procedure.


Chemotherapy is the use of drugs to kill tumor cells, usually by stopping the cells’ ability to grow and divide. Systemic chemotherapy is delivered through the bloodstream to reach tumor cells throughout the body. A chemotherapy regimen (schedule) usually consists of a specific number of cycles given over a set period of time. A patient may receive one drug at a time or combinations of different drugs at the same time. The side effects of chemotherapy depend on the individual and the dose used, but they can include fatigue, risk of infection, nausea and vomiting, loss of appetite, and diarrhea. These side effects usually go away once treatment is finished.

Radiation therapy

Radiation therapy is the use of high-energy x-rays or other particles to kill tumor cells. The most common type of radiation treatment is called external-beam radiation therapy, which is radiation given from a machine outside the body. When radiation treatment is given using implants, it is called internal radiation therapy or brachytherapy. A radiation therapy regimen usually consists of a specific number of treatments given over a set period of time. Side effects from radiation therapy may include fatigue, mild skin reactions, upset stomach, and loose bowel movements. Most side effects go away soon after treatment is finished.

Hormone therapy

The goal of hormone therapy is often to lower the levels of hormones in the body. Hormone therapy may be given to help stop the tumor from growing or to relieve symptoms caused by the tumor. In addition, for thyroid cancer, hormone therapy will be given if the thyroid gland has been removed, to replace the hormone that is needed by the body to function properly.


Immunotherapy (also called biologic therapy) is designed to boost the body’s natural defenses to fight the tumor. It uses materials made either by the body or in a laboratory to bolster, target, or restore immune system function. Examples of immunotherapy include cancer vaccines, monoclonal antibodies, and interferons. Alpha interferon is a form of biologic therapy given as an injection under the skin. This is sometimes used to help relieve symptoms caused by the tumor, but it can have severe side effects including fatigue, depression, and flu-like symptoms.

Targeted therapy

Targeted therapy is a treatment that targets the tumor’s specific genes, proteins, or the tissue environment that contributes to cancer growth and survival. This type of treatment blocks the growth and spread of tumor cells while limiting damage to normal cells, usually leading to fewer side effects than other cancer medications.

Recent studies show that not all tumors have the same targets. To find the most effective treatment, the doctor may run tests to identify the genes, proteins, and other factors in the tumor. As a result, doctors can better match each patient with the most effective treatment whenever possible.

Depending on the type of endocrine tumor, targeted therapy may be a possible treatment option. For instance, targeted therapies, such as sunitinib (Sutent) and everolimus (Afinitor), have been approved for treating advanced islet cell tumors. Early results of clinical trials (research studies) with targeted therapy drugs for other types of endocrine tumors are promising, but more research is needed to prove they are effective.

Recurrent endocrine tumor

Once the treatment is complete and there is a remission (absence of symptoms; also called “no evidence of disease” or NED). Many survivors feel worried or anxious that the tumor will come back. If the tumor does return after the original treatment, it is called a recurrent tumor. It may come back in the same place (called a local recurrence), nearby (regional recurrence), or in another place (distant recurrence). When this occurs, a cycle of testing will begin again to learn as much as possible about the recurrence. Often the treatment plan will include the therapies described above (such as surgery, chemotherapy, and radiation therapy) but may be used in a different combination or given at a different pace. People with a recurrent tumor often experience emotions such as disbelief or fear. Patients are encouraged to talk with their health care team about these feelings and ask about support services to help them cope.

Metastatic endocrine tumor

If a cancerous tumor has spread to another location in the body, it is called metastatic cancer. A treatment plan that includes a combination of surgery, chemotherapy, radiation therapy, hormone therapy, immunotherapy, or targeted therapy may be recommended if required.

In addition to treatment to slow, stop, or eliminate the cancer (also called disease-directed treatment), an important part of cancer care is relieving a person’s symptoms and side effects. It includes supporting the patient with his or her physical, emotional, and social needs, an approach called palliative or supportive care. People often receive disease-directed therapy and treatment to ease symptoms at the same time.

Source References:


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 Curator: Ritu Saxena, Ph.D.

Vitamin C or Ascorbic acid (AA) or Ascorbate

Biochemical role: AA serves a basic biochemical role of accelerating hydroxylation in several biochemical reactions. It provides electrons to metal ions, the reduced forms of which are required for the full enzymatic activity of some enzymes. Most emphasized role of AA is as a cofactor for the enzyme required for the biosynthesis of collagen.

Molecular structure and the oxidized form of AA, dihydroascorbic acid, bear similarity to that of glucose.

Biological role: AA is an essential vitamin for humans and its deficiency leads to disease called Scurvy characterized by initial symptoms of malaise and lethargy, followed by formation of spots on the skin, spongy gums, and bleeding from the mucous membranes. As scurvy advances, there can be open, suppurating wounds, loss of teeth, jaundice, fever, neuropathy and death. AA is water soluble and found in high concentrations in several tissues including eye lens, WBCs, adrenal glad and pituitary gland. Some of the roles of ascorbate include:

  1. Carnitine synthesis from lysine
  2. Neurotransmitter synthesis,
  3. Cytochrome P-450 activity,
  4. Cholesterol metabolism,
  5. Detoxification of exogenous compounds,
  6. Antioxidant
  7. Possibly an ergogenic aid (Ergogenic aids are substances, devices, or practices that enhance an individual’s energy use, production, or recovery.)

Vitamin C and Cancer

As early as in 1949, vitamin C was implicated in cancer therapy. Since then, several research articles have been published exploring the role of ascorbate in cancer therapy. Among the plethora of literature discussing the relationship between vitamin C and cancer, one of the very significant and comprehensive reviews was published in 1979 in Cancer Research (2).

Mechanisms of action of AA (1) with respect to cancer have been divided and subdivided into the following:

  1. Primary mechanisms
  2. Secondary mechanisms
  • Preventive mechanism

Ascorbate acts as a cancer preventive agent by virtue of its strong antioxidant activities. Being one of the strongest reductants and radical scavenger, it absorbs unstable oxygen, nitrogen, and sulphur-centered radicals. AA can prevent biomembranes from peroxidative damage from peroxyl radicals. Ascorbate can trap peroxyl radicals and lead to their peroxidation in the aqueous phase before they reach the lipid rich biomembranes and cause damage. Ascorbate has been speculated to have a biomembrane protective action by its synergistic antioxidant activity with vitamin E (tocopherol).  Vitamin E is lipid-soluble and tocopheroxyl radical is generated in the cell membranes as a result of its antioxidant activity.  Ascorbate reacts with the tocopheroxyl radical and regenerates tocopherol transferring the oxidative challenge to the aqueous phase. At this point, the less active ascorbate radical might be reduced to AA by an NADP-dependent system. The probably mechanism might explain the reduction of nitrates via ascorbate to prevent the formation of carcinogenic nitrosamines.

  • Anticancer mechanisms

1. Primary anticancer mechanisms

i.     Oxidative, oxidant and pro-oxidant properties: Ascorbate has been reported to be cytotoxic at high concentrations, which has been demonstrated in a number of malignant cell lines. Transcription factor NFkB is potentially activated via ascorbate and its radicals leading to the inhibition of cell growth. Also, ascorbate inhibits certain prostaglandins leading to decrease in cell proliferation.

ii.     Hydrogen peroxide: On oxidation with oxygen, ascorbate produces a hydrogen peroxide, a reactive oxygen species. Hydrogen peroxide can generate several other reactive species and can have several damaging effects on cells including decrease in cell viability by damaging cell membranes of malignant cells. The amount of these reactive species produced via oxidation is limited in healthy cells unlike that in malignant cells where they exist in large amounts. The amount of hydrogen peroxide generated has been correlated to the amount of ascorbate in the cells. The reactive species can lead to multiple negative effects on cells including DNA strand breaks, lipid peroxidation leading to membrane function disruption, cellular ATP depletion.

Authors state that “the failure to maintain high ATP production may be a consequence of oxidative inactivation of key enzymes especially those related to the Krebs cycle and the electron transport chain.” This might result in alteration of transmembrane potential and distortion of mitochondrial function, suggestive of the important role of mitochondria in the process of carcinogenesis. In this paper, vitamin C has been correlated with cancer with the involvement of altered mitochondrial function. In addition, ascorbate has been detected in mitochondria where it is also regenerated. Different aspects of mitochondrial involvement in cancer have been discussed in several posts published earlier (3-8).

iii.     Other oxidation products of AA: Other oxidation products of AA include 2,3-diketoglutonic acid, and 5-methyl 1-3, 4-dehydrotetrone and other degradation products, have demonstrated antitumor activity. Additionally, some degradation and oxidation products of AA, gamma-cronolactone and 3-hydroxyl-2-pyrone, have been found to inhibit tumor growth. The mechanism of their antitumor actions is complex and might involve multitude of steps, including generation of reactive oxygen species, lipid peroxidation, inducing structural changes in important cellular proteins, inhibition of mitosis and so on.

iv.     Intracellular transport of ascorbate and its tumor specificity: Oxidized ascorbate, dihydroascorbic acid, is transported intracellularly where it is reduced back to ascorbate. Owing to its structural similarity with glucose, dihydroascorbic transport is facilitated via glucose transporters (GLUTs). Ascrobate in its reduced form is transported through a sodium-dependent cotransporter in some cells. Tumor cells require large amounts of glucose, which leads to an increase in the number of GLUTs, hence, resulting in an increase in ascorbate concentration within cancer cells. Because of this selective increased uptake of ascorbate and its cytotoxic effects in cancer cells (generation of hydrogen peroxide, DNA damage, other cytotoxic effects), AA has become a selective, nontoxic chemotherapeutic agent. The difference in the levels of catalase enzyme has been found to lead to intracellular tumor selectivity in cancer cells.

Ascorbate induced cytotoxicity in cancer cells involves its final electron acceptor, oxygen, which interferes with the anaerobic respiration within malignant cells. This gives an important clue for the involvement of mitochondria in malignant cells.

v.     Intravenous AA: High concentrations of AA in plasma (>200mg/dL) have been found to be cytotoxic to cancer cells. Clinically high plasma concentrations of AA can be achieved by its intravenous administration. It was observed that 60g infusion of AA given to cancer patients for 60 minutes followed by 20g given over the next 60 minutes resulted in a 240 minutes high plasma AA concentration of >400mg/dL, that is known to be cytotoxic.

Lipoic acid when administered with AA, is able to reduce the high-dose requirement of AA for its cytotoxic activity reducing it from 700mg/dL to 120mg/dL. Lipoic acid can recycle vitamin C, mediate the reduction of dihydroascorbic acid and improves mitochondrial function. Thus, energy intermediates such as coenzyme Q, vitamin K3, B-complex vitamins, alpha-ketoglutarate aspartate, magnesium might aid in cancer therapy by intercting with ascorbate, directly or indirectly, thereby stimuating/interacting/correcting aerobic mitochondrial respiration.

Hence, the pro-oxidant activity of vitamin C is being referred to as the primary mechanism of anticancer action.

2. Secondary anticancer mechanisms

i.     AA and intracellular matrix: Collagen is an important constituent of the matrix and its concentration determines the strength of the tissue along with its resistance to the infiltration of malignant cancer cells. In Scurvy, a disease resulting from a chronic deficiency of vitamin C, there is generalized tissue disintegration, dissolution of intercellular ground substance and the disruption of collagen bundles. This disintegration leads to ulceration; bacterial colonization and general undifferentiated cellular proliferation with specialized cells reverting back to their primitive form, very much like cancer.  Lack of ascorbate causes a reduction in the hydroxylation of prolyl and lysyl residues into hydroxyproline and hydroxylysine, leading to instability of the collagen triple helix, a common feature in scurvy and also in cancer. Thus, a secondary mechanism of ascorbic acid anticancer mechanism would be to repair these sites, which is emphasized by its role in wound healing, including surgical recovery and other traumatic injuries.

ii.     Ascorbate and immunocompetence: Ascorbate plays several roles for the efficient functioning of immune system in ways that are invoved in both humoral and cell-mediated.  Ascorbate provides humoral immunocompetence as it is essential for immunoglobulin synthesis. In addition, lymphocytes, seminal cells involved in cell-mediated immunity have been found to contain high concentrations of ascorbate. Other immune system roles include, aid in active phagocytosis and enhancing of interferon production.

Classical vitamin C and Cancer controversy-A possible explanation

Conflicting results were obtained from the studies performed by Pauling (Pauling Institute) and Cameron (Mayo Clinic) with vitamin C and its effect on cancer, the issue was debated a few decades ago. Both the studies, however, used oral doses of ascorbate (10g). Gonzalez et al, authors of the review on which the post is based, analyzed and expressed their views on the controversy. They state that the plasma concentration cannot be replicated when the dose is given orally as opposed to when the dose is given intravenously. According to their research, when AA is administered intravenously, higher plasma levels of ascorbate are achieved that could be retained for longer time periods. Also, the authors advocate the use of substantially higher doses (25-200g) to be given intravenously for selective toxicity towards cancer cells.

Modern vitamin C and Cancer controversy-Chemotherapy and radiation

A recent concern regarding the antioxidants like vitamin C is that they might reduce the effectiveness of chemotherapy and radiation by reducing the potency of free radicals necessary for killing cells. A publication by Agus et al (13) has a major role to play in this misconception. The authors describe how cancer cells acquire and concentrate vitamin C providing malignant cells with metabolic advantage. However, details or explanations regarding the theory are missing. Some studies, on the other hand, explain that high concentrations of AA in cancer cells is cytotoxic and is achieved because of similarity in structure between AA and glucose. Cancer cells uptake AA derivative, dehydroascorbic acid via glucose transporters (GLUTs).

In a case report published in PNAS in 1985 (12), two patients with ovarian cancer stage IIIC were found to respond positively to chemotherapy along with high-dose of antioxidants. Antioxidant, AA was administered intravenously to maintain a high plasma dose of 200 mg/dL. The two patients didn’t show disease recurrence after three years of chemotherapy and vitamin C administration. Vast literature exists on the topic indicating that antioxidants, including ascorbate, provide beneficial effects in several cancers without reducing the efficacy of chemotherapy or radiation during treatment of these cancers. Some data, in fact, suggests increase in effectiveness of chemotherapy when supplemented with antioxidants along with an increase in adverse effects. The topic has been summarized and discussed in a series of articles by Lawson and Brignall (9-11).


The post is primarily based on the following two review articles:

1. González MJ et al. Orthomolecular oncology review: ascorbic acid and cancer 25 years later.  Integr Cancer Ther. 2005 Mar;4(1):32-44.

2. Cameron E, Pauling L, Leibovitz B. Ascorbic acid and cancer: a review. Cancer Res. 1979 Mar;39(3):663-81.

Other articles  on Mitochondria and Cancer were published on this Open Source Online Scientific Journal

3. Ritu Saxena. Mitochondria and Cancer: An overview of mechanisms

4. Ritusaxena. β Integrin emerges as an important player in mitochondrial dysfunction associated Gastric Cancer.

5. Larry H Bernstein. Mitochondria: Origin from oxygen free environment, role in aerobic glycolysis, metabolic adaptation

6. Ritu Saxena. Mitochondria and Cancer: An overview of mechanisms

7. Larry H Bernstein. Mitochondrial Damage and Repair under Oxidative Stress

8. Larry H Bernstein. What can we expect of tumor therapeutic response?

Research articles:

9. Lamson DW, Brignall MS. Antioxidants and cancer, part 3: quercetin. Altern Med Rev. 2000 Jun;5(3):196-208. Review.

10. Lamson DW, Brignall MS. Antioxidants and cancer therapy II: quick reference guide. Altern Med Rev. 2000 Apr;5(2):152-63.

11. Lamson DW, Brignall MS. Antioxidants in cancer therapy; their actions and interactions with oncologic therapies. Altern Med Rev. 1999 Oct;4(5):304-29.

12. Bensch KG, Fleming JE, Lohman W. The role of ascorbic acid in senile cataracts. Proc Natl Acad Sci USA 1985;82:7193-7196.

13. Agus DB, Vera JG, Golde DW. Stand allocation: a mechanism by which tumors obtain vitamin C. Cancer Res. 1999;59:4555-4558.

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Author: Ritu Saxena, Ph.D.

Recently, two world renowned innovators, Steve Jobs-the CEO of Apple Inc. and Dr. Steinman-winner of 2011 Nobel prize in Physiology or medicine lost their life battle against Pancreatic cancer. Although both Jobs and Steinman suffered from the same disease, they were diagnosed with two fundamentally different forms of cancer of pancreas.

Steve lived with the disease for 8 years, a relatively long time for Pancreatic cancer patients to survive. The reason is attributed to the rare form of cancer of pancreas he suffered from-referred to as pancreatic neuroendocrine tumor. Steinman, on the other hand died due to a more common form of pancreatic cancer, the adenocarcenoma.

Neuroendocrine tumors arise from islands of hormone-producing cells (islets), that happen to be in that organ. Jobs learned in 2003 that he had an extremely rare form of this cancer, an islet-cell neuroendocrine tumor. In his email to  Apple employees in 2004, Steven Jobs wrote “I have some personal news that I need to share with you, and I wanted you to hear it directly from me,” Jobs said in the message, which he sent from his hospital bed. “I had a very rare form of pancreatic cancer called an islet cell neuroendocrine tumor, which represents about 1 percent of the total cases of pancreatic cancer diagnosed each year, and can be cured by surgical removal if diagnosed in time (mine was). I will not require any chemotherapy or radiation treatments.”

About 2,500 cases of pancreatic islet cell tumors are seen in the United States each year, according to the University of Southern California’s Center for Pancreatic and Biliary Diseases. These tumors, which are derived from neuroendocrine cells, tend to be slow growing and are treatable even after they have metastasized, said the center’s Web site.

The management strategy of neuroendrocrine tumors (NET) like any other disease is supposed to be curative where possible. As suggested by several researchers including Ramage et al (, ), surgery is the only curative option currently available for NETs. The updated guidelines published for the NET management state the over the past few years, there have been advances in the management of neuroendocrine tumours, which have included clearer characterisation, more specific and therapeutically relevant diagnosis, and improved treatments. However, because of the uncommon nature of the disease, there remain few randomised trials in the field, hence all evidence mentioned in the research article is considered relatively weak compared with other more common cancers. For patients who are diagnosed early enough to be candidates for surgery, the aim is to keep the patient disease- and symptom-free for as long as possible. For patients suffering from advanced-stage NETs, operative therapy is rarely curative and chemotherapy could be used on metastasized NETs.

As reported in a story covered by CNN in 2008, there was a lot of speculation when he appeared rail-thin at the unveiling of the new iPhone. Jobs eventually said in January 2009 that doctors said he dropped so much weight because of “a hormone imbalance that has been ‘robbing’ me of the proteins my body needs to be healthy. Sophisticated blood tests have confirmed this diagnosis.” This statement explains how symptoms of hormonal excess in NET patients must be controlled before surgical procedure is followed. Also, recommended management of the symptoms of hormonal hypersecretion depends on the hormone secreted. For example, glucose levels in patients with insulinomas should be stabilized with diet and/or diazoxide. Gastrin hypersecretion in patients with gastrinomas may be managed with proton pump inhibitors (PPIs).

Steinman, on the other hand, suffered from adenocarcenoma that arises from the pancreatic cells themselves, referred to as the “far more common form of pancreatic cancer” by Jobs. He further wrote in his memo “…(adenocarcenoma) is currently not curable and usually carries a life expectancy of around one year after diagnosis. I mention this because when one hears ‘pancreatic cancer’ (or Googles it), one immediately encounters this far more common and deadly form, which, thank God, is not what I had.”

Dr. Steinman won the 2011 Nobel Prize for Medicine or Physiology for his early-career landmark discovery about the immune system in the 1970s when he first described ‘dendritic cells’ with the help of his mentor Zanvil Cohn at Rockefeller University. Unfortunately, he died just three days before the official announcement. He had been suffering from pancreatic cancer for four years, had been undergoing treatment using a pioneering immunotherapy based on his own research. Dendritic cells from his body were deployed to mount an assault on his cancer. His early research at Rockefeller, began as an attempt to understand the primary white cells of the immune system — the large “eating” macrophages and the exquisitely specific lymphocytes, which operate in a variety of ways to spot, apprehend and destroy infectious microorganisms and tumor cells. Steinman’s subsequent research pointed to dendritic cells as important and unique accessories in the onset of several immune responses, including clinically important situations such as rejection of graft, resistance to tumors, autoimmune diseases and infections including AIDS.

The standard of care in the United States for the treatment of locally advanced pancreatic cancer is a combination of low-dose chemotherapy given simultaneously with radiation treatments to the pancreas and surrounding tissues. Radiation treatments are designed to lower the risk of local growth of the cancer, thereby minimizing the symptoms that local progression causes (back or belly pain, nausea, loss of appetite, intestinal blockage, jaundice).

Research Efforts on Pancreatic Cancer: The untimely passing of the geniuses reminds us how important research in the area of pancreatic cancer is which lead to finding new therapeutic targets that might stem reliable therapies. A recent example is the report published in Science Daily stating that the protein RGL2 might be a promising therapeutic target for pancreatic cancer. The conclusion was derived via research published in November in the Journal of Biological Chemistry by a team led by Channing Der, PhD from UNC Lineberger Cancer Center.   For almost three decades, scientists and physicians have known that a gene called the KRAS oncogene is mutated in virtually all pancreatic cancers, making it an important target for scientists looking for a way to stop the growth of pancreatic cancer tumors. The problem is that the KRAS gene triggers cancer cell growth in numerous ways, through multiple cell signaling pathways, and scientists have had difficulty determining which one will be the most promising to block — an important first step in designing a drug for use in patients. Dr. Der said that “We are particularly optimistic about RGL2 because we know that this protein is a critical component of KRAS signaling to another class of proteins called Ral GTPases, which are essential for the growth of almost all pancreatic tumors.”

Another groundbreaking research was published in the journal Nature talks about discovering the link between a gene and the prognosis of Pancreatic Ductal Adenocarcenoma. The team found that when a gene involved in protein degradation is switched-off through chemical tags on the DNA’s surface, pancreatic cancer cells are protected from the bodies’ natural cell death processes, become more aggressive, and can rapidly spread. Their research study proposed USP9X to be a major tumour suppressor gene with prognostic and therapeutic relevance in pancreatic cancer.

Although, most of the research efforts are concentrated on the more common form of cancer, pancreatic adenocarcenoma, similar research efforts are needed for developing cure for the uncommon form, the one Steve Jobs suffered from, neuroendocrine cancer.

What we lost to the disease is more than the two geniuses, we lost the possibility of further innovation that might have changed the world in ways we could not imagine. The loss, though, sheds light on the importance of finding a cure for the disease and its different types. Hope the research community is able to interpret and find answers to the enigma of Pancreatic cancer and its diverse forms in which it strikes.

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Writer: Venkat Karra, Ph.D.

This study was reported today in the Optical Society’s (OSA) open-access journal Optics Express (Optics Express, Vol. 20, Issue 11, pp. 11582-11597 (2012)), and provide proof-of-concept support that the technology can distinguish malignant tissue by providing high-contrast images of tumors.

In breast cancer screening, x-ray mammography and ultrasonography are primarily used to understand any morphological changes of breast tissue. However, these conventional techniques have their own drawbacks because of for example ionizing radiation that could cause leukemia after prolonged/ repeated exposure where as ultrasonography is strongly operator dependent.

Tumor vascularization is a crucial feature in breast imaging. One commonly used method that focuses on tumor vascularization is Dynamic Contrast Enhanced MRI (DCE-MRI). The high sensitivity of this technique for detecting breast cancer proves that vascularity can indeed provide additional information about the nature of tissue. However, DCE-MRI suffers from a limited specificity, requires the injection of contrast agents and is relatively expensive.

Far-red and near-infrared (NIR): It is gaining attention in (non-invasively) visualizing cancer and its associated vasculature due to its ability to provide functional and molecular information without the use of ionizing radiation. In recent studies, it has been shown that optical imaging in the form of diffuse optical tomography (DOT) can indeed visualize breast malignancies, primarily because of the high absorption of hemoglobin in the NIR regime. However, DOT suffers from low spatial resolution.

Several groups have studied the feasibility of photoacoustic image (PAI) in breast imaging due to their superior resolution capabilities to that of pure optical techniques. Photoacoustic imaging exploits the high NIR light absorption contrast between benign and malignant tissue, but provides superior resolution arising from ultrasound detection.

Scientists from Center for Breast Care, Medisch Spectrum Twente hospital,  University of Twente and University of Amsterdam have developed the Twente Photoacoustic Mammoscope (PAM), to image the breast in transmission mode. The authors say that, in a first pilot study with this system in 2007, it was possible to get technically acceptable measurements on five patients with radiographically proven breast malignancies. Of those, four cases revealed a high photoacoustic contrast with respect to the background associated with tumor related vasculature. Now the authors have recently started an extended clinical study using PAM, as a continuation of the study performed in 2007.

In this new study, they have investigated the clinical feasibility of photoacoustic mammography in a larger group of patients with different types of breast lesions to obtain more information about the clinical feasibility and limitations of photoacoustic mammography and the results were compared with conventional imaging and histopathology.

Ten technically acceptable measurements on patients with malignancies (BI-RADS 5) and two measurements on patients with cysts (BI-RADS 2) were performed. In the reconstructed volumes of all ten malignant lesions, a confined region with high contrast with respect to the background was seen. In all malignant cases, the PA contrast of the abnormality was higher than the contrast on x-ray mammography. The PA contrast appeared to be independent of the mammographically estimated breast density and was absent in the case of cysts.

Authors say that technological improvements to the instrument and further studies on less suspicious lesions are planned to further investigate the potential of PAM. The authors from University of Twente hope that these early results will one day lead to the development of a safe, comfortable, and accurate alternative or adjunct to conventional techniques for detecting breast tumors.

Twente Photoacoustic Mammoscope (PAM):

This techniques combines the light-based system’s to distinguish between benign and malignant tissue with ultrasound to achieve superior targeting ability. The device is built into a hospital bed, where the patient lies prone and positions her breast for imaging. Laser light at a wavelength of 1,064 nm scans the breast. Because there is increased absorption of the light in malignant tissue the temperature slightly increases. With the rise in temperature, thermal expansion creates a pressure wave, which is detected by an ultrasound detector placed on one side of the breast. The resulting photoacoustic signals are then processed by the PAM system and reconstructed into images. These images reveal abnormal areas of high intensity (tumor tissue) as compared to areas of low intensity (benign tissue). This is one of the first times that the technique has been tested on breast cancer patients.

Note: Breast cancer is one of the most common forms of cancer among females and each year more than 450,000 women are diagnosed worldwide with the disease.


Reporter: Venkat Karra

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Reporter: Aviva Lev-Ari, PhD, RN

To: Radial Assist, LLC

Re: Radiation Scatter Survey of Radial Assist RAD BOARD by Alliance Medical Physics LLC

Enclosed please find the results of the radiation scatter survey conducted on the RAD BOARD on April 20, 2012. The RAD BOARD is an arm board utilized in cardiac catheterization and interventional labs for radial access. It has the added feature of being partially lined with a 15″ by 9″ layer of Xenolite TB for additional radiation scatter protection. Xenolite TB, which is a lead-free, super-lightweight 2-element composite equivalent to 0.35mm Pb protection, is embedded in the board under the company logo label. The survey was performed to quantify the ability of the RAD BOARD to reduce radiation scatter to the physician performing the vascular procedure.



The resultsof the survey indicate that when utilizing the RAD BOARD, radiation scatter exposure levels were reduced by 33% – 40% at waist height, and 21% – 30% at neck height (See Figures 1 & 2).

Sincerely yours, ALLIANCE MEDICAL PHYSICS LLC Michael S. Glaser, M.S. Certified Medical Physicist Diplomat-American Board of Radiology

Alliance Medical Physics LLC 2500 Abbey Court · Alpharetta GA 30004 ·770.751.9707 · (fax) 770.753.4305

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