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At least 19 records
All sourcesNASA NTRSDOE OSTI
NASA NTRS2002

Monoclonal antibody to a cancer-specific and drug-responsive hydroquinone (NADH) oxidase from the sera of cancer patients

Monoclonal antibodies were generated in mice to a 34-kDa circulating form of a drug-responsive hydroquinone (NADH) oxidase with a protein disulfide-thiol interchange activity specific to the surface of cancer cells and the sera of cancer patients. Screening used Western blots with purified 34-kDa tNOX from HeLa cells and the sera of cancer patients. Epitopes were sought that inhibited the drug-responsive oxidation of NADH with the sera of cancer patients, but which had no effect on NADH oxidation with the sera of healthy volunteers. Two such antisera were generated. One, designated monoclonal antibody (mAb) 12.1, was characterized extensively. The NADH oxidase activity inhibited by mAb 12.1 also was inhibited by the quinone site inhibitor capsaicin (8-methyl- N-vanillyl-6-noneamide). The inhibition was competitive for the drug-responsive protein disulfide-thiol interchange activity assayed either by restoration of activity to scrambled RNase or by cleavage of a dithiodipyridine substrate, and was uncompetitive for NADH oxidation. Both the mAb 12.1 and the postimmune antisera immunoprecipitated drug-responsive NOX activity and identified the same 34-kDa tNOX protein in the sera of cancer patients that was absent from sera of healthy volunteers, and was utilized as immunogen. Preimmune sera from the same mouse as the postimmune antisera was without effect. Both mouse ascites containing mAb 12.1 and postimmune sera (but not preimmune sera) slowed the growth of human cancer cell lines in culture, but did not affect the growth of non-cancerous cell lines. Immunocytochemical and histochemical findings showed that mAb 12.1 reacted with the surface membranes of human carcinoma cells and tissues.

NASA Discipline Cell Biology↗
NASA NTRS2009

A New View of Radiation-Induced Cancer: Integrating Short- and Long-Term Processes. Part II: Second Cancer Risk Estimation

As the number of cancer survivors grows, prediction of radiotherapy-induced second cancer risks becomes increasingly important. Because the latency period for solid tumors is long, the risks of recently introduced radiotherapy protocols are not yet directly measurable. In the accompanying article, we presented a new biologically based mathematical model, which, in principle, can estimate second cancer risks for any protocol. The novelty of the model is that it integrates, into a single formalism, mechanistic analyses of pre-malignant cell dynamics on two different time scales: short-term during radiotherapy and recovery; long-term during the entire life span. Here, we apply the model to nine solid cancer types (stomach, lung, colon, rectal, pancreatic, bladder, breast, central nervous system, and thyroid) using data on radiotherapy-induced second malignancies, on Japanese atomic bomb survivors, and on background US cancer incidence. Potentially, the model can be incorporated into radiotherapy treatment planning algorithms, adding second cancer risk as an optimization criterion.

Shuryak, Igor↗
NASA NTRS2011

Space Radiation Cancer, Circulatory Disease and CNS Risks for Near Earth Asteroid and Mars Missions: Uncertainty Estimates for Never-Smokers

The uncertainties in estimating the health risks from galactic cosmic rays (GCR) and solar particle events (SPE) are a major limitation to the length of space missions and the evaluation of potential risk mitigation approaches. NASA limits astronaut exposures to a 3% risk of exposure induced cancer death (REID), and protects against uncertainties in risks projections using an assessment of 95% confidence intervals after propagating the error from all model factors (environment and organ exposure, risk coefficients, dose-rate modifiers, and quality factors). Because there are potentially significant late mortality risks from diseases of the circulatory system and central nervous system (CNS) which are less well defined than cancer risks, the cancer REID limit is not necessarily conservative. In this report, we discuss estimates of lifetime risks from space radiation and new estimates of model uncertainties are described. The key updates to the NASA risk projection model are: 1) Revised values for low LET risk coefficients for tissue specific cancer incidence, with incidence rates transported to an average U.S. population to estimate the probability of Risk of Exposure Induced Cancer (REIC) and REID. 2) An analysis of smoking attributable cancer risks for never-smokers that shows significantly reduced lung cancer risk as well as overall cancer risks from radiation compared to risk estimated for the average U.S. population. 3) Derivation of track structure based quality functions depends on particle fluence, charge number, Z and kinetic energy, E. 4) The assignment of a smaller maximum in quality function for leukemia than for solid cancers. 5) The use of the ICRP tissue weights is shown to over-estimate cancer risks from SPEs by a factor of 2 or more. Summing cancer risks for each tissue is recommended as a more accurate approach to estimate SPE cancer risks. 6) Additional considerations on circulatory and CNS disease risks. Our analysis shows that an individual s history of smoking exposure has a larger impact on GCR risk estimates than amounts of radiation shielding or age at exposure (amongst adults). Risks for never-smokers compared to the average U.S. population are estimated to be reduced between 30% and 60% dependent on model assumptions. Lung cancer is the major contributor to the reduction for never-smokers, with additional contributions from circulatory diseases and cancers of the stomach, liver, bladder, oral cavity and esophagus, and leukemia. The relative contribution of CNS risks to the overall space radiation detriment is potentially increased for never-smokers such as most astronauts. Problems in estimating risks for former smokers and the influence of second-hand smoke are discussed. Compared to the LET approximation, the new track structure derived radiation quality functions lead to a reduced risk for relativistic energy particles and increased risks for intermediate energy particles. Revised estimates for the number of safe days in space at solar minimum for heavy shielding conditions are described for never-smokers and the average U.S. population. Results show that missions to near Earth asteroids (NEA) or Mars violate NASA's radiation safety standards with the current levels of uncertainties. Greater improvements in risk estimates for never-smokers are possible, and would be dependent on improved understanding of risk transfer models, and elucidating the role of space radiation on the various stages of disease formation (e.g. initiation, promotion, and progression).

Cucinotta, Francis A.↗
NASA NTRS2024

Combining Large Datasets - Cancer Moonshot Task Group Final Summary

In February 2022, President Biden re-ignited the Cancer Moonshot with bold new goals: to reduce the cancer death rate by half within 25 years and improve the lives of people with cancer and cancer survivors. To achieve these ambitious goals, the White House convened the first-ever Cancer Cabinet, bringing together departments and agencies from across the federal government to end cancer as we know it.The Cancer Cabinet convened three task forces and supporting task groups, including the Data and Innovation Task Force, which supported the Cancer Moonshot priority to “Deliver innovation to patients and communities.” In early 2023, the “Combining Large Datasets” (CoLD) Task Group was created within the Data and Innovation Task Force. The scope of the CoLD Task Group was how federal agencies combine large datasets for broad applications across cancer prevention and control, including nutrition, epidemiology, and military/Veteran health. Within this scope, the group sought to better leverage the immense potential of data and power of data tools to increase our understanding of cancer incidence, causes, mortality, treatments, prevention, outcomes, costs, and all other aspects of the burden of cancer.

data integration↗
NASA NTRS2012

Technical Evaluation of the NASA Model for Cancer Risk to Astronauts Due to Space Radiation

At the request of NASA, the National Research Council's (NRC's) Committee for Evaluation of Space Radiation Cancer Risk Model reviewed a number of changes that NASA proposes to make to its model for estimating the risk of radiation-induced cancer in astronauts. The NASA model in current use was last updated in 2005, and the proposed model would incorporate recent research directed at improving the quantification and understanding of the health risks posed by the space radiation environment. NASA's proposed model is defined by the 2011 NASA report Space Radiation Cancer Risk Projections and Uncertainties 2010 (Cucinotta et al., 2011). The committee's evaluation is based primarily on this source, which is referred to hereafter as the 2011 NASA report, with mention of specific sections or tables cited more formally as Cucinotta et al. (2011). The overall process for estimating cancer risks due to low linear energy transfer (LET) radiation exposure has been fully described in reports by a number of organizations. They include, more recently: (1) The "BEIR VII Phase 2" report from the NRC's Committee on Biological Effects of Ionizing Radiation (BEIR) (NRC, 2006); (2) Studies of Radiation and Cancer from the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR, 2006), (3) The 2007 Recommendations of the International Commission on Radiological Protection (ICRP), ICRP Publication 103 (ICRP, 2007); and (4) The Environmental Protection Agency s (EPA s) report EPA Radiogenic Cancer Risk Models and Projections for the U.S. Population (EPA, 2011). The approaches described in the reports from all of these expert groups are quite similar. NASA's proposed space radiation cancer risk assessment model calculates, as its main output, age- and gender-specific risk of exposure-induced death (REID) for use in the estimation of mission and astronaut-specific cancer risk. The model also calculates the associated uncertainties in REID. The general approach for estimating risk and uncertainty in the proposed model is broadly similar to that used for the current (2005) NASA model and is based on recommendations by the National Council on Radiation Protection and Measurements (NCRP, 2000, 2006). However, NASA's proposed model has significant changes with respect to the following: the integration of new findings and methods into its components by taking into account newer epidemiological data and analyses, new radiobiological data indicating that quality factors differ for leukemia and solid cancers, an improved method for specifying quality factors in terms of radiation track structure concepts as opposed to the previous approach based on linear energy transfer, the development of a new solar particle event (SPE) model, and the updates to galactic cosmic ray (GCR) and shielding transport models. The newer epidemiological information includes updates to the cancer incidence rates from the life span study (LSS) of the Japanese atomic bomb survivors (Preston et al., 2007), transferred to the U.S. population and converted to cancer mortality rates from U.S. population statistics. In addition, the proposed model provides an alternative analysis applicable to lifetime never-smokers (NSs). Details of the uncertainty analysis in the model have also been updated and revised. NASA's proposed model and associated uncertainties are complex in their formulation and as such require a very clear and precise set of descriptions. The committee found the 2011 NASA report challenging to review largely because of the lack of clarity in the model descriptions and derivation of the various parameters used. The committee requested some clarifications from NASA throughout its review and was able to resolve many, but not all, of the ambiguities in the written description.

Source record↗
NASA NTRS2007

Second Cancers After Fractionated Radiotherapy: Stochastic Population Dynamics Effects

When ionizing radiation is used in cancer therapy it can induce second cancers in nearby organs. Mainly due to longer patient survival times, these second cancers have become of increasing concern. Estimating the risk of solid second cancers involves modeling: because of long latency times, available data is usually for older, obsolescent treatment regimens. Moreover, modeling second cancers gives unique insights into human carcinogenesis, since the therapy involves administering well characterized doses of a well studied carcinogen, followed by long-term monitoring. In addition to putative radiation initiation that produces pre-malignant cells, inactivation (i.e. cell killing), and subsequent cell repopulation by proliferation can be important at the doses relevant to second cancer situations. A recent initiation/inactivation/proliferation (IIP) model characterized quantitatively the observed occurrence of second breast and lung cancers, using a deterministic cell population dynamics approach. To analyze ifradiation-initiated pre-malignant clones become extinct before full repopulation can occur, we here give a stochastic version of this I I model. Combining Monte Carlo simulations with standard solutions for time-inhomogeneous birth-death equations, we show that repeated cycles of inactivation and repopulation, as occur during fractionated radiation therapy, can lead to distributions of pre-malignant cells per patient with variance >> mean, even when pre-malignant clones are Poisson-distributed. Thus fewer patients would be affected, but with a higher probability, than a deterministic model, tracking average pre-malignant cell numbers, would predict. Our results are applied to data on breast cancers after radiotherapy for Hodgkin disease. The stochastic IIP analysis, unlike the deterministic one, indicates: a) initiated, pre-malignant cells can have a growth advantage during repopulation, not just during the longer tumor latency period that follows; b) weekend treatment gaps during radiotherapy, apart from decreasing the probability of eradicating the primary cancer, substantially increase the risk of later second cancers.

Sachs, Rainer K.↗
NASA NTRS2017

Cancer Risk in Astronauts: A Constellation of Uncommon Consequences

Excess cancers resulting from external radiation exposures have been noted since the early 1950s, when a rise in leukemia rates was first reported in young atomic bomb survivors [1]. Further studies in atomic bomb survivors, cancer patients treated with radiotherapy, and nuclear power plant workers have confirmed that radiation exposure increases the risk of not only leukemia, but also a wide array of solid cancers [2,3]. NASA has long been aware of this risk and limits astronauts' risk of exposure-induced death (REID) from cancer by specifying permissible mission durations (PMD) for astronauts on an individual basis. While cancer is present among astronauts, current data does not suggest any excess of known radiation-induced cancers relative to a comparable population of U.S. adults; however, very uncommon cancers have been diagnosed in astronauts including nasopharyngeal cancer, lymphoma of the brain, and acral myxoinflammatory fibroblastic sarcoma. In order to study cancer risk in astronauts, a number of obstacles must be overcome. Firstly, several factors make the astronaut cohort considerably different from the cohorts that have previously been studied for effects resulting from radiation exposure. The high rate of accidents and the much healthier lifestyle of astronauts compared to the U.S. population make finding a suitable comparison population a problematic task. Space radiation differs substantially from terrestrial radiation exposures studied in the past; therefore, analyses of galactic cosmic radiation (GCR) in animal models must be conducted and correctly applied to the human experience. Secondly, a large enough population of exposed astronauts must exist in order to obtain the data necessary to see any potential statistically significant differences between the astronauts and the control population. Thirdly, confounders and effect modifiers, such as smoking, diet, and other space stressors, must be correctly identified and controlled for in those analyses. In order to begin work assessing the astronaut population, the earliest groups of astronauts (selection groups 1-7) provide a unique model. These astronauts were relatively homogenous, white males whose lifestyle characteristics were similar to an average U.S. citizen of the same birth cohort. This work reviews radiation exposure levels, age, and causes of mortality among these early NASA astronauts and discusses the benefits and limitations of assessing such a cohort for radiation-induced cancer risk.

Milder, Caitlin M.↗
NASA NTRS2012

Technical Evaluation of the NASA Model for Cancer Risk to Astronauts Due to Space Radiation

At the request of NASA, the National Research Council's (NRC's) Committee for Evaluation of Space Radiation Cancer Risk Model1 reviewed a number of changes that NASA proposes to make to its model for estimating the risk of radiation-induced cancer in astronauts. The NASA model in current use was last updated in 2005, and the proposed model would incorporate recent research directed at improving the quantification and understanding of the health risks posed by the space radiation environment. NASA's proposed model is defined by the 2011 NASA report Space Radiation Cancer Risk Projections and Uncertainties--2010 . The committee's evaluation is based primarily on this source, which is referred to hereafter as the 2011 NASA report, with mention of specific sections or tables. The overall process for estimating cancer risks due to low linear energy transfer (LET) radiation exposure has been fully described in reports by a number of organizations. The approaches described in the reports from all of these expert groups are quite similar. NASA's proposed space radiation cancer risk assessment model calculates, as its main output, age- and gender-specific risk of exposure-induced death (REID) for use in the estimation of mission and astronaut-specific cancer risk. The model also calculates the associated uncertainties in REID. The general approach for estimating risk and uncertainty in the proposed model is broadly similar to that used for the current (2005) NASA model and is based on recommendations by the National Council on Radiation Protection and Measurements. However, NASA's proposed model has significant changes with respect to the following: the integration of new findings and methods into its components by taking into account newer epidemiological data and analyses, new radiobiological data indicating that quality factors differ for leukemia and solid cancers, an improved method for specifying quality factors in terms of radiation track structure concepts as opposed to the previous approach based on linear energy transfer, the development of a new solar particle event (SPE) model, and the updates to galactic cosmic ray (GCR) and shielding transport models. The newer epidemiological information includes updates to the cancer incidence rates from the life span study (LSS) of the Japanese atomic bomb survivors, transferred to the U.S. population and converted to cancer mortality rates from U.S. population statistics. In addition, the proposed model provides an alternative analysis applicable to lifetime never-smokers (NSs). Details of the uncertainty analysis in the model have also been updated and revised. NASA's proposed model and associated uncertainties are complex in their formulation and as such require a very clear and precise set of descriptions. The committee found the 2011 NASA report challenging to review largely because of the lack of clarity in the model descriptions and derivation of the various parameters used. The committee requested some clarifications from NASA throughout its review and was able to resolve many, but not all, of the ambiguities in the written description.

Source record↗
NASA NTRS2011

Cancer Risk Map for the Surface of Mars

We discuss calculations of the median and 95th percentile cancer risks on the surface of Mars for different solar conditions. The NASA Space Radiation Cancer Risk 2010 model is used to estimate gender and age specific cancer incidence and mortality risks for astronauts exploring Mars. Organ specific fluence spectra and doses for large solar particle events (SPE) and galactic cosmic rays (GCR) at various levels of solar activity are simulated using the HZETRN/QMSFRG computer code, and the 2010 version of the Badhwar and O Neill GCR model. The NASA JSC propensity model of SPE fluence and occurrence is used to consider upper bounds on SPE fluence for increasing mission lengths. In the transport of particles through the Mars atmosphere, a vertical distribution of Mars atmospheric thickness is calculated from the temperature and pressure data of Mars Global Surveyor, and the directional cosine distribution is implemented to describe the spherically distributed atmospheric distance along the slant path at each elevation on Mars. The resultant directional shielding by Mars atmosphere at each elevation is coupled with vehicle and body shielding for organ dose estimates. Astronaut cancer risks are mapped on the global topography of Mars, which was measured by the Mars Orbiter Laser Altimeter. Variation of cancer risk on the surface of Mars is due to a 16-km elevation range, and the large difference is obtained between the Tharsis Montes (Ascraeus, Pavonis, and Arsia) and the Hellas impact basin. Cancer incidence risks are found to be about 2-fold higher than mortality risks with a disproportionate increase in skin and thyroid cancers for all astronauts and breast cancer risk for female astronauts. The number of safe days on Mars to be below radiation limits at the 95th percent confidence level is reported for several Mission design scenarios.

Kim, Myung-Hee Y.↗
NASA NTRS1993

Measuring the metastatic potential of cancer cells

Cancer cells must secrete proteolytic enzymes to invade adjacent tissues and migrate to a new metastatic site. Urokinase (uPA) is a key enzyme related to metastasis in cancers of the lung, colon, gastric, uterine, breast, brain, and malignant melanoma. A NASA technology utilization project has combined fluorescence microscopy, image analysis, and flow cytometry, using fluorescent dyes, and urokinase-specific antibodies to measure uPA and abnormal DNA levels (related to cancer cell proliferation) inside the cancer cells. The project is focused on developing quantitative measurements to determine if a patient's tumor cells are actively metastasizing. If a significant number of tumor cells contain large amounts of uPA (esp. membrane-bound) then the post-surgical chemotherapy or radiotherapy can be targeted for metastatic cells that have already left the primary tumor. These analytical methods have been applied to a retrospective study of biopsy tissues from 150 node negative, stage 1 breast cancer patients. Cytopathology and image analysis has shown that uPA is present in high levels in many breast cancer cells, but not found in normal breast. Significant amounts of uPA also have been measured in glioma cell lines cultured from brain tumors. Commercial applications include new diagnostic tests for metastatic cells, in different cancers, which are being developed with a company that provides a medical testing service using flow cytometry for DNA analysis and hormone receptors on tumor cells from patient biopsies. This research also may provide the basis for developing a new 'magic bullet' treatment against metastasis using chemotherapeutic drugs or radioisotopes attached to urokinase-specific monoclonal antibodies that will only bind to metastatic cells.

Morrison, Dennis R.↗
NASA NTRS2002

Ocular input for human melatonin regulation: relevance to breast cancer

The impact of breast cancer on women across the world has been extensive and severe. As prevalence of breast cancer is greatest in industrialized regions, exposure to light at night has been proposed as a potential risk factor. This theory is supported by the epidemiological observations of decreased breast cancer in blind women and increased breast cancer in women who do shift-work. In addition, human, animal and in vitro studies which have investigated the melatonin-cancer dynamic indicate an apparent relationship between light, melatonin and cancer, albeit complex. Recent developments in understanding melatonin regulation by light in humans are examined, with particular attention to factors that contribute to the sensitivity of the light-induced melatonin suppression response. Specifically, the role of spectral characteristics of light is addressed, and recent relevant action spectrum studies in humans and other mammalian species are discussed. Across five action spectra for circadian and other non-visual responses, a peak sensitivity between 446-484 nm was identified. Under highly controlled exposure circumstances, less than 1 lux of monochromatic light elicited a significant suppression of nocturnal melatonin. In view of the possible link between light exposure, melatonin suppression and cancer risk, it is important to continue to identify the basic related ocular physiology. Visual performance, rather than circadian function, has been the primary focus of architectural lighting systems. It is now necessary to reevaluate lighting strategies, with consideration of circadian influences, in an effort to maximize physiological homeostasis and health.

Review↗
NASA NTRS2011

Organ Dose Assessment and Evaluation of Cancer Risk on Mars Surface

Organ specific fluence spectra and doses for large solar particle events (SPE) and galactic cosmic rays (GCR) at various levels of solar activity are simulated on the surface of Mars using the HZETRN/QMSFRG computer code and the 2010 version of the Badhwar and O Neill GCR model. The NASA JSC propensity model of SPE fluence and occurrence is used to consider upper bounds on SPE fluence for increasing mission lengths. To account for the radiation transmission through the Mars atmosphere, a vertical distribution of Mars atmospheric thickness is calculated from the temperature and pressure data of Mars Global Surveyor. To describe the spherically distributed atmospheric distance on the Mars surface at each elevation, the directional cosine distribution is implemented. The resultant directional shielding by Mars atmosphere at each elevation is then coupled with vehicle and body shielding for organ dose estimates. Finally, cancer risks for astronauts exploring Mars can be assessed by applying the NASA Space Radiation Cancer Risk 2010 model with the resultant organ dose estimates. Variations of organ doses and cancer risk quantities on the surface of Mars, which are due to a 16-km elevation range between the Tharsis Montes and the Hellas impact basin, are visualized on the global topography of Mars measured by the Mars Orbiter Laser Altimeter. It is found that cancer incidence risks are about 2-fold higher than mortality risks with a disproportionate increase in skin and thyroid cancers for male and female astronauts and in breast cancer for female astronauts. The number of safe days, defined by the upper 95% percent confidence level to be below cancer limits, on Mars is analyzed for several Mars mission design scenarios.

Kim, Myung-Hee↗
NASA NTRS2018

Persistence of Gamma-H2AX Foci in Irradiated Bronchial Cells Correlates with Susceptibility to Radiation Associated Lung Cancer in Mice

The risk of developing radiation-induced lung cancer differs between different strains of mice, but the underlying cause of the strain differences is unknown. Strains of mice also differ in their ability to efficiently repair DNA double strand breaks resulting from radiation exposure. We phenotyped mouse strains from the CcS/Dem recombinant congenic strain set for their efficacy in repairing DNA double strand breaks during protracted radiation exposures. We monitored persistent gamma-H2AX radiation induced foci (RIF) 24 hours after exposure to chronic gamma-rays as a surrogate marker for repair deficiency in bronchial epithelial cells for 17 of the CcS/Dem strains and the BALB/cHeN founder strain. We observed a very strong correlation R2 = 79.18%, P < 0.001) between the level of persistent RIF and radiogenic lung cancer percent incidence measured in the same strains. Interestingly, spontaneous levels of foci in non-irradiated strains also showed good correlation with lung cancer incidence (R2=32.74%, P =0.013). These results suggest that genetic differences in DNA repair capacity largely account for differing susceptibilities to radiation-induced lung cancer among CcS/Dem mouse strains and that high levels of spontaneous DNA damage is also a relatively good marker of cancer predisposition. In a smaller pilot study, we found that the repair capacity measured in peripheral blood leucocytes also correlated well with radiogenic lung cancer susceptibility, raising the possibility that such phenotyping assay could be used to detect radiogenic lung cancer susceptibility in humans.

Ochola, Donasian O.↗
NASA NTRSDate not supplied

Plausible Biological Mechanisms Underlying Sex Differences in Radiation-Induced Lung Cancer Risk

Some epidemiological studies suggest that women are at greater risk for radiation-induced lung cancer than men, but this observation is not consistent across all studies. A scientific committee formed by the National Council on Radiation Protection and Measurement evaluated evidence for a sex difference in lung cancer risk from radiation exposuresby reviewing animal studies and assessing the biological plausibility that such a difference might exist. The committee identified four mechanisms that could potentially result in greater radiogenic lung cancer risks for women. The first of these is that radiation exposure increases the relative risk for a molecular subtype of spontaneous lung cancer that occurs predominantly in women. The second is that is that sex chromosome or gene expression differences between men and women places women at greater risk. The third is that hormonal differences between men and women, particularly for estrogen levels, puts women at greater risk. The fourth mechanism is that sex differences in immune system function underlie a sex difference in radiation associated lung cancer risk.None of these mechanisms hasyet been proven to play a role in radiogenic lung cancer risk.

radiation↗
NASA NTRS1993

Screening for prostate cancer

Despite recent advances in both the survival and cure rates for many forms of cancer, unfortunately the same has not been true for prostate cancer. In fact, the age-adjusted death rate from prostate cancer has not significantly improved since 1949, and prostate cancer remains the most common cancer in American men, causing the second highest cancer mortality rate. Topics discussed include the following: serum testosterone levels; diagnosis; mortality statistics; prostate-sppecific antigen (PSA) tests; and the Occupational Medicine Services policy at LeRC.

Weirich, Stephen A.↗
NASA NTRS2002

Cancer Risk Assessment for Space Radiation

Predicting the occurrence of human cancer following exposure to any agent causing genetic damage is a difficult task. This is because the uncertainty of uniform exposure to the damaging agent, and the uncertainty of uniform processing of that damage within a complex set of biological variables, degrade the confidence of predicting the delayed expression of cancer as a relatively rare event within any given clinically normal individual. The radiation health research priorities for enabling long-duration human exploration of space were established in the 1996 NRC Report entitled "Radiation Hazards to Crews of Interplanetary Missions: Biological Issues and Research Strategies". This report emphasized that a 15-fold uncertainty in predicting radiation-induced cancer incidence must be reduced before NASA can commit humans to extended interplanetary missions. That report concluded that the great majority of this uncertainty is biologically based, while a minority is physically based due to uncertainties in radiation dosimetry and radiation transport codes. Since that report, the biologically based uncertainty has remained large, and the relatively small uncertainty associated with radiation dosimetry has increased due to the considerations raised by concepts of microdosimetry. In a practical sense, however, the additional uncertainties introduced by microdosimetry are encouraging since they are in a direction of lowered effective dose absorbed through infrequent interactions of any given cell with the high energy particle component of space radiation. The biological uncertainty in predicting cancer risk for space radiation derives from two primary facts. 1) One animal tumor study has been reported that includes a relevant spectrum of particle radiation energies, and that is the Harderian gland model in mice. Fact #1: Extension of cancer risk from animal models, and especially from a single study in an animal model, to humans is inherently uncertain. 2) One human database is predominantly used for assessing cancer risk caused by space radiation, and that is the Japanese atomic bomb survivors. Fact #2: The atomic-bomb-survivor database, itself a remarkable achievement, contains uncertainties. These include the actual exposure to each individual, the radiation quality of that exposure, and the fact that the exposure was to acute doses of predominantly low-LET radiation, not to chronic exposures of high-LET radiation expected on long-duration interplanetary manned missions.

Richmond, Robert C.↗
NASA NTRS2000

Breast Cancer Detection

The BioScan System was developed by OmniCorder Technologies, Inc. at the Jet Propulsion Laboratory. The system is able to locate cancerous lesions by detecting the cancer's ability to recruit a new blood supply. A digital sensor detects infrared energy emitted from the body and identifies the minute differences accompanying the blood flow changes associated with cancerous cells. It also has potential use as a monitoring device during cancer treatment. This technology will reduce the time taken to detect cancerous cells and allow for earlier intervention, therefore increasing the overall survival rates of breast cancer patients.

Source record↗