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At least 973 records · Page 54Linked to original sources
PubMed2002

Increased radioresistance, modelling of carcinogenesis and low-dose risk estimation.

Increased radioresistance for exposures to low-LET radiation with doses exceeding a few hundred milligray is a well established fact for cell inactivation in vitro and in vivo. Cell inactivation and the subsequent replacement by intermediate cells is a possible mechanism for a radiation-induced increase of the number of intermediate cells in carcinogenesis in an irradiated organ. In the present work this mechanism has been implemented in the two-step clonal expansion model for carcinogenesis in the lung in addition to the conventionally assumed radiation-induced initiation. Compared with the original TSCE model, the new model has the same number of parameters and fits the lung cancer incidence data for the atomic bomb survivors slightly better. The resulting estimate of the lung cancer risk after low-dose exposures of persons with an age of 20 or 40 years is similar in the two models; however, it is higher by about an order of magnitude in the new model for an age-at-exposure of 60 years. Age-at-exposure dependence and risk estimates at low dose turn out to be closer to best estimates obtained with a constant-excess-relative-risk model for different age-at-exposure subgroups.

Animals↗
PubMed2004

Using Medicare data to estimate the number of cases missed by a cancer registry: a 3-source capture-recapture model.

BACKGROUND: Cancer surveillance is essential for assessing patterns of cancer occurrence. State cancer registries do not capture all available cases potentially biasing results. Secondary data may be useful in identifying new cases and estimating the number of cases missed. OBJECTIVE: We sought to create 2 distinct data sources from Medicare claims to use in combination with registry data as 3 sources for a capture-recapture analysis to estimate the capture rate and bias in capture of a statewide cancer registry. METHODS: Data from the Virginia cancer registry (Registry) were merged with Medicare inpatient (Part A) as well as Medicare outpatient and physician claims (Part B) to provide 3 sources to estimate missing cases. A 3-source loglinear model was used to estimate the number of missing cancer cases for breast, lung, colorectal, and prostate cancer. Models included main effects and interactions. Additional analysis looked at the effect of demographic and comorbidity variables. RESULTS: Loglinear models demonstrated mostly positive dependence between the 3 sources, implying that 2-source models would underestimate missing cases and overestimate capture rates. Using capture-recapture estimates of total number of cancer cases as the denominator, capture rates for Registry ranged from 59% (colorectal) to 74% (lung). When the aggregate of cases found by either Medicare or Registry were used the capture rates ranged from 74% (prostate) to 89% (breast). Further analysis indicated that capture rates differed by demographic characteristics. CONCLUSION: We conclude that Medicare claims are useful to supplement a Registry, estimate the number of missing cases, and assess bias in capture.

Aged↗
PubMed1964

TUMOURS OF THE CENTRAL NERVOUS SYSTEM IN CHILDREN.

One hundred and fifty-five tumours of the central nervous system which occurred in children in the north west of England during a period of nine years are analysed from a pathological point of view. It is probable that these represent over 90% of all such tumours occurring in the region at that time and that the relative incidence of various tumour types is, therefore, a true one: just over a fifth (35) were medulloblastomas; just under a fifth (29) were juvenile astrocytomas; a similar group (33) were of the adult astrocytic type; there were 24 ependymomas and 34 in miscellaneous minor groups.

Adolescent↗
PubMed2005

Alteration of protein expression pattern of vascular endothelial growth factor (VEGF) from soluble to cell-associated isoform during tumourigenesis.

BACKGROUND: Vascular endothelial growth factor (VEGF) is a potent mitogen for endothelial cells, and its expression has been correlated with increased tumour angiogenesis. Although numerous publications dealing with the measurement of circulating VEGF for diagnostic and therapeutic monitoring have been published, the relationship between the production of tissue VEGF and its concentration in blood is still unclear. The aims of this study were to determine: 1) The expression pattern of VEGF isoforms at the protein level in colorectal and lung adenocarcinoma in comparison to the pattern in corresponding adjacent normal tissues 2) The relationship between the expression pattern of VEGF and total level of circulating VEGF in the blood to clarify whether the results of measuring circulating VEGF can be used to predict VEGF expression in tumour tissues. METHODS: Ninety-four tissue samples were obtained from patients, 76 colorectal tumour tissues and 18 lung tumour tissues. VEGF protein expression pattern and total circulating VEGF were examined using western blot and capture ELISA, respectively. RESULTS: Three major protein bands were predominately detected in tumour samples with an apparent molecular mass under reducing conditions of 18, 23 and 26 kDa. The 18 kDa VEGF protein was expressed equally in both normal and colorectal tumour tissues and predominately expressed in normal tissues of lung, whereas the 23 and 26 kDa protein was only detected at higher levels in tumour tissues. The 18, 23 and 26 kDa proteins are believed to represent the VEGF121, the VEGF165 and the VEGF189, respectively. There was a significant correlation of the expression of VEGF165 with a smaller tumour size maximum diameter < 5 cm (p < 0.05), and there was a significant correlation of VEGF189 with advanced clinical stage of colorectal tumours. The measurement of total circulating VEGF in serum revealed that cancer patients significantly (p < 0.001) possessed a higher level of circulating VEGF (1081 +/- 652 pg/ml in colorectal and 1,251 +/- 568 pg/ml in lung) than a healthy volunteer group (543 +/- 344 pg/ml). No correlation between the level of circulating VEGF and the pathologic features of tumours was observed. CONCLUSION: Our findings indicate that the expression patterns of VEGF isoforms are altered during tumourigenesis as certain isoform overexpression in tumour tissues correlated with tumour progression indicating their important role in tumour development. However, measurement of VEGF in the circulation as a prognostic marker needs to be carefully evaluated as the cell-associated isoform (VEGF189), but not the soluble isoform (VEGF121 and VEGF165) appears to play important role in tumour progression.

Adenocarcinoma↗