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J Peto

Publications and source records attributed to J Peto.

At least 73 records · Page 4Linked to original sources
PubMed1990

An overview of prognostic factors in small cell lung cancer. A report from the Subcommittee for the Management of Lung Cancer of the United Kingdom Coordinating Committee on Cancer Research.

Several studies of small cell lung cancer (SCLC) treatments have been performed in the United Kingdom. In some, prognostic factor analyses were carried out but the results were not entirely consistent. The Lung Cancer Subcommittee of the United Kingdom Coordinating Committee on Cancer Research (UKCCCR) consequently initiated an overview of these studies with the aim of identifying the important prognostic factors using a large number of patients. Information on almost 4,000 patients was available, but it was necessary to perform analyses on smaller subsets because the variables recorded in individual studies were inconsistent. A number of variables contributed significantly to the prediction of likely survival over the 6 months after starting treatment, but performance status (PS), alkaline phosphatase (AlkP) and disease stage were shown to be the most important; aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) may also be useful. A prognostic index was devised for this initial period and validated using independent data. For patients who survived the first 6 months, the pre-treatment variables important for prognosis in the 6-24 month period were stage, PS and plasma sodium (Na). The Subcommittee recommends that performance status, disease stage, AlkP, Na, AST and LDH should be measured in all future SCLC studies to assist comparisons between studies and possibly the selection of patients for different treatment strategies. The additional recording of five other variables would allow a more definitive overview to be performed at some future date.

Adult↗
PubMed1990

An update of cancer mortality among chrysotile asbestos miners in Balangero, northern Italy.

The mortality experience of a cohort of chrysotile miners employed since 1946 in Balangero, northern Italy was updated to the end of 1987 giving a total of 427 deaths out of 27,010 man-years at risk. A substantial excess mortality for all causes (standardised mortality ratio (SMR) = 149) was found, mainly because of high rates for some alcohol related deaths (hepatic cirrhosis, accidents). For mortality from cancer, however, the number of observed deaths (82) was close to that expected (76.2). The SMR was raised for oral cancer (SMR 231 based on six deaths), cancer of the larynx (SMR 267 based on eight deaths), and pleura (SMR 667 based on two deaths), although the excess only reached statistical significance for cancer of the larynx. Rates were not increased for lung, stomach, or any other type of cancer. No consistent association was seen with duration or cumulative dust exposure (fibre-years) for oral cancer, but the greatest risks for laryngeal and pleural cancer were in the highest category of duration and degree of exposure to fibres. Although part of the excess mortality from laryngeal cancer is probably attributable to high alcohol consumption in this group of workers, the data suggest that exposure to chrysotile asbestos (or to the fibre balangeroite that accounts for 0.2-0.5% of total mass in the mine) is associated with some, however moderate, excess risk of laryngeal cancer and pleural mesothelioma. The absence of excess mortality from lung cancer in this cohort is difficult to interpret.

Alcohol Drinking↗
PubMed1990

The contribution of inherited predisposition to cancer incidence.

Only a small proportion of cancers, arising in inherited syndromes such as polyposis coli, have an unequivocally inherited basis. Nevertheless, most common cancers show familial clustering, much of which may be due to inherited predisposition. If so, there may be wide variation in genetic susceptibility to common cancers. The precise models of susceptibility are unclear, but for ovarian cancer and breast cancer there is some evidence that a small proportion of cases result from highly penetrant dominant genes. This has been confirmed recently for breast cancer by genetic linkage studies. Clear evidence for genetic susceptibility has been obtained for Hodgkin's disease and nasopharyngeal carcinoma, where the existence of susceptibility genes at the HLA locus has been demonstrated by linkage analysis. These genes could account for the majority of cases of these cancers. Identification of other cancer susceptibility genes should be possible, either directly using linkage analysis, or through identification of constitutional phenotypes related to cancer risk.

Disease Susceptibility↗
PubMed1989

Cancer treatment trials--past failures, current progress and future prospects.

Randomized trials are usually too small to provide decisive evidence on the effectiveness of cancer therapy, and most therapeutic developments have been based on studies of tumour response. This approach, together with survival comparisons using historical controls, has led to the development of effective chemotherapy for a few very responsive tumours, but not for most common cancers, where the impact of treatment on survival is quite small. It is difficult to distinguish effective and ineffective innovations in the treatment of such cancers, and consistent progress, in which the more effective treatments are developed and the less effective ones discarded, cannot be achieved without comparisons based on large numbers of randomized patients. The combined evidence on adjuvant therapy for breast cancer and colorectal cancer is reviewed, and a new meta-analysis of published chemotherapy trials in advanced ovarian cancer is presented. The evidence that certain adjuvant regimens can prolong survival is conclusive for breast cancer and quite strong for colorectal cancer, and there is suggestive evidence that cis-platinum prolongs survival in advanced ovarian cancer. Such results illustrate the importance of large randomized trials in evaluating and improving the treatment of common cancers. The major difficulty in achieving large patient entry to randomized studies is the reluctance of many oncologists to participate in collaborative clinical research. The reasons underlying this reluctance, and the way in which such collaboration should be organized to meet these objections, are also discussed.

Clinical Trials as Topic↗
PubMed1988

Cancers of the respiratory tract in mustard gas workers.

In a study of a cohort of 2498 men and 1032 women employed in the manufacture of mustard gas in Cheshire during the second world war 3354 (95%) individuals were successfully traced for mortality to the end of 1984. Large and highly significant excesses were observed as compared with national death rates for deaths from cancer of the larynx (11 deaths observed, 4.04 expected, p = 0.003), pharynx (15 observed, 2.73 expected, p less than 0.001), and all other buccal cavity and upper respiratory sites combined (lip, tongue, salivary gland, mouth, nose) (12 observed, 4.29 expected, p = 0.002). For lung cancer, a highly significant but more moderate excess was observed (200 observed, 138.39 expected, p less than 0.001). Significant excesses were also observed for deaths from acute and chronic non-malignant respiratory disease (131 observed, 91.87 expected and 185 observed, 116.31 expected, respectively). The risks for cancers of the pharynx and lung were significantly related to duration of employment. None of these results is substantially altered when expected numbers are calculated from Cheshire urban areas rather than national rates, although the relative risks for lung cancer and non-malignant respiratory disease are substantially reduced if rates for Merseyside, the nearest large conurbation, are used. The results provide strong evidence that exposure to mustard gas can cause cancers of the upper respiratory tract and some evidence that it can cause lung cancer and non-malignant respiratory disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Cohort Studies↗
PubMed1987

Medical Research Council Childhood Leukaemia Trial VIII compared with trials II-VII: lessons for future management.

This improvement in medium disease-free survival is probably a result of sustained early cell kill, and UKALL VIII has enabled us to define risk categories requiring even further continuous intensification, as now introduced in MRC UKALL X. Thanks to the greater availability of blood products, for example, the rational use of antibiotics and the development of expertise amongst nurses and doctors, such sustained therapy can now be delivered on a multi-centre basis, but only in experienced centres. The monitoring and removal of morbidity are essential if the advantages of this more sustained chemotherapy are to be realised. All elements of therapy require controlling and patients, parents and, above all, doctors must comply with protocol requirements in order to build further upon these initial promising results.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

AIDS and promiscuity.

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Acquired Immunodeficiency Syndrome↗
PubMed1986

Passive smoking.

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Adult↗
PubMed1986

Cohort study analysis with a FORTRAN computer program.

We describe the analysis of cohort study data with a standard FORTRAN program which should run on most computers. It provides a summary measure of the mortality (or incidence) rate ratio between the study cohort and some standard population, based either on person-years at risk or on proportional mortality, and adjusted for age, sex and calendar period; a test of the statistical significance of the ratio; and a set of observed death rates in the study cohort. Results may also be produced in a form suitable for use with GLIM. The analysis may be subdivided into a range of time intervals since each subject was first exposed to risk. The program provides for movement of subjects between different 'level-of-exposure' subgroups within the cohort, and for various methods of censoring. It allows considerable flexibility in data management, and is available with complete documentation and a worked example. The program should enable epidemiologists with little computing experience to carry out formal analysis of cohort studies.

Adolescent↗
PubMed1986

Contribution of environmental fibers to respiratory cancer.

This article reviews studies of the carcinogenicity of mineral fibers, notably asbestos, and presents seven major recommendations for further research. Mineral fibers represent the greatest cause--after cigarette smoke--of respiratory cancer due to air pollutants. Past asbestos exposure may currently account for 2000 mesothelioma deaths per year and 4000 to 6000 lung cancer deaths per year. All major commercial types of asbestos (crocidolite, amosite, and chrysotile) can cause each of the major asbestos-related respiratory diseases. Lung cancers in asbestos-exposed individuals probably do not have a different distribution of histological types from that of non-asbestos-related lung cancers. Nonoccupational exposures are likely to be associated with malignant disease outcomes qualitatively similar to those associated with occupational exposures. Further investigations of fibers are needed to characterize the relationships among physicochemical properties, patterns of migration and clearance, dose, and adverse health effects. Transmission electron microscopy has been found to be the preferred method of analysis of environmental fibers. Relations among time factors (e.g., age at first exposure), dose, and risk for adverse health effects require analyses of existing and new epidemiologic studies of exposed cohorts. Concomitant exposure, behavioral factors, and host factors affecting susceptibility to asbestos should be identified.

Air Pollutants↗
PubMed1986

Models for respiratory cancer in nickel refinery workers.

Lung and nasal sinus cancer death rates among employees of a nickel refinery in South Wales were examined from the standpoint of quantifying the relationship between exposure and the risk of these two cancers. Areas in the refinery associated with high risk were identified by using a matched case-control approach, and a simple index of exposure for each man was constructed accordingly based on the duration of time spent in these areas. The dependence of relative risk and absolute excess risk for lung and nasal sinus cancers on age at first employment, calendar period of first employment, time since first employment, and duration of exposure in high-risk areas was then analyzed. The relative risk for nasal sinus cancer increased sharply with increasing age at first exposure but remained roughly constant throughout the period of follow-up, while that for lung cancer was independent of age at first exposure and dropped sharply with increasing time since first employment. The implications and limitations of these analyses are discussed in relation to the multistage theory of carcinogenesis and occupational risk assessment.

Adult↗
PubMed1985

Prospective study of cancer in patients with hypogammaglobulinaemia.

Among 377 patients with primary hypogammaglobulinaemia, mainly common variable immunodeficiency (CVID), 316 patients survived the first 2 years after diagnosis and were the subject of a study of cancer incidence. Among the 220 patients with CVID, there was a 5-fold increase of cancer due mainly to large excesses of stomach cancer (47-fold) and lymphomas (30-fold). The excess of stomach cancer is probably related to the high frequency of achlorhydria in CVID. 3 of the 7 patients with stomach cancer and CVID survived for 5 years or longer.

Adolescent↗
PubMed1985

Bladder cancer mortality of workers exposed to aromatic amines: analysis of models of carcinogenesis.

The effects of various factors were evaluated on both relative risk (multiplicative model), and absolute excess risk (additive model) of bladder cancer among 664 workers of a dyestuff factory in Northern Italy. These workers were exposed to aromatic amines in fairly constant working conditions from 1922 to 1970, and were employed for at least one year. They were followed up till the end of 1981 for a total of 12,302 man-years at risk. Under both models, the risk was greater for workers directly involved in aromatic amine manufacture than for those with only intermittent exposure. There was no marked effect of age at first exposure on the absolute excess risk of bladder cancer, but the relative risk was strongly and negatively related to age at first exposure. Under the multistage theory of carcinogenesis, this pattern of risk indicates an early stage effect. Absolute excess risk increased sharply during exposure, and continued to rise, although less sharply, after exposure had ceased. Relative risk, however, decreased after cessation of exposure, indicating a possible late stage effect. Thus, the results derived from both additive and multiplicative models are not in contrast when interpreted in terms of the multistage theory of carcinogenesis, though they are not totally consistent with a single-stage effect, either early or late. Aromatic amines may act on a stage somewhere between the first and penultimate, or on more than one stage of the process of carcinogenesis. Alternatively, it is possible that imprecision in the job classification or other observational problems may obscure the trends, or produce fictitious trends in the effects of variables such as age at first exposure and time since last exposure. Finally, such a pattern of trends could emerge if there were only two stages and the first and penultimate stage were the same.

Amines↗