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Biomedical subjects

H S Evans

Publications and source records attributed to H S Evans.

17 recordsLinked to original sources

The risk of cancer in HIV-infected people in southeast England: a cohort study.

This study used data from the Communicable Disease Surveillance Centre's national HIV database and the Thames Cancer Registry to assess the risk of cancer in HIV-infected people in southeast England. Among 26 080 HIV-infected men with 158,660 person-years follow-up, 1851 cancers, and among 7110 HIV-infected women (31 098 person-years), 171 cancers were identified. The standardised incidence ratio (SIR) for all non-AIDS-defining cancers was significantly increased in HIV-infected men (2.8, 95% confidence interval (CI) 2.6-3.1) but was nonsignificant in HIV-infected women (1.1, 95% CI 0.8-1.6). Most of the cancers observed were in men (n = 1559) and women (n = 127) with AIDS, and among them, the SIR for all non-AIDS-defining cancers was significantly increased in men (8.2, 95% CI 7.2-9.2) and women (2.8, 95% CI 1.6-4.6). The SIR for all non-AIDS-defining cancers was only just significantly increased in men with HIV-infection but not AIDS (1.2, 95% CI 1.0-1.5) and was nonsignificant in such women (0.8, 95% CI 0.5-1.2).

Acquired Immunodeficiency Syndrome↗

Second primary cancers after cervical intraepithelial neoplasia III and invasive cervical cancer in Southeast England.

OBJECTIVE: Multiple primary cancers may arise in an individual because they share a common environmental risk factor (such as smoking); genetic predisposition or immunodeficiency may predispose to both cancers, or treatment for one cancer may cause a second cancer. The objective of this analysis was to identify which, if any, cancers occur more often than would be expected in a cohort of women diagnosed with cervical intraepithelial neoplasia III (CIN III) and in women with invasive cervical cancer. METHODS: The Thames Cancer Registry was used to identify two cohorts of women diagnosed with either CIN III or invasive cervical cancer. The number of subsequent cancers at other sites was observed and compared to the expected number, based on relevant age-, sex-, and period-specific incidence rates. Standardised incidence rates (SIRs) were calculated assuming a Poisson distribution. RESULTS: The following cancer sites were significantly increased after a diagnosis of either CIN III or cervical cancer: anus (SIR 5.9 and 6.3, respectively), lung (SIR 1.8 and 2.5), vulva (SIR 4.4 and 1.9), vagina (SIR 18.5 and 8.0), and kidney (SIR 1.6 and 1.9). In addition, the incidence of cancers of the rectum, bladder, and connective tissue was significantly increased after invasive cervical cancer. Cervical cancers were seen significantly more often than expected after cancers of the anus and vagina. CONCLUSION: These results support the hypothesis that cancers of the cervix, anus, vulva, and vagina share common risk factors such as human papillomavirus and smoking.

Adult↗

The risk of subsequent primary cancers after colorectal cancer in southeast England.

BACKGROUND: Multiple cancers may occur in an individual because of a genetic predisposition, environmental exposure, cancer therapy, or immunological deficiency. Colorectal cancer is one of the most commonly diagnosed cancers, and inherited factors play an important role in its aetiology. AIMS: To characterise the occurrence of multiple primary cancers in patients diagnosed with colorectal cancer and explore the possibility of a common aetiology for different cancer sites. PATIENTS: The Thames Cancer Registry database was used to identify patients with a first colorectal cancer, resident in the North or South Thames region, diagnosed between 1 January 1961 and 31 December 1995. A total of 127 281 patients were included, 61 433 men and 65 848 women. METHODS: Observed numbers of cancers occurring after the diagnosis of colorectal cancer were compared with expected numbers, calculated using appropriate age, sex, and period specific rates, to obtain standardised incidence ratios. The occurrence of colorectal cancers subsequent to cancers at other sites was also examined. RESULTS: Small intestinal cancer was significantly increased in men diagnosed with colorectal cancer before the age of 60 years and in women diagnosed with colorectal cancer after the age of 65 years. Colorectal cancer was also significantly increased after a first diagnosis of cancer of the small intestine. Other cancer sites with a significant increase after colorectal cancer included the cervix uteri, corpus uteri, and ovary. CONCLUSIONS: Patients with colorectal cancer are at increased risk of developing cancer at a number of other sites. Some of these associations are consistent with the effects of known inherited cancer susceptibility genes.

Adult↗

Cancer risks in women with 2 breast or ovarian cancers: clues to genetic cancer susceptibility.

Women diagnosed with 2 cancers of the breast and/or ovary are at higher risk of developing subsequent cancers. Using registrations from the Thames Cancer Registry, we quantified the risks at different cancer sites. Increased risks were found for cancers that are part of the BRCA1 and BRCA2 tumour spectrum: oropharyngeal cancer, malignant melanoma of the skin (BRCA2) and colon cancer (BRCA1). We also found significantly increased risks of myeloid leukaemia (probably due to radiotherapy) and of cancer of the corpus uteri (which may be due to hormonal factors).

Breast Neoplasms↗

Incidence of multiple primary cancers in a cohort of women diagnosed with breast cancer in southeast England.

Among women in the Thames Cancer Registry database with a first breast cancer diagnosed between 1961-1995 observed numbers of subsequent cancers were compared with expected numbers and standardized incidence ratios were calculated. The occurrence of breast cancers subsequent to cancers at other sites was also examined. Women diagnosed with breast cancer before age 50 had significantly elevated risks for 9 cancer sites namely, oesophagus, stomach, lung, bone, connective tissue, breast, corpus uteri, ovary and myeloid leukaemia compared with 2 sites (corpus uteri and myeloid leukaemia) in women diagnosed at age 50 and above. Some of these associations are consistent with the effects of known inherited cancer susceptibility genes, shared environmental factors, or therapy.

Age Factors↗

Outbreaks of waterborne infectious intestinal disease in England and Wales, 1992-5.

Following the introduction of an improved surveillance system for infectious intestinal disease outbreaks in England and Wales, the Public Health Laboratory Service Communicable Disease Surveillance Centre received reports of 26 outbreaks between 1 January 1992 and 31 December 1995 in which there was evidence for waterborne transmission of infection. In these 26 outbreaks, 1756 laboratory confirmed cases were identified of whom 69 (4%) were admitted to hospital. In 19 outbreaks, illness was associated with the consumption of drinking water from public supplies (10 outbreaks) or private supplies (9 outbreaks). The largest outbreak consisted of 575 cases. In 4 of the remaining 7 outbreaks, illness was associated with exposure to swimming pool water. Cryptosporidium was identified as the probable causative organism in all 14 outbreaks associated with public water supplies and swimming pools. Campylobacter was responsible for most outbreaks associated with private water supplies. This review confirms a continuing risk of cryptosporidiosis from chlorinated water supplies in England and Wales, and reinforces governmental advice to water utilities that water treatment processes should be rigorously applied to ensure effective particle removal. High standards of surveillance are important for prompt recognition of outbreaks and institution of control measures. As microbiological evidence of water contamination may be absent or insufficient to implicate a particular water supply, a high standard of epidemiological investigation is recommended in all outbreaks of suspected waterborne disease.

Communicable Diseases↗

General outbreaks of infectious intestinal disease in England and Wales: 1995 and 1996.

One thousand nine hundred and nineteen general outbreaks of infectious intestinal disease in England and Wales were reported to the PHLS Communicable Disease Surveillance Centre (CDSC) between 1 January 1995 and 31 December 1996, compared with 1073 in the previous two years. A minimum data set was received for 1568 (82%) of the 1919 outbreaks. Over 40,000 people were affected and about 2% of those who were ill were admitted to hospital. Seventy-one deaths were reported. The duration of outbreaks varied between less than one day and 202 days (median six days) according to the pathogen. Small round structured virus (SRSV) (43%) and salmonellas (15%) were the most commonly reported pathogens. In almost a quarter of the outbreaks (24%) the aetiology was unknown. Over half the outbreaks (64%) were reported to be transmitted from person to person, most of which were due to SRSV and occurred in residential homes and hospitals. Twenty-two per cent of outbreaks were described as mainly foodborne, 51% of which were due to salmonellas. The number of outbreaks reported in each region ranged from 52 in Wales to 512 in Northern and Yorkshire.

Caliciviridae Infections↗

Outbreaks of infectious intestinal disease in residential institutions in England and Wales 1992-1994.

Data from the surveillance scheme of all general outbreaks of infectious intestinal disease in England and Wales reported to or otherwise identified, by the Public Health Laboratory Service Communicable Disease Surveillance Centre (CDSC) in 1992 and 1994 were used to describe the epidemiology of outbreaks of infectious intestinal disease in residential institutions. Outbreaks in residential institutions accounted for 22% (282/1275) of all outbreaks with most, 95% (268/282), occurring in homes for the elderly. The commonest pathogens in these 282 outbreaks were small round structured viruses 48% (132), salmonellas 17% (49). Clostridium perfringens 8% (23), rotavirus 5% (15) and Shigella sonnei 2% (6). The mode of transmission was described as mainly person to person in 71% (200 outbreaks) and mainly foodborne in 21% (58 outbreaks). The mean duration of outbreaks was 9 days. Duration of outbreaks varied with both the mode of transmission and the pathogen involved. The mean attack rate was 37%. Illness was reported in 5872 people. One or more individuals were admitted to hospital in 22% of outbreaks. Twenty-six deaths were reported, of which 18 were attributed to salmonellosis. Outbreaks in residential institutions are common. Attack rates are high and outbreaks are often prolonged, with high morbidity and mortality. There is a need for effective infection control policies which include appropriate training of staff, simple surveillance systems and readily available expert advice to ensure outbreaks are rapidly controlled.

Aged↗

Outbreaks of foodborne viral gastroenteritis in England and Wales: 1992 to 1994.

Outbreaks of foodborne viral gastroenteritis in England and Wales from 1992 to 1994 have been analysed using data from the national surveillance scheme for general outbreaks of infectious intestinal disease. The cause was virologically confirmed for 389 (31%) of the 1280 outbreaks for which a minimum set of data were collected. Forty-seven of the 389 were attributed to foodborne transmission, 41 of which were caused by small round structured viruses (SRSV). An infected food handler was suspected to be a contributing factor in 14 and the consumption of oysters in eight of these 41 foodborne SRSV outbreaks. No seasonal pattern emerged. The highest incidences occurred in Wales, West Midlands, and South Western regional health authorities. The annual rate of outbreaks did not increase during the three year period (Chi square for linear trend 0.6; p = 0.4). Much remains to be discovered about the epidemiology of foodborne viruses, and outbreaks present an opportunity to enhance our knowledge. As molecular diagnostic techniques become routinely available, it is likely that the role of viruses in foodborne outbreaks will be increasingly recognised.

Data Collection↗

Outbreaks of infectious intestinal disease in schools and nurseries in England and Wales 1992 to 1994.

We present data on outbreaks of infectious intestinal disease in schools and nurseries obtained from the surveillance scheme of all general outbreaks of infectious intestinal disease in England and Wales reported to the PHLS Communicable Disease Surveillance Centre between 1992 and 1994. A minimum set of data was received for 1280 outbreaks, 95 of which (7%) arose in schools and nurseries. The commonest pathogens were salmonellas, Shigella sonnei, and small round structured viruses. The mode of transmission was described as mainly from person to person in 55 outbreaks and mainly foodborne in 30. The mean attack rate was 30% and median duration was 10 days. The attack rate and duration varied with the pathogen involved. Forty-five of the 3118 people reported to have been ill were admitted to hospital. Outbreaks in schools and nurseries are common. Attack rates are high and such outbreaks are often prolonged. Effective infection control policies and appropriate training of staff are needed. Good local systems for surveillance can help identify outbreaks quickly and allow control measures to be applied early.

Adolescent↗

General outbreaks of infectious intestinal disease in England and Wales 1992 to 1994.

Data from the surveillance scheme of general outbreaks of infectious intestinal disease in England and Wales, reported to the PHLS Communicable Disease Surveillance Centre (CDSC), were used to review 1280 of the 1594 outbreaks identified between 1 January 1992 and 31 December 1994 for which a minimum data set was captured. The number of outbreaks reported in each regional health authority ranged from 31 in Mersey to 221 in Yorkshire. The commonest pathogens reported were salmonellas in 32% (412) of outbreaks, small round structured virus (SRSV) in 27% (342), Clostridium perfringens in 7% (90), and Shigella sonnei in 4% (46). The main mode of transmission was described as foodborne in 50% (642), over half of which were caused by salmonellas, and person to person in 39% (496), over half of which were caused by SRSV. Most outbreaks transmitted from person to person occurred in hospitals and in residential institutions for elderly people. Outbreaks lasted from one to 217 days (median five days) and their duration varied with the pathogen. The median attack rate was 37%. Illness was reported in 34,158 people, 751 of whom (2%) were admitted to hospital. There were 55 deaths, 28 of which were associated with salmonella and 12 with SRSV. Most of the outbreaks reported and the associated morbidity and mortality could have been prevented by following standard food hygiene practices, implementing infection control policies, and ensuring that food entering kitchens was of the highest microbiological quality possible.

Clostridium Infections↗

Outbreaks of infectious intestinal disease associated with person to person spread in hotels and restaurants.

Twenty-eight outbreaks of infectious intestinal disease, reported as being transmitted mainly by the person to person route, were identified in association with retail catering premises, such as hotels, restaurants, and public houses, in England and Wales between 1992 and 1994. Five thousand and forty-eight people were at risk in these outbreaks and 1234 were affected. Most of the outbreaks (over 90%) occurred in hotels. Small round structured viruses were the most commonly detected pathogens. Diarrhoea and vomiting were common symptoms and most of the outbreaks occurred in the summer months. Control measures to contain infectious individuals and improved hygiene measures are necessary to contain such outbreaks.

Communicable Diseases↗

The Public Health Laboratory Service national case-control study of primary indigenous sporadic cases of campylobacter infection.

The aetiology of sporadic campylobacter infection was investigated by means of a multicentre case-control study. During the course of the study 598 cases and their controls were interviewed. Conditional logistic regressional analysis of the data collected showed that occupational exposure to raw meat (odds ratio [OR] 9.37; 95% confidence intervals [CI] 2.03, 43.3), having a household with a pet with diarrhoea (OR 2.39; CI 1.09, 5.25), and ingesting untreated water from lakes, rivers and streams (OR 4.16; CI 1.45, 11.9) were significant independent risk factors for becoming ill with campylobacter. Handling any whole chicken in the domestic kitchen that had been bought raw with giblets, or eating any dish cooked from chicken of this type in the home (OR 0.41-0.44; CI 0.24, 0.79) and occupational contact with livestock or their faeces (OR 0.44; CI 0.21, 0.92) were significantly associated with a decrease in the risk of becoming ill with campylobacter.

Adolescent↗

Analysis of HPV-1 E4 gene expression using epitope-defined antibodies.

Six monoclonal antibodies (mAbs) have been raised against the E4 proteins of HPV-1. Five of these were found to recognize denaturation-resistant epitopes as determined by Western blotting--and their binding sites were identified by determining their reactivity against a panel of bacterial E4--beta-galactosidase fusion proteins which contained progressive deletions at the C-terminal end of the E4 region. The five mAbs were found to bind to four distinct sites. By using these epitope-defined mAbs, along with anti-peptide antibodies raised against putative N- and C-terminal E4 sequences, we have determined the relationships between the eight distinct polypeptides (mol. wt 10/11 kd, 16/17 kd, 21/23 kd and 32/34 kd) previously shown to be expressed from the E4 gene of HPV-1 in productively infected papillomas. The 17 kd E4 polypeptide appears to be the product of a spliced mRNA encoding five amino acids from open reading frame (ORF) E1 joined onto 120 from the E4 ORF. The 16 kd and 10/11 kd proteins, which may be derived from this, lack sequences (approximately 15 and 70 amino acids respectively) encoded by the 5' end of the E4 gene. The 32/34 kd proteins were detected by all antibodies which reacted with the 16/17 kd polypeptides, suggesting that they represent dimers of the latter species. The 21/23 kd polypeptides, however, do not appear to be simple dimers of the 10/11 kd protein as previously predicted, and reacted with antibodies whose epitopes mapped in the N-terminal half of the E4 protein.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

Monoclonal antibodies to the latent membrane protein of Epstein-Barr virus reveal heterogeneity of the protein and inducible expression in virus-transformed cells.

Monoclonal antibodies specific for the 'latent membrane protein' (LMP) of Epstein-Barr virus (EBV), one of the effector proteins of EBV-induced B cell transformation, have been generated from mice immunized with a beta-galactosidase fusion protein containing the carboxyl half of the B95.8 strain LMP sequence. Four monoclonal IgG1 antibodies, designated CS.1, CS.2, CS.3 and CS.4, which together recognized at least three different epitopes on the molecule, were used to examine various aspects of LMP expression in B cell lines transformed in vitro. The pooled CS.1 to 4 reagent detected the LMPs encoded by each of 20 geographically distinct EBV isolates, despite a degree of inter-isolate heterogeneity in the size and antigenicity of the protein. In cell lines carrying the prototype B95.8 virus strain, particularly if these were virus producers, an additional lower molecular weight LMP was also detected; this appeared to correspond to the truncated form of the protein already predicted to exist from the analysis of B95.8 lytic cycle mRNAs. Attempts were made to identify an analogous truncated form of LMP in cell lines carrying other virus isolates after treatment with phorbol ester and/or sodium butyrate to induce virus production. Surprisingly these experiments showed that expression of the full length LMP molecule was itself strongly inducible by these agents; when monitored at the single cell level, this was a generalized response and was not restricted to cells entering a lytic cycle. Expression of LMP in EBV-transformed B cells therefore appears to be subject to a distinct type of regulation.

Antibodies, Monoclonal↗