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F Xavier Bosch

Publications and source records attributed to F Xavier Bosch.

At least 37 records · Page 2Linked to original sources
PubMed2004

Cervical cancer control, priorities and new directions.

Cervical cancer is caused by infection with a range of high risk "oncogenic" human papillomavirus (HPV) types, and it is now accepted that >99% of cervical cancer is initiated by HPV infection. The estimated lifetime risk of cervical cancer is nevertheless relatively low (less than 1 in 20 for most community based studies). Although sensitivity and specificity of the available diagnostic techniques are suboptimal, screening for persistent HPV infection is effective in reducing the incidence of cervical cancer. Infection can be detected by molecular techniques or by cytological examination of exfoliated cervical cells. Persistent infection is the single best predictor of risk of cervical cancer. The latest findings of HPV and cervical cancer research need to be widely disseminated to the scientific and medical societies that are updating screening and management protocols, public health professionals, and to women and clinicians. This report reviews current evidence, clinical implications and directions for further research in the prevention, control and management of cervical cancer. We report the conclusions of the Experts' Meeting at the EUROGIN 2003 conference.

Female↗
PubMed2004

Primary liver cancer: worldwide incidence and trends.

Estimates from the year 2000 indicate that liver cancer remains the fifth most common malignancy in men and the eighth in women worldwide. The number of new cases is estimated to be 564,000 per year, including 398,000 in men and 166,000 in women. In high-risk countries, liver cancer can arise before the age of 20 years, whereas, in countries at low risk, liver cancer is rare before the age of 50 years. Rates of liver cancer in men are typically 2 to 4 times higher than in women. The incidence of primary liver cancer is increasing in several developed countries, including the United States, and the increase will likely continue for some decades. The trend is a result of a cohort effect related to infection with hepatitis B and C viruses, the incidence of which peaked in the 1950s to 1980s. In selected areas of some developing countries, the incidence of primary liver cancer has decreased, possibly as a result of the introduction of hepatitis B virus vaccine. The geographic variability in incidence of primary liver cancer is largely explained by the distribution and the natural history of the hepatitis B and C viruses. The attributable risk estimates for the combined effects of these infections account for well over 80% of liver cancer cases worldwide. Primary liver cancer is the first human cancer largely amenable to prevention using hepatitis B virus vaccines and screening of blood and blood products for hepatitis B and C viruses.

Adolescent↗
PubMed2004

Time trends in incidence and mortality for chronic liver disease and liver cancer in the interval 1980-1997 in Catalonia, Spain.

BACKGROUND AND AIMS: It has been reported that the incidence of liver cancer and intrahepatic bile duct tumours might be increasing in some developed countries. The purpose of this study was to examine time trends of incidence and mortality rates of liver cirrhosis and liver cancer for the period 1980-1997 in Catalonia, Spain. METHODS: Data were obtained from the Catalan Mortality Registry and the Tarragona Cancer Registry. Joinpoint analysis was used to detect time-related changes in incidence and mortality of liver diseases. The cohort effect on mortality and incidence rates was explored by an age-period-cohort model. RESULTS: Mortality from liver cirrhosis decreased during the study period for both sexes and all age groups, with the exception of men aged between 25 and 35 years. No changes in incidence or mortality rates were observed for liver cancer. Mortality rates for intrahepatic bile duct tumours increased in men and women, while incidence rates remained stable. CONCLUSIONS: This study identified in Catalonia an increase in mortality due to liver cirrhosis among 25-35-year-old men. Mortality rates for intrahepatic bile duct tumours increased for all age groups and both sexes. The former could be related to hepatitis C or B viruses and human immunodeficiency virus co-infection, while the latter remains unexplained.

Adult↗
PubMed2003

Human papillomavirus and oral cancer: the International Agency for Research on Cancer multicenter study.

BACKGROUND: Human papillomavirus (HPV), the causal agent of cervical cancer, appears to be involved in the etiology of cancer of the oral cavity and oropharynx. To investigate these associations, we conducted a multicenter case-control study of cancer of the oral cavity and oropharynx in nine countries. METHODS: We recruited 1670 case patients (1415 with cancer of the oral cavity and 255 with cancer of the oropharynx) and 1732 control subjects and obtained an interview, oral exfoliated cells, and blood from all participants and fresh biopsy specimens from case patients. HPV DNA was detected by polymerase chain reaction (PCR). Antibodies against HPV16 L1, E6, and E7 proteins in plasma were detected with enzyme-linked immunosorbent assays. Multivariable models were used for case-control and case-case comparisons. RESULTS: HPV DNA was detected in biopsy specimens of 3.9% (95% confidence interval [CI] = 2.5% to 5.3%) of 766 cancers of the oral cavity with valid PCR results and 18.3% (95% CI = 12.0% to 24.7%) of 142 cancers of the oropharynx (oropharynx and tonsil combined) with valid PCR results. HPV DNA in cancer biopsy specimens was detected less frequently among tobacco smokers and paan chewers and more frequently among subjects who reported more than one sexual partner or who practiced oral sex. HPV16 DNA was found in 94.7% of HPV DNA-positive case patients. HPV DNA in exfoliated cells was not associated with cancer risk or with HPV DNA detection in biopsy specimens. Antibodies against HPV16 L1 were associated with risk for cancers of the oral cavity (odds ratio [OR] = 1.5, 95% CI = 1.1 to 2.1) and the oropharynx (OR = 3.5, 95% CI = 2.1 to 5.9). Antibodies against HPV16 E6 or E7 were also associated with risk for cancers of the oral cavity (OR = 2.9, 95% CI = 1.7 to 4.8) and the oropharynx (OR = 9.2, 95% CI = 4.8 to 17.7). CONCLUSIONS: HPV appears to play an etiologic role in many cancers of the oropharynx and possibly a small subgroup of cancers of the oral cavity. The most common HPV type in genital cancers (HPV16) was also the most common in these tumors. The mechanism of transmission of HPV to the oral cavity warrants further investigation.

Adult↗
PubMed2003

Prevalence of BRCA1 and BRCA2 germline mutations in young breast cancer patients: a population-based study.

Our aim was to estimate the prevalence of mutations in the BRCA1 and BRCA2 genes among unselected incident cases of breast cancer in young women. We identified 158 incident breast cancer cases diagnosed before age 46 years in predefined geographic areas in Girona and Tarragona, Spain, during 1995-1997. Of these, 136 (86%) provided information on family history of cancer and were screened for BRCA1 and BRCA2 mutations. Nine of the 136 (6.6%) were found to carry BRCA deleterious mutations (MUT) (1 BRCA1 and 8 BRCA2), and 20 were detected with rare BRCA variants of unknown significance (UV). Both MUT and US BRCA alterations were more frequent in younger patients: 7 (11.6%) MUT and 12 (19.3%) UV carriers were found in the group of 62 patients younger than 40 years, whereas 2 (2.7%) MUT and 9 (12%) US carriers were identified in the group of 74 patients aged 40-45. Family history of breast and ovarian cancers suggestive of hereditary condition (at least 2 first- or second-degree relatives affected with breast cancer or at least 1 relative affected with ovarian cancer or early-onset breast cancer) was absent for 5 of 9 MUT carriers. This suggests that BRCA screening policies based on family history of cancer would miss a considerable proportion of BRCA mutations. Mutations in the BRCA1 and BRCA2 genes explain at least 10% of breast cancer cases diagnosed before age 40 years. The contribution of these genes to early-onset breast cancer is likely to be even higher given that certain UV cases might be disease-associated.

Adult↗
PubMed2003

Epidemiologic classification of human papillomavirus types associated with cervical cancer.

BACKGROUND: Infection with human papilloma virus (HPV) is the main cause of cervical cancer, but the risk associated with the various HPV types has not been adequately assessed. METHODS: We pooled data from 11 case-control studies from nine countries involving 1918 women with histologically confirmed squamous-cell cervical cancer and 1928 control women. A common protocol and questionnaire were used. Information on risk factors was obtained by personal interviews, and cervical cells were collected for detection of HPV DNA and typing in a central laboratory by polymerase-chain-reaction-based assays (with MY09/MY11 and GP5+/6+ primers). RESULTS: HPV DNA was detected in 1739 of the 1918 patients with cervical cancer (90.7 percent) and in 259 of the 1928 control women (13.4 percent). With the GP5+/6+ primer, HPV DNA was detected in 96.6 percent of the patients and 15.6 percent of the controls. The most common HPV types in patients, in descending order of frequency, were types 16, 18, 45, 31, 33, 52, 58, and 35. Among control women, types 16, 18, 45, 31, 6, 58, 35, and 33 were the most common. For studies using the GP5+/6+ primer, the pooled odds ratio for cervical cancer associated with the presence of any HPV was 158.2 (95 percent confidence interval, 113.4 to 220.6). The odds ratios were over 45 for the most common and least common HPV types. Fifteen HPV types were classified as high-risk types (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82); 3 were classified as probable high-risk types (26, 53, and 66); and 12 were classified as low-risk types (6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81, and CP6108). There was good agreement between our epidemiologic classification and the classification based on phylogenetic grouping. CONCLUSIONS: In addition to HPV types 16 and 18, types 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, and 82 should be considered carcinogenic, or high-risk, types, and types 26, 53, and 66 should be considered probably carcinogenic.

Adenocarcinoma↗
PubMed2003

Smoking and cervical cancer: pooled analysis of the IARC multi-centric case--control study.

BACKGROUND: Smoking has long been suspected to be a risk factor for cervical cancer. However, not all previous studies have properly controlled for the effect of human papillomavirus (HPV) infection, which has now been established as a virtually necessary cause of cervical cancer. To evaluate the role of smoking as a cofactor of progression from HPV infection to cancer, we performed a pooled analysis of 10 previously published case-control studies. This analysis is part of a series of analyses of cofactors of HPV in the aetiology of cervical cancer. METHODS: Data were pooled from eight case-control studies of invasive cervical carcinoma (ICC) and two of carcinoma in situ (CIS) from four continents. All studies used a similar protocol and questionnaires and included a PCR-based evaluation of HPV DNA in cytological smears or biopsy specimens. Only subjects positive for HPV DNA were included in the analysis. A total of 1463 squamous cell ICC cases were analyzed, along with 211 CIS cases, 124 adeno- or adeno-squamous ICC cases and 254 control women. Pooled odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression models controlling for sexual and non-sexual confounding factors. RESULTS: There was an excess risk for ever smoking among HPV positive women (OR 2.17 95%CI 1.46-3.22). When results were analyzed by histological type, an excess risk was observed among cases of squamous cell carcinoma for current smokers (OR 2.30, 95%CI 1.31-4.04) and ex-smokers (OR 1.80, 95%CI 0.95-3.44). No clear pattern of association with risk was detected for adenocarcinomas, although the number of cases with this histologic type was limited. CONCLUSIONS: Smoking increases the risk of cervical cancer among HPV positive women. The results of our study are consistent with the few previously conducted studies of smoking and cervical cancer that have adequately controlled for HPV infection. Recent increasing trends of smoking among young women could have a serious impact on cervical cancer incidence in the coming years.

Adenocarcinoma↗
PubMed2003

Chapter 1: Human papillomavirus and cervical cancer--burden and assessment of causality.

Cervical cancer remains the second most common cancer in women worldwide and the most frequent in developing countries. Pre-neoplasic cervical lesions represent an additional burden in countries where screening is widespread. The human papillomavirus (HPV) prevalence and type distribution in normal smears and in cancer specimens are being described and show relatively small international variation. State-of-the-art detection techniques have unequivocally shown that HPV-DNA can be detected in 95% to 100% of adequate specimens of cervical cancer, supporting the claim that HPV is the necessary cause. The odds ratios for cervical cancer related to a cross sectional detection of HPV-DNA range from 50 to several hundred in all studies. The risk for any of 15 high-risk types is not statistically different from the risk reported for HPV16. The estimates of the attributable fraction range from 90% to 98%. Additional work should be done in providing information on incidence of cervical cancer and on HPV infection in areas where the disease is common. Theoretical work including modeling of the incidence could be of potential use in the evaluation of the existing and novel preventive strategies. Research is currently being conducted on the mechanisms of HPV carcinogenesis. These include the determinants of the systemic and cellular immune response to the viral infection, the interaction between the host and the virus and the relevance of the different strains and variants of the HPV viral types. Technology developments in this area suitable for epidemiological studies are needed.

Age Distribution↗
PubMed2003

Cervical human papillomavirus infection in the female population in Barcelona, Spain.

BACKGROUND AND OBJECTIVE: Human papillomavirus (HPV) is a major cause of invasive cervical cancer. Identification of HPV determinants might allow for targeting of high-risk groups for cervical cancer. GOAL: The goal was to estimate the HPV prevalence and its determinants among women from the general population of Barcelona. STUDY DESIGN: We studied a random sample of female residents in metropolitan Barcelona, Spain (n = 973). Information was obtained through personal interviews and laboratory testing of cervical exfoliated cells. HPV was detected using a GP5+/6+ polymerase chain reaction assay. RESULTS: The average age of participants was 43 years (standard deviation = 16.1 y) and the percentage of lifetime monogamy was 79%. The age-adjusted HPV prevalence was 3.0%. Independent HPV determinants were being born overseas (odds ratio [OR], 8.1; 95% confidence interval [CI], 1.9-33.5), being divorced (OR, 6.7; 95% CI, 1.9-24.3), reporting more than one sexual partner (OR, 2.6; 95% CI, 1.0-6.5), and smoking marijuana and related products (OR, 5.2; 95% CI, 1.2-21.7). Use of condoms with regular partner was protective (OR, 0.14; 95% CI, 0.02-1.0). CONCLUSION: The study confirms a low overall HPV prevalence in a largely monogamous population. The protection observed with condom use needs further evaluation.

Adolescent↗
PubMed2003

Epidemiology of human papillomavirus infections: new options for cervical cancer prevention.

In the last two decades, the cervical cancer puzzle has become a coherent description that includes the identification of human papillomavirus (HPV) as the sexually transmitted etiologic agent and the characterization of the major determinants of HPV acquisition. Triage studies have consistently shown that HPV testing is more sensitive that repeated cytology in identifying underlying high-grade lesions in women with atypical squamous cells of undetermined significance (ASCUS). Studies that reflect primary screening conditions have shown that the sensitivity of HPV tests is higher than standard cytology in detecting high-grade lesions whereas the specificity is similar only in women aged 30-35 and above. HPV vaccines have an intrinsic attraction as a preventive strategy in populations with limited resources. However, vaccines designed to widespread use are still in development and testing phases. Time is ripe for exploring in depth the clinical implications of current achievements and to devise novel strategies for the prevention of cervical cancer. This paper is available too at: http://www.insp.mx/salud/index.html.

Adolescent↗
PubMed2003

The male role in cervical cancer.

Experimental, clinical, and epidemiological evidence strongly suggests that genital Human Papillomaviruses (HPVs) are predominantly sexually transmitted. Epidemiological studies in virginal and HPV-negative women clearly indicate that sexual intercourse is virtually a necessary step for acquiring HPV. As with any other sexually transmitted disease (STD) men are implicated in the epidemiological chain of the infection. Penile HPVs are predominantly acquired through sexual contacts. Sexual contacts with women who are prostitutes play an important role in HPV transmission and in some populations sex workers may become an important reservoir of high-risk HPVs. Acting both as "carriers" and "vectors" of oncogenic HPVs male partners may markedly contribute to the risk of developing cervical cancer in their female partners. Thus, in the absence of screening programs, a woman's risk of cervical cancer may depend less on her own sexual behavior than on that of her husband or other male partners. Although more rarely than women, men may also become the "victims" of their own HPV infections as a fraction of infected men are at an increased risk of developing penile and anal cancers. Male circumcision status has been shown to reduce the risk not only of acquiring and transmitting genital HPVs but also of cervical cancer in their female partners. More research is needed to better understand the natural history and epidemiology of HPV infections in men. This paper is available too at: http://www.insp.mx/salud/index.html.

Adolescent↗
PubMed2002

Herpes simplex virus-2 as a human papillomavirus cofactor in the etiology of invasive cervical cancer.

BACKGROUND: Human papillomavirus (HPV) infection is the main cause of invasive cervical cancer, but cofactors may act in conjunction with HPV. We performed a pooled analysis of seven case-control studies to examine the effect of one possible HPV cofactor, herpes simplex virus-2 (HSV-2) infection, in the etiology of invasive cervical cancer. METHODS: Blood and exfoliated cervical specimens were obtained from 1263 case patients with invasive cervical cancer (1158 with squamous-cell carcinomas and 105 with adeno- or adenosquamous-cell carcinomas) and 1117 age-matched control subjects. Western blot analysis and/or an enzyme-linked immunosorbent assay were used to detect type-specific serum antibodies to HSV-2 and HSV-1, and Chlamydia trachomatis serum antibodies were detected using a micro-immunofluorescence assay. HPV DNA was detected using a polymerase chain reaction assay. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were computed from unconditional logistic regression models. RESULTS: Overall, HSV-2 seropositivity was higher among case patients with squamous-cell carcinoma (44.4%, 95% CI = 41.5% to 47.3%) or adeno- or adenosquamous-cell carcinoma (43.8%, 95% CI = 34.2% to 53.5%) than among control subjects (25.6%, 95% CI = 23.0% to 28.2%). Cervical specimens from 1098 (94.8%) squamous-cell carcinoma case patients, 95 (90.5%) adeno- or adenosquamous carcinoma case patients, and 164 (14.7%) control subjects were positive for HPV DNA. Among the HPV DNA-positive women, HSV-2 seropositivity was associated with increased risks of squamous-cell carcinoma (OR = 2.19, 95% CI = 1.41 to 3.40) and adeno- or adenosquamous-cell carcinoma (OR = 3.37, 95% CI = 1.47 to 7.74) after adjustment for potential confounders. A similar association between HSV-2 seropositivity and squamous-cell carcinoma risk was observed after further controlling for markers of sexual behavior (OR = 1.96, 95% CI = 1.24 to 3.09). Among control subjects, HSV-2 seropositivity was associated with markers of sexual behavior, but not with cervical HPV DNA positivity. CONCLUSION: HSV-2 infection may act in conjunction with HPV infection to increase the risk of invasive cervical carcinoma.

Adult↗
PubMed2002

Male circumcision, penile human papillomavirus infection, and cervical cancer in female partners.

BACKGROUND: It is uncertain whether male circumcision reduces the risks of penile human papillomavirus (HPV) infection in the man and of cervical cancer in his female partner. METHODS: We pooled data on 1913 couples enrolled in one of seven case-control studies of cervical carcinoma in situ and cervical cancer in five countries. Circumcision status was self-reported, and the accuracy of the data was confirmed by physical examination at three study sites. The presence or absence of penile HPV DNA was assessed by a polymerase-chain-reaction assay in 1520 men and yielded a valid result in the case of 1139 men (74.9 percent). RESULTS: Penile HPV was detected in 166 of the 847 uncircumcised men (19.6 percent) and in 16 of the 292 circumcised men (5.5 percent). After adjustment for age at first intercourse, lifetime number of sexual partners, and other potential confounders, circumcised men were less likely than uncircumcised men to have HPV infection (odds ratio, 0.37; 95 percent confidence interval, 0.16 to 0.85). Monogamous women whose male partners had six or more sexual partners and were circumcised had a lower risk of cervical cancer than women whose partners were uncircumcised (adjusted odds ratio, 0.42; 95 percent confidence interval, 0.23 to 0.79). Results were similar in the subgroup of men in whom circumcision was confirmed by medical examination. CONCLUSIONS: Male circumcision is associated with a reduced risk of penile HPV infection and, in the case of men with a history of multiple sexual partners, a reduced risk of cervical cancer in their current female partners.

Adult↗
PubMed2002

Effect of oral contraceptives on risk of cervical cancer in women with human papillomavirus infection: the IARC multicentric case-control study.

BACKGROUND: Use of oral contraceptives could increase risk of cervical cancer; however the effect of human papillomavirus (HPV), the main cause of cervical cancer, is not usually taken into account. We aimed to assess how use of oral contraceptives affected risk of cervical cancer in women who tested positive for HPV DNA. METHODS: We pooled data from eight case-control studies of patients with histologically confirmed invasive cervical carcinoma (ICC) and from two studies of patients with carcinoma in situ (ISC). Information about use of oral contraceptives was obtained from personal interviews. Effects were estimated as odds ratios, with logistic-regression models adjusted for possible confounders. FINDINGS: 1465 of 1561 (94%) patients with ICC, 211 of 292 (72%) with ISC, and 255 of 1916 (13%) controls were positive for HPV DNA. Compared with never-users, patients who had used oral contraceptives for fewer than 5 years did not have increased risk of cervical cancer (odds ratio 0.73; 95% CI 0.52-1.03). The odds ratio for use of oral contraceptives was 2.82 (95% CI 1.46-5.42) for 5-9 years, and 4.03 (2.09-8.02) for use for 10 years or longer, and these risks did not vary by time since first or last use. INTERPRETATION: Long-term use of oral contraceptives could be a cofactor that increases risk of cervical carcinoma by up to four-fold in women who are positive for cervical HPV DNA. In the absence of worldwide information about HPV status, extra effort should be made to include long-term users of oral contraceptives in cervical screening programmes.

Age of Onset↗
PubMed2002

Role of parity and human papillomavirus in cervical cancer: the IARC multicentric case-control study.

BACKGROUND: High parity has long been suspected of being associated with an increased risk of cervical cancer, but previous analyses of this association have not taken the strong effect of human papillomavirus (HPV) into account. To assess the role of reproductive factors in the progression from HPV infection to cancer, we did a pooled analysis including only HPV-positive women. METHODS: We pooled data from eight case-control studies on invasive cervical carcinoma (ICC) and two on in-situ carcinoma (ISC) from four continents. 1465 patients with squamous-cell ICCs, 211 with ISCs, 124 with adenocarcinomas or adenosquamous ICCs, and 255 control women, all positive for HPV DNA by PCR-based assays, were analysed. We calculated pooled odds ratios by means of unconditional multiple logistic regression models, and adjusted them for sexual and non-sexual confounding factors. The 95% CI were estimated by treating the odds ratio as floating absolute risk. FINDINGS: We found a direct association between the number of full-term pregnancies and squamous-cell cancer risk: the odds ratio for seven full-term pregnancies or more was 3.8 (95% CI 2.7-5.5) compared with nulliparous women, and 2.3 (1.6-3.2) compared with women who had one or two full-term pregnancies. There was no significant association between risk of adenocarcinoma or adenosquamous carcinoma and number of full-term pregnancies. INTERPRETATION: High parity increases the risk of squamous-cell carcinoma of the cervix among HPV-positive women. A general decline in parity might therefore partly explain the reduction in cervical cancer recently seen in most countries.

Adenocarcinoma↗