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PubMedDate not supplied

Apoptosis in cervical cancer cells: implications for adjunct anti-estrogen therapy for cervical cancer.

BACKGROUND: Many tumors show dependence on estrogen for growth and establishment of drug resistance. We examined the effects of estrogen on cervical cancer cells exposed to apoptotic agents including drugs used for treatment. MATERIALS AND METHODS: We tested the effect of estradiol on apoptosis in three cervical cancer cell lines. Apoptosis was measured by endonucleolytic degradation of DNA. Bcl-2 was measured by Western analysis. RESULTS: Estradiol reduced the percentage of cells undergoing apoptosis after exposure to the DNA-damaging agents UVB, mitomycin-C and cisplatin. Protection against taxol-induced apoptosis was marginal. Protection was independent of HPV gene expression, and not specific to apoptosis induced by DNA damage, since estradiol significantly reduced the number of apoptotic cells produced after exposure to indole-3-carbinol (I3C), a non-genotoxic phytochemical effective in preventing HPV-induced tumors. Higher concentrations of I3C overcame the anti-apoptotic effect of estradiol. Treatment with I3C resulted in loss of the survival protein Bcl-2, and estradiol partially reversed this effect. CONCLUSION: Estrogen protects cervical cancer cells treated with DNA-damaging agents; UVB, mitomycin-C and cisplatin, from apoptotic death. For I3C, which induces apoptosis and is anti-estrogenic, the amount of apoptosis versus survival and the level of Bcl-2 depend on the I3C/estradiol ratio.

Antineoplastic Agents↗
PubMed2006

Risk of second cancers after radiotherapy for cervical cancer.

Radiotherapy for cervical cancer has both beneficial and detrimental effects: improvement of patient survival and potential induction of a second cancer among long-term survivors. Large epidemiological studies have demonstrated small, but significant, increases of second cancers with radiotherapy compared with the general population. The risk of second cancer has been characterized by organ sites, dose, time since radiotherapy and age at the time of radiotherapy. Analyses of genetic susceptibility and molecular carcinogenesis can be used to develop more appropriate strategies for radiation therapy for cervical cancers.

Cell Transformation, Neoplastic↗
PubMed1991

Clinical experience in gynecological cancer management. c). Cervical cancer: report from the Gynecologic Institutes of Padua University (1963-1989).

The retrospective analysis of 1876 cases of invasive cervical cancer allows some considerations and conclusions on the clinical management of this neoplasia. Always led by the Gynaecologist, in the aims of prophylaxis and early diagnosis, personalized screening are necessary, with regard to risk factors. Surgical Pathological Staging (SPS) is mandatory for adequate treatment and prognosis. By personalizing surgical radicality and avoiding the application, in all cases, of the routine and standard extended operations of the past, it may be possible to reduce the complication rate with 5 year survival rate unchanged. In early stages personalized radical operations with systemic pelvic lymphadenectomy allow the best results (94% 5 year survival rate). Integrated therapies must be planned only in lymph nodal positive or in vascular space invasion cases. In advanced cases, surgery must be personalized in enlarged operations and integrated with adjuvant treatments on the basis of surgical pathological findings. In very advanced stages, integrated therapies, even without surgery, are justified, due to the poor prognosis of these cases.

Combined Modality Therapy↗
PubMed2005

The impact of anti HPV vaccination on cervical cancer incidence and HPV induced cervical lesions: consequences for clinical management.

Cervical cancer is the second most common cause of cancer-related deaths in women worldwide. Screening for cervical cancer is accomplished utilizing a Pap smear and pelvic exam. While this technology is widely available and has reduced cervical cancer incidence in industrialized nations, it is not readily available in third world countries in which cervical cancer incidence and mortality is high. Development of cervical cancer is associated with infection with high risk types of human papillomavirus (HPV) creating a unique opportunity to prevent or treat cervical cancer through anti-viral vaccination strategies. Several strategies have been examined in clinical trials for both the prevention of HPV infection and the treatment of pre-existing HPV-related disease. Clinical trials utilizing prophylactic vaccines containing virus-like particles (VLPs) indicate good vaccine efficacy and it is predicted that a prophylactic vaccine may be available within the next five years. But, preclinical research in this area continues in order to deal with issues such as cost of vaccination in underserved third world populations. A majority of clinical trials using therapeutic agents which aim to prevent the progression of pre-existing HPV associated lesions or cancers have shown limited efficacy in eradicating established tumors in humans possibly due to examining patients with more advanced-stage cancer who tend to have decreased immune function. Future trends in clinical trials with therapeutic agents will examine patients with early stage cancers or pre-invasive lesions in order to prevent invasive cervical cancer. Meanwhile, preclinical studies in this field continue and include the further exploration of peptide or protein vaccination, and the delivery of HPV antigens in DNA-based vaccines or in viral vectors. Given that cervical cancers are caused by the human papillomavirus, the prospect of therapeutic vaccination to treat existing lesions and prophylactic vaccination to prevent persistent infection with the virus are high and may be implemented in the near future. The consequences for clinical management may include a significant reduction in the frequency of Pap smear screening in the case of prophylactic vaccines, and the availability of less invasive and disfiguring treatment options for women with pre-existing HPV associated lesions in the case of therapeutic vaccines. Implementation of both prophylactic and therapeutic vaccine regimens could result in a significant reduction of health care costs and reduction of worldwide cervical cancer incidence.

Female↗
PubMed2002

[Second vulvar cancer after treatment for cervical cancer].

OBJECTIVES: The purpose of this study was to evaluate the incidence of subsequent vulvar cancer in a group treated previously for cervical cancer. MATERIAL AND METHODS: Between 1965 and 1993 180 patients with vulvar cancer were treated in the Great Poland Cancer Center. 10 of them were irradiated earlier for inoperable cervical cancer. Median age of patients with second cancer was 61.2 years old, ranging from 52 to 77 years. Period between occurrence of both tumors ranged from 4 months to 36 years (median--14 years and 4 month). RESULTS: 5-year survival rate was 60.0% (6/10), 5 of the patients survived this period without symptoms, one was treated successfully surgically. Length of time passed between first and second cancer seems to have no influence one the survival rate, other correlations not being found. CONCLUSIONS: 1. Second vulvar cancer can develop at different times after recognizing of the first. Long-term careful clinical controlling of groups of patients treated for cervical cancer is necessary. 2. In 6 cases (60.0%) patients were treated successfully by surgery.

Adult↗
PubMed2002

The cervical cancer screening programme in Norway, 1992-2000: changes in Pap smear coverage and incidence of cervical cancer.

OBJECTIVES: Changes in the incidence of cervical cancer were studied to assess the impact of the Norwegian coordinated cervical cancer screening programme introduced in 1995. Attention was given as to whether recommendation letters sent to women without a screen in the previous 3 years could be an alternative to a conventional screening programme that invites women irrespectively of their spontaneous screening. SETTING: A population based, nationwide, screening programme in which women of 25 to 69 are recommended to have a conventional Pap smear every 3 years. METHODS: The impact of the screening programme was assessed indirectly by comparing trends in invasive cervical cancer, changes in coverage, and changes in interval between Pap smears in the 3 year period (1992-4) before screening with the two first screening rounds (1995-7 and 1998-2000). All Pap smears taken from women of all ages were included, a total of 4 744 967 Pap smears from more than 1.4 million women. Further, the impact was assessed directly by logistic regression by comparing the screening results of women recruited for the programme with women who had regularly had Pap smears. RESULTS: In the last 2 years studied, the incidence of invasive cancer was 22% lower than in the period before the programme. The proportion of women who had a Pap smear was higher after the implementation of the coordinated screening programme. The number of smears taken was less as the interval after a normal smear was greater. The newly recruited women had a threefold risk of having a high grade precursor and a 20-fold higher risk of cancer than the women who had had regular smears. CONCLUSIONS: The coordinated screening programme provides a low cost way of increasing the coverage of the female population, and consequently has reduced the rate of invasive cervical cancer.

Adolescent↗
PubMed2006

A truncated P2X7 receptor variant (P2X7-j) endogenously expressed in cervical cancer cells antagonizes the full-length P2X7 receptor through hetero-oligomerization.

A truncated naturally occurring variant of the human receptor P2X7 was identified in cancer cervical cells. The novel protein (P2X7-j), a polypeptide of 258 amino acids, lacks the entire intracellular carboxyl terminus, the second transmembrane domain, and the distal third of the extracellular loop of the full-length P2X7 receptor. The P2X7-j was expressed in the plasma membrane; it showed diminished ligand-binding and channel function capacities and failed to form pores and mediate apoptosis in response to treatment with the P2X7 receptor agonist benzoyl-ATP. The P2X7-j interacted with the full-length P2X7 in a manner suggesting heterooligomerization and blocked the P2X7-mediated actions. Interestingly, P2X7-j immunoreactivity and mRNA expression were similar in lysates of human cancer and normal cervical tissues, but full-length P2X7 immunoreactivity and mRNA expression were higher in normal than in cancer tissues, and cancer tissues lacked 205-kDa P2X7 immunoreactivity suggesting lack of P2X7 homo(tri)-oligomerization. These results identify a novel P2X7 variant with apoptosis-inhibitory actions, and demonstrate a distinct regulatory property for a truncated variant to antagonize its full-length counterpart through hetero-oligomerization. This may represent a general paradigm for regulation of a protein function by its variant.

Alternative Splicing↗
PubMed2004

Detection of human papillomavirus DNA in breast cancer of patients with cervical cancer history.

BACKGROUND: Recent studies have revealed a possible role for the human papillomavirus (HPV) in the pathogenesis of breast cancer. In this study, patients having both a history of invasive cervical cancer and breast cancer as second primary cancer were selected for enrolment in a study of breast carcinomas for the presence of HPV. METHODS: Paraffin-embedded tissue from cervical cancer, pelvic lymph nodes, breast cancer and axillary lymph nodes of eleven patients were examined for the presence of HPV DNA using a polymerase chain reaction - enzyme immuno assay. DNA extraction was performed with the "QIAamp Tissue Kit" according to the manufacturer's instructions. Additionally, serum samples taken between diagnosis of cervical and breast cancer, were analyzed for the presence of HPV DNA to examine a possible haematogenous spread of oncogenic HPV DNA. RESULTS: All cervical carcinomas were HPV-positive. HPV DNA was detected in seven out of eleven cases in breast cancer and/or axillary lymph node tissue. Six patients had the same HPV type (HPV-16) in cervical cancer and in the corresponding breast cancer/lymph node tissue. In one case, the same HPV DNA type (HPV 16) was detected in cervical cancer, breast cancer and serum sample. CONCLUSION: These results suggest that HPV DNA might be transported from the original site of infection to the breast tissue by the bloodstream, and that it is possibly involved in the carcinogenesis of breast neoplasia in some patients.

Adult↗
PubMed2005

Apoptosis effects of Xrel3 c-Rel/Nuclear Factor-kappa B homolog in human cervical cancer cells.

Cervical cancer is considered a common yet preventable cause of death in women. In this report, we studied the role of the NF-kappaB gene family in HeLa human cervical cancer cells, using the Xrel3 c-Rel homologue of Xenopus laevis. The expression of Xrel3/c-Rel slowed cell growth 6-fold, consistent with an upregulated expression of the cell cycle inhibitor p21. The activated PARP apoptosis effector was significantly increased (P<0.01). Based on cell viability assays Xrel3 provided an anti-apoptotic effect in 1 microM cisplatin, and this was associated with significantly lower levels of the apoptotic proteins Bax and MDM-2 (P<0.05). Furthermore, there was a 3-fold drop in the level of the tumor suppressor protein p53. In 5 microM cisplatin, expression of HeLa Xrel3 enhanced apoptosis by significantly increasing the expression of the apoptotic proteins Bax and MDM-2 (P<0.05). However, the tumor suppressor protein p53 showed a significant decrease (P<0.05) relative to the control. Thus, c-Rel/NF-kappaB may potentially be of clinical significance, especially in tumors exhibiting resistance to high-level chemotherapy.

Animals↗
PubMed1988

Second primary cancer after treatment for cervical cancer. Late effects after radiotherapy.

Using data from the population-based Danish Cancer Registry, the relative risk (RR) of second primary cancer was assessed among 24,970 women with invasive cervical cancer (1943-1982) and 19,470 women with carcinoma in situ of the cervix. The analysis was stratified according to treatment with (+) and without (-) radiation. For all second primaries combined, a RR+ = 1.1 (95% confidence interval (CI) = 1.06-1.18) and a RR- = 1.3 (95% CI = 1.13-1.40) was observed after invasive cervical cancers and a RR+ = 3.5 (95% CI = 1.4-7.2) and RR- = 1.1 (95% CI = 0.7-1.6) following in situ cancer. The small overall excess of second primary cancer is accounted for by an increase of some cancers such as lung, bladder, and a concurrent decrease in others such as breast. Although not statistically different from nonirradiated, the RR increased with time since treatment among irradiated invasive cervical cancer patients in organs close to and at intermediate distance from the cervix, reaching a maximum after 30 or more years of follow-up (RR = 1.9; 95% CI = 1.4-2.5). Altogether, for these sites an excess of 64 cases per 10,000 women per year were attributable to radiation among survivors of 30+ years. The highest risks among long-term survivors were observed for the following: other genital organs (RR = 5.8; 95% CI = 1.8-13.0) bladder (RR = 5.5; 95% CI = 2.8-9.5), connective tissue (RR = 3.3; 95% CI = 0.4-12.0), stomach (RR = 2.5; 95% CI = 1.1-4.7) and rectum (RR = 2.4; 95% CI = 1.1-4.6). A significant deficit of risk for breast cancer (RR = 0.7, 95% CI = 0.6-0.8) was observed for 10+ years, may be attributable to the effect of ovarian ablation by radiotherapy. It is speculated that the same effect also may explain the observed deficits of brain tumors (RR = 0.6; 95% CI = 0.4-1.0) and skin melanomas (RR = 0.6; 95% CI = 0.3-1.0). It is concluded that cancers attributable to radiation, apart from acute nonlymphocytic leukemias, tend to appear late (10 or more years after radiotherapy), and that the risk remains elevated for more than 30 years.

Carcinoma in Situ↗
PubMed1988

Adjuvant chemotherapy after radical hysterectomy for cervical cancer.

Invasive cervical cancer can be treated by surgery, radiotherapy, and cytostatic chemotherapy. For decades, surgery alone or in combination with radiotherapy was the treatment of choice. At our hospital, primary radiotherapy was reserved for patients with advanced disease. Antineoplastic agents, especially combinations which included cisplatin, achieved good results in patients with advanced disease--or after other therapeutic modalities had been exhausted. This led us to use postoperative chemotherapy for high-risk patients with positive pelvic or parametrial nodes or vascular invasion. Radiotherapy had not improved the survival of such patients. A combination of bleomycin, vincristine, mitomycin C and cisplatin was used. The results were compared with those of patients who had received radical abdominal surgery only (n = 166) or surgery and postoperative radiotherapy (n = 170). The 29 patients who underwent surgery and chemotherapy had a statistically higher incidence of all risk factors. Nonetheless, after a three-year follow-up they had fewer recurrences and fewer deaths than did the other patients. We believe that systemic antineoplastic treatment can reduce recurrences and death in patients with invasive systemic cervical cancer.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

A report on the current status of European research on the use of human papillomavirus testing for primary cervical cancer screening.

Cervical cancer remains a significant public health concern, both at a global and a European level. A number of new technologies such as diagnostic tests for human papillomavirus (HPV) have a potential to assist with the reduction of this disease. However, both the efficacy and the cost-effectiveness of these new technologies must be established in properly designed trials before they can be implemented within national public health programs. Our study reviews the randomized controlled trials that are currently being conducted in Europe to establish the performance of HPV testing as a primary cervical cancer screening test.

DNA, Viral↗
PubMed1990

[Perspectives and plans to improve the prognosis of cervical cancer].

The cervical cancer has already attained high survival rate and there is a little room to improve the prognosis. The examination of recurred patients reveals that the recurrence was often found in the cervix, parametrium, pelvic wall, and distant organs. More intensive treatment to such part may be of beneficial to reduce recurrence. Post operative radiation to the pelvis for high risk patients seemed to improve the survival rate, although some authors failed to show its merit. Radiation to the para-aortic lymph node is matter of controversial. Chemotherapy is now expected to play an important role to control or prevent distant metastasis. Considering these facts, improvement of prognosis of the cervical cancer will be expected by 1. early detection by mass screening and 2. centralization the treatment facilities in order to do the individualized and multidisciplinary treatment.

Antineoplastic Combined Chemotherapy Protocols↗
PubMedDate not supplied

CD8+CD45RA+CD27-CD28-T-cell subset in PBL of cervical cancer patients representing CD8+T-cells being able to recognize cervical cancer associated antigens provided by HPV 16 E7.

OBJECTIVE: In response to antigenic stimulation, naive MHC-class I restricted and antigen-specific CD8+CD45RA+CD28+T-cells undergo clonal expansion and differentiate into CD8+CD45RO+ memory T-cells. Upon re- encounter with the nominal antigen, CD45RO+ T-cells are able to convert to CD8+CD45RA+CD28-T-cells displaying potent immune effector functions, including TNF-alpha production. This T-cell subpopulation constitutes a minor population in healthy individuals. In the present study we are currently evaluating whether this particular T-cell subset in PBL represents CD8+T-cells which may be able to recognize cervical cancer associated antigens provided by HPV 16 E7. MATERIAL AND METHODS: Flow-cytometric cell sorted CD8+CD45RA+CD28- and CD8+CD45RA+CD28-T-cells were obtained from patients with cervical cancer and tested for recognition of HLA-A2 restricted peptides derived from the human papillomavirus (HPV)16-E7 gene product using ELISA. HPV DNA in tumor tissue was detected by PCR. RESULTS: We show that the effector CD8+CD45RA+CD28-T-cell subset is expanded in peripheral blood lymphocytes (PBL) from patients with cervical cancer, but also in PBL from patients with an acute mycobacterial infection. CD8+T-cells from 3/6 cancer patients showed a peptide-specific immune response which could be segregated in peptide epitopes which elicited either a strong TNF-alpha production, or GM-CSF and IL-2 secretion. Peptide-reactivity could exclusively be detected in the ex vivo freshly isolated CD8+CD45RA+CD28-T-cell population. A similar situation was found to be true for HLA-A2 presented peptide epitopes derived from M. tuberculosis-associated antigens presented to T-cells obtained from patients with tuberculosis. CONCLUSIONS: The sorting of CD8+CD45RA+CD28-T-cells enables to determine the fine specificity of CD8+ effector T-cells without the need for in vitro manipulation and aids to define the most appropriate target epitopes for novel vaccine designs.

Amino Acid Sequence↗
PubMed2004

Recent trends in cervical cancer mortality in Britain and Ireland: the case for population-based cervical cancer screening.

This study used published mortality data and regression techniques to look at time trends in cervical cancer mortality between 1970 and 2000 in the UK and the Republic of Ireland. Mortality from cancer of the cervix has been declining in the UK for at least the past 30 years. The rate of decrease has been greatest in England, Wales and Scotland and has accelerated in these countries since the reorganisation of screening services in the late 1980s. Mortality in Northern Ireland is also decreasing, but at a lesser rate and without significant change over the same period. In contrast, cervical cancer mortality in the Irish Republic, which, unlike the UK, does not have comprehensive population-based screening, has been increasing by an average of 1.5% per year since 1978. The mortality rate, which was half of that in the UK in the late 1970s, now exceeds that in any of the region of the UK. The absence of population-based screening for cervical cancer in the Republic of Ireland is the most plausible explanation for these differences in trend.

Adult↗
PubMed1988

Cervical cancer screening practices among older women: results from the Maryland Cervical Cancer Case-Control Study.

Considerable evidence shows a large proportion of older women have either never had a Pap test or have significant gaps in their history of cervical cancer screening. Differences in health care utilization patterns by age, cohort differences in use of medical subspecialities, and provider reluctance to perform cancer screening within the general medical care encounter have been suggested as reasons for underscreening. Our study conducted in 1985 documents prior health care utilization patterns of 153 cases of Maryland women with invasive cervical cancer compared with a matched control group. Analysis within three age groups showed that cases were significantly less likely to have ever had a Pap test or to receive regular Pap testing, primarily due to differences in medical care utilization patterns. Never having an obstetrician-gynecology visit, a recent (less than 3 years) internist visit, or not having any out-patient visit were significant risk factors. Other risks included older age at first Pap test, reporting not being told to have routine Pap tests, and not using contraceptives. In a multiple logistic regression analysis, recent out-patient visits and lifetime use of an obstetrician-gynecologist remained significant after adjusting for age interactions with recent Pap test history, underscoring the importance of medical care utilization patterns for screening of cancer of the uterine cervix among the elderly.

Adult↗
PubMed2003

Comparative analysis of cervical cancer in women and in a human papillomavirus-transgenic mouse model: identification of minichromosome maintenance protein 7 as an informative biomarker for human cervical cancer.

Human papillomaviruses (HPVs), such as HPV-16, are associated with >99% of cervical cancers in women. Two viral oncogenes, E6 and E7, are selectively expressed in these cancers. K14E6 and K14E7 transgenic mouse strains, which express the HPV16 E6 or E7 gene in stratified squamous epithelia, display many acute and long-term phenotypes indicative of the oncogenic potential of E6 and E7 including epithelial hyperplasia, abrogation of normal DNA damage responses, and spontaneous skin tumors. When treated with estrogen, these HPV-16 transgenic mice develop a progressive disease leading to cervical cancer that shows many histopathological parallels to cervical cancer in women. In this study, we evaluated the cervical lesions that arise in these transgenic mice for the expression of biomarkers induced in human cervical cancer. These analyses, which showed close parallels in the timing and pattern of expression of cyclin E and Ki-67 in the mouse cervical disease compared with that in humans, provided further validation of this HPV-16 transgenic mouse model for human cervical cancer. We then used our mouse model to identify minichromosome maintenance protein 7 (MCM7), an E2F-induced cellular DNA replication factor, as a novel biomarker for cervical cancer. In both the mouse and human disease, strong, full thickness staining for MCM7 was seen selectively in the epithelium of high-grade intraepithelial lesions and in frank cancer. The uniform staining pattern and strong signal for MCM7 suggest that MCM7 may be a highly informative biomarker for cervical cancer.

Animals↗