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PubMed1995

Molecular biology of cervical cancer and its precursors.

Cervical cancer develops from well-defined precursor lesions referred to as either cervical intraepithelial neoplasia or squamous intraepithelial lesions. It is now known that specific types of human papillomaviruses (HPV) are the principal etiologic agents for both cervical cancer and its precursors. The high-oncogenic-risk HPV types associated with invasive cervical cancer produce two oncoproteins, designated E6 and E7, which interact with endogenous cell cycle regulatory proteins, including p53 and Rb. The interaction of virally derived and endogenous cellular proteins converges in deregulation of cell cycle progression and appears to be critical for the development of cervical cancers. However, the development of cervical cancer is a multistep process that cannot be explained simply by infection with specific types of HPV. One additional event that appears to play a role in tumor progression is integration of HPV DNA into the host genome. Integration of HPV DNA frequently disrupts the E2 open reading frames, resulting in overexpression of the E6 and E7 oncoproteins and possibly causing genomic instability. Additional cofactors and mutational events may be important in the pathogenesis of invasive cervical cancers and may include chromosomal rearrangements, loss of constitutional heterozygosity, and proto-oncogene activation.

Cell Transformation, Viral↗
PubMed1990

The social and demographic characteristics of women dying from cervical cancer in Nottingham.

Cervical cancer accounted for 57 deaths to women in Nottingham District in 1986 and 1987. 28% were women aged under 50 years of age. Using age specific death rates, the greatest risk was among women aged 60-69 years. However, when expressed as a proportion of all deaths, cervical cancer represents 8.5% of deaths in women aged 25-45, but only 0.6% of deaths to women over 46. There was no significant difference in relative risk between the five social classes, even when social class V was compared to aggregated data for social classes I-IV. This supports other evidence that the social class gradient in cervical cancer mortality is lessening. There was no excess risk shown to women resident in the inner city or in areas of social deprivation. This finding is in contrast to the work of others who have shown an increased incidence in areas of social deprivation. The evidence from this study would support those who suggested over 20 years ago that it is not social deprivation or occupation that constitute an increased risk to women, but sexual behaviour and other habits such as smoking.

Adult↗
PubMed2025

Serum, Cell-Free, HPV-Human DNA Junction Detection and HPV Typing for Predicting and Monitoring Cervical Cancer Recurrence.

Almost all cervical cancers are caused by human papillomaviruses (HPVs). In most cases, HPV DNA is integrated into the human genome. We found that tumor-specific, HPV-human DNA junctions are detectable in serum cell-free DNA of a fraction of cervical cancer patients at the time of initial treatment and/or at six months following treatment. Retrospective analysis revealed these junctions were more frequently detectable in women in whom the cancer later recurred. We also found that cervical cancers caused by HPV types outside of phylogenetic clade α9 had a higher recurrence frequency than those caused by α9 types in both our study and The Cancer Genome Atlas cervical cancer database, despite the higher prevalence of α9 types including HPV16 in cervical cancer. Thus, HPV-human DNA junction detection in serum cell-free DNA and HPV type determination in tumor tissue may help predict recurrence risk. Screening serum cell-free DNA for junctions may also offer an unambiguous, non-invasive means to monitor absence of recurrence following treatment.

DNA integration↗
PubMed2026

Serum, cell-free, HPV-human DNA junction detection and HPV typing for predicting and monitoring cervical cancer recurrence.

Almost all cervical cancers are caused by human papillomaviruses (HPVs). In most cases, HPV DNA is integrated into the human genome. We found that tumor-specific, HPV-human DNA junctions are detectable in serum cell-free DNA of a fraction of cervical cancer patients at the time of initial treatment and/or at 6 months following treatment. Retrospective analysis revealed these junctions were more frequently detectable in women in whom the cancer later recurred. We also found that cervical cancers caused by HPV types outside of phylogenetic clade α9 had a higher recurrence frequency than those caused by α9 types in both our study and The Cancer Genome Atlas cervical cancer database, despite the higher prevalence ofα9 types, including HPV16, in cervical cancer. Thus, HPV-human DNA junction detection in serum cell-free DNA and HPV type determination in tumor tissue may help predict recurrence risk. Screening serum cell-free DNA for junctions may also offer an unambiguous non-invasive means to monitor absence of recurrence following treatment.

Humans↗
PubMed1995

Intra-arterial chemotherapy with cisplatin followed by radical radiotherapy for locally advanced cervical cancer.

Locally advanced cervical cancer has a dismal prognosis, with a high local failure rate and a poor survival rate. To improve the cure rate for advanced carcinoma of the cervix, we initiated a study of intra-arterial (I-A) chemotherapy with cisplatin via the uterine artery prior to definitive radiotherapy. I-A chemotherapy via the internal iliac artery has been used to treat advanced cervical cancer; however, access by way of the uterine artery has not been tested for this purpose. Thirty-four patients with central tumor > or = 5 cm in anteroposterior diameter observed on CT scans were treated with I-A chemotherapy. I-A chemotherapy consisted of unilateral catheterization of the uterine artery using 120 mg/m2 cisplatin. After assessment of I-A chemotherapy, all but 3 patients were treated with a combination of whole-pelvis external irradiation and intracavitary irradiation. The 3 patients underwent external radiotherapy alone. Twenty-seven of 34 patients treated were evaluable for response to I-A chemotherapy. Eleven patients (41%) experienced a partial response. Seventy-six percent of the 34 patients treated with I-A chemotherapy followed by radiotherapy exhibited a complete response by the end of treatment. Toxicity was well tolerated and no death due to treatment occurred. The 2- and 5-year actuarial survival rates were 64 and 55%, respectively. The crude incidences of pelvic recurrence and distant metastasis observed at a median follow-up of 54 months were both 47%. This study for locally advanced cervical cancer suggests there is benefit to be derived from our I-A chemotherapy followed by radical radiotherapy.

Adult↗
PubMed2003

KCl cotransport is an important modulator of human cervical cancer growth and invasion.

Cervical cancer is a major world health problem for women, but the pathophysiology of this disease has received scant attention. Here we show that the growth and invasion of cervical cancer cells are strongly linked the expression and activity of the KCl cotransporter (KCC), an important regulator of the ionic and cellular osmotic homeostasis. Functional assays of KCl cotransport activation by osmotic swelling, staurosporine, and N-ethylmaleimide indicate that removal of the N-terminal 117 amino acids from KCC1 produces a dominant-negative loss-of-function phenotype for KCl cotransport in human cervical cancer cells. The capability for regulatory volume decrease is much attenuated in the loss-of-function KCC mutant cervical cancer cells. The loss-of-function KCC mutant cervical cancer cells exhibit inhibited cell growth accompanied by decreased activity of the cell cycle gene products retinoblastoma and cdc2 kinase. Reduced cellular invasiveness is in parallel by reduced expression of alpha v beta 3 and alpha 6 beta 4 integrins, accompanied by decreased activity of matrix metalloproteinase 2 and 9. Inhibition of tumor growth in SCID mice confirms the crucial role of KCC in promoting cervical cancer growth and invasion. Thus, blockade of KCl cotransport may be a useful therapeutic adjunctive strategy to retard or prevent cervical cancer invasion.

Animals↗
PubMed1998

Factors leading to delay in diagnosis of invasive cervical cancer.

Objective: Screening for cervical cancer has been one of the major successes in American health care. The reasons for screening failure have not been well described. We have encountered 24 patients in the past year on our gynecologic oncology service who have presented with grossly visible stage IB or higher cervical cancers. A questionnaire was developed to determine why these patients presented with invasive cervical cancer, a theoretically preventable disease.Methods: All patients seen at our hospital center with grossly visible cervical cancer were offered entry into this prospective study, approved by the IRB. After informed consent was obtained, a questionnaire was administered to the patients by a physician. The questions involved sexual and gynecologic history, symptom review, social history, and personal concerns involving gynecologic exams. Twenty-four patients were approached for the study and 20 were enrolled. Four patients were unable to participate secondary to medical or social conditions that did not allow them to complete the questionnaire.Results: Of the 20 patients enrolled in this study, 14 of 20 (70%) presented with bleeding irregularities. Upon further questioning, 19 of 20 (95%) reported a history of abnormal bleeding. Only 3 of 20 (15%) patients reported a history of an abnormal Papanicolaou smear, and 7 of 20 (35%) reported not having had a Papanicolaou in the past 5 years. Two patients had never had a Papanicolaou smear. Seventeen of 20 (85%) of all patients in the study had medical insurance at the time of diagnosis, and only 2 patients reported lack of insurance as the reason they had not been seen by a gynecologist in the past 2 years. The majority of the study patients, 17 of 20 (85%) had contact with medical personnel in the 2 years prior to diagnosis. Sixteen of the 20 patients had been seen by a physician, 5 of 20 had surgery or other invasive procedures, and 6 of 20 had been seen in an emergency department. Only 5 of 20 patients knew that a Papanicolaou smear is a screening test for cervical cancer. Five of the 20 thought it to be a test for infections, and 10 of 20 did not know the purpose of a Papanicolaou smear. The main reason women gave for not having had a Papanicolaou smear in the past 2 years was that they felt healthy and had no symptoms (12/20).Conclusion: The majority of patients in our study (17/20) reported contact with a physician within 2 years of diagnosis of their invasive cervical cancer. It appears that failure to screen and lack of understanding regarding Papanicolaou smear screening, rather than lack of access to medical care, is a major cause for delay in diagnosis of cervical cancer.

Journal Article↗
PubMed1993

[Cervical cancer before 35 years of age: epidemiological and prognostic aspects. Retrospective study of 46 cases of cervical cancer before 35 years of age in a series of 449 cases in stages IA2 and IV].

OBJECTIVE: To investigate the diagnosis and prognosis aspects of carcinoma of the cervix in a group of young patients less 35 years old, not very clear in literature. STUDY: Retrospective and comparative diagnostic and prognostic study. This study is related to the epidemiology and prognosis of such cervical cancer in young women. SUBJECTS: Of 449 new patients with carcinoma of cervix FIGO stages IA2-IV treated between 1972-1990 inclusive, 46 patients were aged less than 35 years old. RESULTS: The frequency is about 10.2%; during the last 20-year period, there was a gradual rise in the proportion of young women with invasive carcinoma of the cervix (7.6% between January 1972 and June 1981, 13.9% between July 1981 and December 1990). There is more frequent incidence of adenocarcinoma in the young women group (19.6% adenocarcinoma < 35 years, 8.2% > 35 years). The overall 5-year survival all stages together is better before 35 years (71% < 35 years, 50% > 35 years), because in women aged less than 35 years, early stages disease (IA2, IB), predominated. Stage for stage, the 5-year survival is a little lower for stage I (78.6% < 35 years, 88.5% > 35 years) and much lower for stage II (45.5% < 35 years, 71% > 35 years). The young age is an independent prognosis factor, predicting early recurrences within 20 months: the relative risk is 3.7. CONCLUSION: The young age (less than 35 years), is a worse prognosis factor of carcinoma of the cervix; the treatment is very difficult: heavy (radiotherapy, neoadjuvant chemotherapy), efficient, problem of femininity.

Adenocarcinoma↗
PubMed2005

Vaccines against human papillomavirus and cervical cancer: promises and challenges.

Cervical cancer and precancerous lesions of the genital tract are major threats to the health of women worldwide. The introduction of screening tests to detect cervical cancer precursor lesions has reduced cervical cancer rates in the developed world, but not in developing countries. Human papillomavirus (HPV) is the primary etiologic agent of cervical cancer and dysplasia. Thus, cervical cancer and other HPV-associated malignancies might be prevented or treated by HPV vaccines. Two vaccine strategies have been developed. First, prevention of HPV infection through induction of capsid-specific neutralizing antibodies has been studied in clinical trials. However, because the capsid proteins are not expressed at detectable levels by infected basal keratinocytes or in HPV-transformed cells, a second approach of developing therapeutic vaccines by targeting nonstructural early viral antigens has also been developed. Because two HPV oncogenic proteins, E6 and E7, are critical to the induction and maintenance of cellular transformation and are coexpressed in the majority of HPV-containing carcinomas, most therapeutic vaccines target one or both of these gene products. A variety of approaches is being tested in therapeutic vaccine clinical trials, whereby E6 and/or E7 are administered in live vectors, as peptides or protein, in nucleic acid form, or in cell-based vaccines. The paradigm of preventing HPV infection through vaccination has been tested, and two vaccines are currently in phase III clinical trials. However, current therapeutic vaccine trials are less mature with respect to disease clearance. A number of approaches have shown significant therapeutic benefit in preclinical papillomavirus models and await testing in patient populations to determine the most effective curative strategy.

Cancer Vaccines↗
PubMed2004

TSLC1 gene silencing in cervical cancer cell lines and cervical neoplasia.

BACKGROUND: Cervical carcinogenesis is initiated by infection with high-risk (i.e., carcinogenic) human papillomavirus (HPV) types. The subsequent progression from premalignant cervical intraepithelial neoplasia (CIN) to invasive cancer is driven by both genetic and epigenetic processes. We assessed the role of the gene encoding the adhesion molecule tumor suppressor in lung cancer 1 (TSLC1) in this progression. METHODS: We analyzed TSLC1 gene expression by real-time quantitative reverse transcription-polymerase chain reaction, promoter methylation by sodium bisulfite genomic DNA sequencing, and allelic loss by microsatellite analysis in primary keratinocytes, in four non-tumorigenic HPV-immortalized human keratinocyte cell lines, and in 11 human cervical cancer cell lines that were positive for a high-risk HPV DNA type and in normal cervical epithelial cells. We transfected cervical cancer SiHa cells that did not express TSLC1 mRNA with an expression vector containing the TSLC1 complementary DNA (cDNA) or an empty vector and analyzed transfectants for anchorage-independent growth and tumorigenicity in nude mice. We also examined TSLC1 promoter methylation in premalignant cervical lesions and in cervical carcinomas and smears. All statistical tests were two-sided. RESULTS: TSLC1 mRNA was strongly reduced, relative to levels in primary keratinocytes, or absent in 10 (91%) of 11 cervical carcinoma cell lines but in none (0%) of the four HPV-immortalized cell lines (difference = 91%, 95% confidence interval [CI] = 74% to 100%; P =.004). The TSLC1 promoter was hypermethylated, relative to normal foreskin and cervical epithelial cells, in nine (82%) of the 11 cervical carcinoma cell lines but in none (0%) of the four HPV-immortalized cell lines (difference = 82%, 95 CI = 59% to 100%; P =.01). Seven (88%, 95% CI = 47% to 100%) of the eight SiHa/TSLC1 transfectants displayed a marked reduction in anchorage-independent growth (i.e., 0-100 colonies per 5000 cells) compared with none of the four (0%, 95% CI = 0% to 60%) SiHa transfectants bearing the empty vector (i.e., SiHa/hygro transfectants; difference = 88%, 95% CI = 65% to 100%; P =.01) or untransfected SiHa cells. All seven mice (100%, 95% CI = 59% to 100%) injected with untransfected SiHa cells or SiHa/hygro transfectants displayed tumors of at least 50 mm(3) by 2-6 weeks after injection compared with none of eight mice (0%, 95% CI = 0% to 37%) injected with the SiHa/TSLC1 transfectants (difference = 100%, 95% CI = 68% to 100%; P<.001). We detected TSLC1 promoter hypermethylation in seven (35%, 95% CI = 15% to 59%) of 20 high-grade CIN lesions (i.e., CIN II and III) and in 30 (58%, 95% CI = 43% to 71%) of 52 cervical squamous cell carcinomas compared with none (0%, 95% CI = 0% to 34%) of nine normal cervical epithelial biopsy samples and none (0%, 95% CI = 0% to 22%) of 12 CIN I lesions (P<.001 for cervical squamous cell cancer versus normal epithelial biopsy samples plus CIN I lesions). CONCLUSIONS: TSLC1 gene silencing via promoter hypermethylation is a frequent event in the progression from high-risk HPV-containing, high-grade CIN lesions to invasive cervical cancer.

Animals↗
PubMed2004

Cervical cancer in Hispanic/Latino women.

Cervical cancer is largely preventable if detected early. Minority populations and people of low socioeconomic status are affected disproportionately by cervical cancer. When compared to non-Hispanic white women, Hispanic/Latino women residing in the United States have twice the incidence rate of and 1.4 times the mortality from cervical cancer. Contributing factors include lack of awareness about cancer prevention and available services; lack of access to quality health care; feelings of embarrassment, fear, and fatalism; and limited linguistically and ethnically sensitive information about cervical cancer prevention and detection. Education and screening programs targeted at this population have the potential to decrease the morbidity and mortality associated with cervical cancer, and nurses play an important role in educating Hispanic/Latino women about cervical cancer.

Adult↗
PubMedDate not supplied

Deregulation of D-type cyclins in uterine cancers. Cyclin D1/D3 is differentially expressed in cervical cancer.

BACKGROUND: We have previously found cyclin D1 to be overexpressed in 45% of corpus cancers, but in only 3% of cervical cancers. To see whether and how D-type cyclins contribute to the neoplastic phenotype in uterine cancers, aberrant expression and association between cyclins D1 and D3 proteins were studied. MATERIALS AND METHODS: Expression of cyclin D3 was investigated by immunohistochemistry in 51 patients with primary cancer of the corpus and 73 cases of primary cervical carcinomas. Amplification of the cyclin D1 and D3 genes was investigated by fluorescence in situ hybridisation (FISH). RESULTS: We found high/moderate levels of cyclin D3 in 53.5% of cervical cancers and 55% of corpus cancers. High/moderate expression of cyclin D1 and D3 was associated in the corpus cancers, but not in cervical cancers. The accumulation of cyclin D3 but not D1 protein could, in some cases, be explained by increased gene dosage since extra copies of chromosome 6 were found. CONCLUSION: This study demonstrates that in cervical cancers cyclin D3 may compensate for low levels of cyclin D1, whereas in corpus cancers both isoforms may contribute to the neoplastic phenotype.

Cyclin D1↗
PubMedDate not supplied

Arguments for a magnetic resonance imaging-assisted FIGO staging system for cervical cancer.

FIGO staging of cervical cancer is based on anatomic compartmental spread of cervical cancer. This was necessary in the evaluation of surgical resectability in each patient. Even if the surgical resection was not deemed satisfactory, surgical findings and subsequent accurate anatomic pathology findings could be used to prescribe tailored adjuvant therapies. Recently, the management of cervical cancer has been influenced by the evidence from several surgical-pathologic studies and phase II and III combined modality treatment trials. However, the patient selection criteria used in these clinical studies were almost always refined by modern medical imaging and surgical techniques not prescribed in the FIGO staging system. The results obtained from these studies would not correlate with those from the patient population similarly treated but selected strictly along the FIGO staging criteria. This selective, heterogenous, and arbitrary refinement of FIGO staging has certainly given insight into cervical cancer biology but in the process has rendered the current FIGO staging of this disease quite inadequate. Prior knowledge of these factors through modern imaging in these patients could be used in staging and selecting the optimum treatment modality while minimizing the treatment-related morbidity. A magnetic resonance imaging-assisted FIGO staging system for cervical cancer as proposed here could be used for selecting patients appropriately for a given treatment package.

Female↗
PubMed1993

[Chemoprevention of cervical cancer--intervention study of cervical precancerous lesions by retinamide II and riboflavin].

Patients with cervical precancerous lesions were double blindly divided into 2 groups and treated with either Retinamide II (RII) or Riboflavin (VB2) suppository. The suppository containing RII 20mg or VB2 5mg was given intravaginally daily for 100 days, divided into 2 courses. Clinical examination, papanicolaou cytology and tissue biopsy under colposcope were carried out before and after treatment. The results showed that the disappearance rates of precancerous lesions (DRPL) after the second course of treatment with RII or VB2 were 68.5% and 52.00%, and the overall response rates were 74.29% and 56.0%, respectively. 1 or 2 yrs after treatment, DRPL of the RII, Riboflavin and laser groups did not show significant difference (P > 0.05). The statistically significant differences were among the RII, Riboflavin, laser groups and antiphlogistic treatment group (P < 0.01). The results indicate that local application of RII and Riboflavin may serve as chemopreventive agents for cervical cancer.

Administration, Intravaginal↗
PubMed2000

Cervical cancer screening in Germany.

Cervical cancer is one of the target cancers covered by the statutory German cancer screening programme which was introduced in West Germany in 1971 and expanded to the eastern part of the country in 1991. Women covered by statutory health insurance (over 90% of the female population) are eligible to receive an annual cervical examination including a Papanicolaou (PAP) smear beginning at age 20 years. Annual uptake currently slightly exceeds 50% of the eligible population. Shortly after implementation of the national screening programme in the early 1970s the incidence of invasive cervical cancer decreased moderately and the incidence of cervical carcinoma in situ increased substantially in the state of Saarland. These observations would be expected as a result of a cervical cancer screening programme with substantial uptake. Although quality assurance guidelines for cervical cancer screening have been adopted and updated since the inception of the screening programme, only minor changes have been made in the cross-sectional programme documentation. Implementation of population-based documentation and evaluation of screening activities is currently being developed for the German cancer screening programme in pilot studies implementing the European guidelines on the quality assurance of mammography screening. After demonstration of feasibility and effectiveness, improvements in the quality management of breast cancer screening will subsequently be applied to the cervical cancer screening programme.

Adult↗
PubMed2000

Interval cervical cancer following treatment for cervical intraepithelial neoplasia.

The objective of this study was to determine whether those women who developed cervical cancer following treatment for preinvasive disease had common features in their history which could identify those at increased risk of progression and therefore be used to modify management protocols. A retrospective case note review from clinical and histopathologic records was undertaken at a teaching hospital in Wessex, Southern England. The review included 33 women diagnosed with cervical carcinoma between 1985 and 1996 who had previously undergone treatment for cervical intraepithelial neoplasia (CIN) or cervical glandular intraepithelial neoplasia (CGIN). The diagnosis prior to treatment was CIN 3 in 19 cases, CGIN 3 in 2 cases, CIN 2 in 9 cases (97% high grade CIN/CGIN) and CIN 1 in 1 case. At primary treatment, among those treated by knife cone biopsy or Large Loop Excision of the Transformation Zone (LLETZ), and for whom the margins of the treatment specimen were reported, 14 out of 15 had incomplete margins. Local ablation (in which completeness of excision could not be histologically assessed) was performed in 12 cases. In 58% (19/33) of cases, the patient was 40 years or older at the time of initial treatment. Fifteen women had one or more negative smears after treatment, of which only 6 had transformation zone sampling. The interval between treatment of CIN/CGIN and diagnosis of invasion ranged from 8 to 216 months. (mean 40.4 months), with 67% of cases of invasive cancer occurring within 5 years of treatment for CIN/CGIN and 94% within 10 years. Screen detection was achieved in 91% (30/33) of cases with 53% diagnosed while stage 1A. In conclusion, most treatment screen detection of invasive disease at an early (and often microinvasive) stage was achieved for most patients, although a third of patients were diagnosed more than 5 years after initial treatment. The data suggest the need to follow up longer than 5 years when there are risk factors such as incomplete excision of high grade CIN/CGIN and in women over 40 years of age at the time of initial diagnosis.

Journal Article↗