Racial disparities in cancer-specific survival between 1973 and 2015 persist for uterine cancer and are growing for breast, ovarian and cervical cancer
Cassandra PrestiChunqiao TianAmanda JacksonKathryn Osei-BonsuMichael RichardsonJ.K. ChanRodney P. RocconiNathaniel JonesCraig D. ShriverNicholas W. BatemanC.A. HamiltonThomas P. ConradsYovanni CasablancaGeorge L. MaxwellK.M. Darcy
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Uterine cancer
Background. Valid inference on cervical cancer mortality is very difficult since – on the basis of death certificates – it is not always possible to distinguish between cervix, corpus and unspecified uterine cancer deaths. Our aim was to estimate the extent to which cervical cancer as the official cause of death reflects the true mortality from cervical cancer in Slovenia. Material and methods. The data on 2245 deaths from cervix, corpus uteri, and uterus-unspecified cancers for the period 1985-1999 were linked to the Cancer Registry of Slovenia database from the mortality database of Slovenia. Results. Officially, in the period 1985-1999, there were 878 cervical cancer deaths. The comparison of these causes of death with the cancer sites registered in the Cancer Registry revealed that they include only 87.7% patients with a previous diagnosis of cervical cancer. Of 650 corpus uteri cancer deaths, 17. 1 % of patients were registered to have cervical cancer, and of 717 unspecified uterine cancer deaths, 31.4% were registered. Taking into account the correctly identified cervical cancer cases among cervical cancer deaths and misclassified cervical cancer deaths as corpus uteri and unspecified uterine, the corrected number of deaths would be 1106. Conclusions. When evaluating the impact of cervical cancer mortality from national mortality rates, the stated underestimation should be taken into account. However, this does not hold for some other cancers.
Corpus Uteri
Uterine cancer
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Limited evidence suggests that inherited predisposing risk variants might affect the disease outcome. In this study, we analyzed the effect of genome-wide association studies—identified breast cancer-risk single nucleotide polymorphisms on survival of early-stage breast cancer patients in a Chinese population. This retrospective study investigated the relationship between 21 GWAS-identified breast cancer-risk single nucleotide polymorphisms and the outcome of 1177 early stage breast cancer patients with a long median follow-up time of 174 months. Cox proportional hazards regression models were used to estimate the hazard ratios and their 95% confidence intervals. Primary endpoints were breast cancer special survival and overall survival while secondary endpoints were invasive disease free survival and distant disease free survival. Multivariate survival analysis showed only the rs2046210 GA genotype significantly decreased the risk of recurrence and death for early stage breast cancer. After grouping breast cancer subtypes, significantly reduced survival was associated with the variant alleles of rs9485372 for luminal A and rs4415084 for triple negative breast cancer. Importantly, all three single-nucleotide polymorphisms, rs889312, rs4951011 and rs9485372 had remarkable effects on survival of luminal B EBC, either individually or synergistically. Furthermore, statistically significant multiplicative interactions were found between rs4415084 and age at diagnosis and between rs3803662 and tumor grade. Our results demonstrate that breast cancer risk susceptibility loci identified by GWAS may influence the outcome of early stage breast cancer patients’ depending on intrinsic tumor subtypes in Chinese women.
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Objective : To evaluate the distributing and expression of insulin-like growth,factor-1 receptor of LN( - ) breast cancer, UN( + ) breast cancer and normal breast tissue. Methods: The IGF-1R expression on LN( - )breast cancer, LN( + ) breast cancer and normal breast tissue was tested by im-munohistochemistry. Results: The positive rateon LN( - ) breast cancer was 94.12%o(16/17), on LN/( + )breast cancer was 91.30%o(21/23) ,and on normal breast tissue was 58.33% (7/12) . The number of strongstein was 12 on LN( - )breast cancer(strong stein rayte70.59%) , and 8 on LN( + ) breast cancer(strong stein rate 34.78% ) . The positive rate on the LN( - )breast cancer and LN( + ) breast cancer was higer than it on the normal breast tissue( P 0.05) , the overexpression rate on the LN ( - ) breast cancer was higher than it on LN ( + ) breast cancer( P 0.05 ) . Conclusion : These data suggested that IGF-1R play an important role in pathogenesis and development of breast cancer. IGF-1R maybe a adjuvant indexfor diagnosing to breast cancer and estimating prognosis.
CA 15-3
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The serum levels of Trx1 in patients with ovarian cancer were significantly higher than those in normal persons and patients with non-cancer inflammatory diseases. The level of Trx1 increased with the Figo stage. Ovarian cancer patients who were determined to be negative for CA125, were observed to have serum Trx1 levels as high as those of CA125-positive patients. In addition, patients with non-cancer inflammatory diseases had lower plasma Trx1 1 levels than did controls, showing that Trx1 allows clear distinctions between ovarian cancer and these non-cancer diseases. Combinational analysis of CA125 with Trx1 for the detection of ovarian cancer suggests that the diagnostic capacity of CA125 alone for the early detection of ovarian cancer, especially regarding sensitivity, is significantly improved by its combination with Trx1. Taken together, we conclude that serum Trx1 is useful for the early diagnosis of ovarian cancer.
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We aimed to estimate the 15-year and lifetime risks of contralateral breast cancer in breast cancer patients according to the age of diagnosis of the first cancer and the history of breast cancer in the mother. The risks of contralateral breast cancer were estimated for all 78,775 breast cancer patients in the Swedish Family-Cancer Database (age at diagnosis of first breast cancer <70 years). The risk of experiencing a contralateral breast cancer within 15 years of diagnosis was 8.4% [95% confidence interval (CI): 8.1-8.7%] for women with an unaffected mother, was 12% (95%CI: 11-13%) for a woman with a mother with unilateral breast cancer and was 13% (95%CI: 9.5-17%) for women with a mother with bilateral breast cancer. In early-onset diagnosed women (<50 years) with an unaffected mother, the risk of contralateral breast cancer until age 80 was 23% (95%CI: 20-26%) and for late-onset (50-69 years) diagnosed women it was 17% (95%CI: 14-21%). In a woman with a mother with an early-onset unilateral breast cancer, risk of contralateral breast cancer by age 80 was 35% (95%CI: 25-46%). Women with a mother with early-onset bilateral breast cancer had 31% (95%CI: 12-67%) lifetime risk of contralateral breast cancer. The risk of contralateral breast cancer is higher for daughters of breast cancer patients than for daughters of women without breast cancer. Maternal cancer history and age at onset of first breast cancer in women should be taken into account when counseling breast cancer patients about their risk of contralateral breast cancer.
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Abstract Mice have been used in ovarian cancer research mainly as hosts for cell lines derived from human ovarian tumors and ascites. Such models provided valuable information into the nature of metastatic ovarian cancer and possible treatment strategies. However, the complexity of genetic aberrations in human ovarian cancer cell lines precluded understanding of the initiating events responsible for ovarian cancer induction. Since the majority of ovarian cancer patients present at an advanced stage of the disease, it has been difficult to identify the precursor lesions that could be used to study the early morphologic and genetic changes in ovarian cancer. It is thought that the development of animal models in which ovarian cancer can be induced and studied during its early stages will enable better understanding of early ovarian cancer lesions and elucidate molecular events that support ovarian cancer progression. The difficulties in generating such models include the lack of an adequate ovary‐specific promoter, the uncertainty about the tissue of origin for different histologic types of ovarian cancer, and the deficiency in understanding the genetic aberrations responsible for ovarian cancer induction. In spite of these difficulties, the first advances toward generating mouse models for ovarian cancer have been made.
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Gynecologic oncology
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There are operative method and radiotherapy and immunotherapy in the treatment for the uterine cervical cancer. For the satisfactory treatment, several conditions must be considered, such as, the extension of the cancer, age, physical status or complication of the patient, side effect of the treatment and sensitivity to the radiation or anti-cancer agent. In the present time, without the profound understanding of the characteristics and biological behaviors of the uterine cervical cancer, we can not treat the cancer patient correctly. From the several clinical and follow-up data, in this article, time course of the uterine cervical cancer is estimated, and individualization of the treatment for the uterine cervical cancer will be shown.
Uterine cancer
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Ovarian cancer is a major gynecologic cancer and common cause of gynecologic cancer death worldwide. However, the molecular mechanisms of ovarian cancer progression are still unclear. circular RNAs (circRNAs) are recently reported to be involved in cancer progression regulation but the potential functions of circRNAs in ovarian cancer remains unknown. In this study, we explored the expression of circKIF4A in ovarian cancer tissues. Then, a series of experiments were conducted to investigate how circKIF4A functioned in ovarian cancer in vitro and in vivo. The results revealed that circKIF4A was highly expressed in ovarian cancer tissues. Knockdown of circKIF4A suppressed cell proliferation and migration in ovarian cancer. Subsequent mechanism study revealed that circKIF4A acted as a competitive endogenous RNA (ceRNA) to promoted ovarian cancer progression by sponging miR-127 and upregulated the expression of Junctional adhesion molecule 3 (JAM3). Therefore, circKIF4A could be a novel biomarker and therapeutic target for ovarian cancer.
Competing Endogenous RNA
Tumor progression
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