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Researching the Ovarian Cancer Essay (Article)

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Updated: May 10th, 2022

Introduction

The amount of deaths caused by ovarian cancer is alarming in gynecology. It is essential to understand the risk factors of the disease in order to prevent its occurrence. One must also know the pathogenesis of ovarian cancer as well as developments in diagnosis. This report will attempt to demystify these issues.

Epidemiology and risk factors

In the United Kingdom, prevalence rates for ovarian cancer rank second in gynecological cancers (Cervical cancer ranks first while uterine cancer is third). Crude incidence rates for England per 100,000 people are 20.3, while Wales, Scotland, Northern Ireland and the UK have 26.1, 24.3, 20.5 and 20.9 as their crude rates. When age-standardized, these incidence rates become 15.8, 19.6, 18.0, 17.6 and 16.2 respectively. On average, 21 in 100,000 women suffer from ovarian cancer in the United Kingdom (based on crude rates), and this number is 16 when age-standardized (Cancer Research UK 15).

Statistics also indicate that ovarian cancer is more prevalent among postmenopausal females. Only 20% of patients are less than 50 years (UK Association of Cancer Registries 90). Incidence rates rise sharply after this age. However, the highest proportion of patients comes from the 80-84-year-old bracket. These rates decrease dramatically after 85 years. Cases of ovarian cancer have increased gradually over the past quarter-century. Women aged 65 and above account for the highest prevalence rates and their cases have increased by 50% or more. In 1975, incidence rates (Age-standardised) were 15 per 100,000, but this increased to 19 at the end of the century. This number decreased in the first half of the 2000s but increased again in the late 2000s to 16. The age group responsible for the highest decrease lies between 50 and 64 years. At the beginning of the 2000s, patients in that age group were 44 per 100,000 but this reduced to 34 in 2008 (Permuth-Wey and Sellers 430). Experts explain that the increased use of contraceptive pills accounts for the decrease. This method minimizes one’s risk of getting ovarian cancer. Additionally, alterations in classification systems for this type of cancer may also account for the differences. Similar decreases in the 2000s have occurred in Western and Northern Europe, and experts also assert that increases in the use of the contraceptive may also explain this difference.

In the European continent, for every 100,000 females, 12 to 17 will have ovarian cancer, depending on the nation of origin; this is the age-standardized rate. The latter figure represents patients in Northern Europe while the former represents patients in Southern Europe. Portugal and Cyprus have the lowest incidence rates (an average of 7 in every 100,000 women) while Lithuania and Latvia represent the highest incidence rates, which stand at 19 (Bray et. al. 980). In the EU, the UK has the seventh-highest number of ovarian cancer patients.

Internationally, ovarian cancer represents about 4% of all types of cancers among women. The latest statistics, in 2008, indicate that 225,000 cases were reported internationally. Developed nations account for the highest incidence rates as their figures stand at 9 per 100,000. Conversely developing or underdeveloped nations only have incidence rates of 5 in every 100,000 females. Asia and Africa represent the regions with the lowest prevalence rates while Europe and North America account for the highest rates. It is not surprising that this is the case because certain risk factors are higher among affluent groups than deprived ones (DeVita et al. 109).

Most patients tend to live for approximately ten years with ovarian cancer. In the UK, a large number of them have carcinomas or epithelial malignancies; these represent 80% of the cases. Epithelial cancers respond well to chemo action, so they are treatable (Quinn et al. 54).

Risk factors include exposure to asbestos/ talcum powder, age, diet, pregnancy, smoking, hormone replacement therapy, chronic inflammation, use of drugs for infertility, OCP (Oral contraceptive) use, ethnicity, obesity and genetics (McLemore 283). Talcum powder is similar to asbestos and leads to inflammation which brings about DNA damage. Alternatively, it may cause physiological responses when the particles get inside the ovarian epithelium (Mills et. al. 464). Sometimes talc may be used on sanitary towels or applied directly to the genitals. Age is a risk factor when one considers the onset of menses. Early menses and late menopause increase one’s susceptibility owing to the effects of estrogens (Riman et. al. 1012). Dietary factors also account for ovarian cancer risk factors. However, medical practitioners do not agree on the constituents of the diet. Some have found a link between the disease and alcohol consumption, meat and butterfat (LaVecchia et. al. 667) while others have not (Kushi et. al. 23). On the other hand, whole grain wheat products and green vegetables decrease one’s susceptibility. Pregnancy reduces women’s risk of ovarian cancer while abstaining from pregnancy increases this risk (Pike et. al. 189). Women who have never been pregnant have higher cases of ovulation and hence higher levels of estrogen, which heightens the risk of getting ovarian cancer. Chronic inflammation leads to the development of ovarian cancer through the alteration of prostaglandins or the development of epithelial cancer cells (Cramer and Welch 720).

Smoking may lead to ovarian cancer due to the prevalence of nicotine metabolites in ovarian cancer cells (Runnebaum and Stickeler 79). Most studies on ovarian cancer and smoking reveal a strong association between the two. However, a few do not show any association (Modugno et. al. 469). Hormone replacement therapy places women at risk of getting ovarian cancer even though these studies have had different results. Results have been controversy concerning the use of infertility drugs. Some researchers have found that these drugs imitate incessant ovulation and this increases one’s susceptibility to the disease (Brinton et. al. 1199). Others have found no association with ovarian cancer when women utilized gonadotrophins or clomiphene (Rossing et. al. 775). Conversely, others have found a decreased risk for cancer. It is likely that the divergent differences stem from inadequate follow-up, especially since the median age for the disease is 65. OCP use gives protective effects, so failure to use them may increase one’s susceptibility to the disease (McLemore et. al. 287). Ethnicity also plays a part as it determines women’s breastfeeding patterns, pregnancy rates, and use of oral contraceptives. Studies indicate that white women have a higher risk than black women and Ashkenazi Jews have a higher risk of developing the complication (John et. al. 143). Obesity increases steroid hormones which add to the amount of estradiol in the body (Runnebaum and Stickeler 76). This heightens women’s susceptibility to the disease. Having a family history of ovarian or breast cancer also increases a person’s risk because one is likely to possess the BRCA1 and 2 mutations of ovarian cancer.

Role of genetic factors and histopathology of ovarian cancer

BRCA1 and BRCA2 profoundly account for the prevalence of ovarian cancer in patients. The latter are genes that are responsible for DNA cell stability. They ensure this by preventing excessive cell multiplication. In other words, these are tumor suppressors, which are found on chromosome 17q of the cell. Tumor suppression of a normal cell occurs when the BRCA1 gene controls remodeling processes of the concerned chromosomes. The gene also works with the retinoblastoma (Rb) gene during this remodeling process. When a mutation has occurred, then steps in the cell cycle will not include it. This causes tumorigenesis or unchecked growth inside the cell.

If BRCA1 and BRCA2 mutate and a person’s offspring inherits them, then that progeny has a high susceptibility to ovarian cancer even if the disease has not manifested itself in the parent. BRCA2 and BRCA1 mutations may not necessarily cause cancer unless the mutations are harmful. These can then be compounded by the family history of the patient, age or menopausal status, and other risk factors. Therefore, a harmful mutation may not always translate into ovarian cancer. The likelihood of getting ovarian cancer increases fivefold if a patient inherits the BRCA1 or 2 genes than if the person did not have that mutation (Lu 56). It should be noted that the above genes are not the only ones responsible for genetic ovarian cancer risk. Other genes such as Phosphatase and tensin homolog (PTEN), MutL homolog 1 (MLH1), MutS homolog and p53 also account for this disease (Lu 55).

In the case of the BRCA1 and 2 genes, certain criteria ought to be examined in order to understand the likelihood of developing the disease. Women with first-degree relatives, like mothers and sisters, who had been diagnosed with breast cancer at an early age might develop the disease. Another criterion is the existence of more than two second-degree or first-degree relatives, like aunts and grandmothers, with breast cancer. Additionally, the combination of ovarian cancer and breast cancer among the second or first-degree relatives also accounts for an increased level of harmful BRCA1 and BRCA2 mutations. Bilateral breast cancer or cancer in both breasts among first-degree relatives is another criterion. Breast cancer in a male relative is also a cause for alarm. The above criteria apply to non-Ashkenazi Jews. If one belongs to this ethnic community then first-degree relatives with ovarian or breast cancer and 2 second-degree relatives with ovarian cancer and breast cancer have high chances of having the mutations of BRCA1 and BRCA2 (Lu 56). Genetic testing may be done in order to determine whether one has a high risk. If the tests are negative, this does not imply that a person will never have ovarian cancer, it simply demonstrates that their likelihood of contracting the disease is minimal. BRCA1 mutations have a 20 to 63% chance of causing ovarian cancer while BRCA2 mutations have a 10 to 27% chance of causing ovarian cancer.

Females with HNPCC or Lynch Syndrome also have an increased chance of developing ovarian cancer (Russo et. al. 32). This is an autosomal syndrome that increases a woman’s risk of acquiring ovarian, gastric or endometrial cancers. It originates from mutations in the mismatch repair (MMR) gene, which is located in chromosomes 7p, 3p, 2q, and 2p. The purpose of these genes is to ensure that DNA transcription takes place normally by repairing mistakes in the process. Ovarian cancer that comes from this mutation accounts for all histopathologic tumors. They are also heritable and will increase an offspring’s chances of developing ovarian cancer.

Recent progress in the diagnosis of ovarian cancer

Ovarian cancer patients have benefited from the discovery of the BRCA1 and 2 genes in the late 1990s. This discovery illustrated that one has an increased risk of developing the disease when one possesses the above gene mutation. This has caused many women to perform tubal ligation or surgically remove the ovaries. Additionally, the discovery that ovarian cancer does not just consist of one disease but a combination of diseases means that patients can use tailor-made solutions to deal with their illnesses (Jelovac & Armstrong 186).

In 2005, researchers worked on decoding the genome responsible for ovarian cancer. This was done in order to have new targets for the treatment of the ailment. In 2006, scientists discovered that ovarian cancer commences in the fallopian tubes. They carried out surveys amongst women who had removed their fallopian tubes in order to reduce their risk of developing ovarian cancer. They found that these women already had cancer in their fallopian tubes and that cancer often spread to the ovaries. Cancer in the fallopian tubes has characteristics that are different from the ones in the ovaries, so this has serious implications in the diagnosis of the disease (Jelovac & Armstrong 189).

During the late 2000s, researchers found that ovarian cancer has a series of subtypes. The two most prevalent ones are low-grade ovarian tumors; these are quite aggressive and poorly-differentiated tumors, which are slow-growing. The discovery assisted in providing treatments depending on the nature of the tumor. It was unnecessary to subject patients to intense forms of treatment when they had milder forms of the disease.

In 2010, research also found that minimal need exists for continual assessment of the patient after cancer treatment has been completed. In the past, blood tests would be assessed for the CA125 protein. Women with a resurgence of ovarian cancer would record elevated levels of the protein. However, now experts are debating the merit of such tests as physical symptoms of recurrence are sometimes enough to prove its existence. However, no consensus exists in this area (Jelovac & Armstrong 202).

Currently, a number of researches are still being analyzed concerning the diagnosis of the disease. Since epithelial ovarian cancer is still regarded as the most malignant form, then researchers are looking for a method that will enable early detection of the disease. Conventional methods can only facilitate diagnosis in advanced phases of the disease. Scientists are studying how CA 125 tumor markers can assist in the process of diagnosing the disease at an earlier phase. Additionally, even ultrasound use needs to be improved in order to enable early detection of the same. Since BRCA1, BRCA2, and Lynch syndrome account for 10% of hereditary cases, it is imperative to investigate other sources of genetic risks. These are all aspects that scientists are working on presently. As mentioned earlier, a clear etiology of sporadic ovarian cancer does not exist. Consequently, researchers are trying to investigate these components. Surgery plays a unique role in the diagnosis of advanced ovarian cancer; researchers are currently working on methods that can improve the use of such a method in the detection of diseases.

Role of Micro RNAs in ovarian cancer pathogenesis

Micro RNAs are a category of RNA molecules, which are non-coding. They regulate gene expression through mRNA translation inhibition or transcript degradation. In several tumors, it is difficult to observe the phenotype of these molecules; they thus require special approaches to understand their working. The human body has numerous Micro RNA (miR); estimates claim that about 1000 subtypes exist and each carries out various functions in the body (Zhang et. al. 7004). A number of them may be responsible for cell development, differentiation, metabolism and regulations.

In ovarian cancer and other forms of cancer, miRs may be involved in the disease through a number of pathways. Sometimes, their enzymes may be knocked down in a manner that increases transformation and leads to the prevalence of tumorigenesis. Conversely, miR down-regulation may arise as a result of genomic losses associated with epigenetic alterations (Zhang et. al. 7005). Tumor suppressors like miR-15a may also be down-regulated. In fact, it is possible to differentiate between normal cells and cancerous ones on the basis of the down-regulation that takes place.

The let 7 clusters (a group of 12 genes that are precursors for the formation of micro RNA) often target Ras oncogenes (a group of proteins that transmit signals in cells and may cause cancer if they become overactive). During ovarian cancer, the clusters are downregulated (Johnson et al. 640). Therefore, tumourigenesis arises out of these pathways. Other targets for the above category of micro RNAs include cMYC, CDK6 and HMGA2 (Peter 847). Alternatively, miRs may target tumor suppressors such as WTI. The latter is responsible for encoding transcription factors within the cell. As mentioned earlier, p53 is yet another gene that accounts for the prevalence of ovarian cancer. MiR may use p53 as another mechanism for the development of the disease. In this regard, micro RNA, like miR- 34b as well as miR-34c, have been downregulated. Since a number of them are known transcriptional targets of p53, then it is safe to assume that they depend on the existence of such targets. Elevated levels of miRs also prove that they play a role in tumourigenesis (Corney et. 8435). Therefore, analysts can separate normal cells from cancerous ones using this increased expression.

Some of the most over-expressed miRs include miR 200a, 200b, 141, and 200c because they are the most down-modulated ones (Johnson et al. 644). Additionally, the biopathological features of a certain type of ovarian cancer also determine the nature of expression for these types of products. Certain micro RNAs are linked to ovarian surfaces while others specialize in organ invasion. Alternatively, others are lymphovascular while others depend on the histotype of the target.

In essence miR bind with mRNA through perfect or imperfect complementarities. This process can lead to inhibition or degradation. When they target these mRNA, they may either act as tumor suppressors or become oncogenes. Therefore, the involvement of micro RNA in the development of certain types of tumors is the subject of much research interest.

Conclusion

The need for effective screening techniques is essential in the treatment of ovarian cancer as it facilitates early detection. The ovarian cancer genome has complex pathways that explain the incidence and manifestation of the disease, further research on the pathogenesis and the histopathology of ovarian cancer will lead to the use of appropriate methods for management.

References

Bray, Valentine, A. Loos, S. Tognazzo, C. Vecchia. “Ovarian cancer in Europe: Cross-sectional trends in incidence and mortality in 28 countries, 1953-2000.” International Journal of Cancer 113(2005):977-90. Print.

Brinton, L., E. Lamb, and S. Moghissi. “Ovarian cancer risk after use of ovulation-stimulation drugs.” Obstetrics Gynaecology Journal 103.6 (2004):1194-1203. Print.

Cancer Research UK. Ovarian cancer incidence statistics. 2012. Web.

Corney, D., A. Flesken-Nikitin, A. Gowin, W. Wang & A. Nikitin. “MicroRNA 34b are targets of p53 and cooperate in control of cell proliferation and adhesion-independent growth.” Cancer Research 67(2007): 8433-8438. Print.

Cramer, D. and W. Welch. “Determinants of ovarian cancer risk. II. Inferences regarding pathogenesis.” Journal of the National Cancer Institute 71.4(1983):717-721. Print.

DeVita, Vincent, T. Lawrence, and S. Rosenberg. Cancer: Principles and Practice of Oncology. Lippincott: Williams and Wilkins, 2008. Print.

Jelovac, D. & D. Armstrong. “Recent progress in the diagnosis and treatment of ovarian cancer.” CA Cancer Clinical Journal 61.3(2011): 183-203. Print.

John, E., A. Whittemore, R. Harris, and J. Intyre. “Characteristics relating to ovarian cancer risk: collaborative analysis of seven US case-control studies: epithelial ovarian cancer in black women.” Journal of the National Cancer Institute 85.2 (1993):142-146. Print.

Johnson, S., H. Grosshans, J. Shingara, M. Byrom, R. Jarvis, A. Cheng, E. Labourier, & F. Slack. “RAS is regulated by the let-7 microRNA family.” Cell 120(2005): 635–647. Print.

Kushi, L., P. Mink, and A. Folson. “Prospective study of diet and ovarian cancer.” American Journal of Epidemiology 149.1(1999):21-31. Print.

LaVecchia, C., A. Decarli, and E. Negri. “Dietary factors and the risk of epithelial ovarian cancer.” Journal of National Cancer Institute 79.4(1987):663-669. Print.

Lu, K. “Hereditary gynecologic cancers: differential diagnosis, surveillance, management, and surgical prophylaxis.” Fam Cancer 7.1(2008):53-58. Print.

McLemore, Monica, Christine Miaskowski, Bradley Aouizerat, Lee-may Chen, Marylin Dodd. “Epidemiological and Genetic Factors Associated With Ovarian Cancer.” Cancer Nursing 32(2009): 281 – 288. Print.

Mills, P., D. Riordan, R. Cress, and H. Young. “Perineal talc exposure and epithelial ovarian cancer risk in the central valley of California.” International Journal of Cancer 112(2004): 458-464. Print.

Modugno, F., R. Ness, and C. Cottreau. “Cigarette smoking and the risk of mucinous and non-mucinous epithelial ovarian cancer.” Epidemiology 13(2002):467-471. Print.

Permuth-Wey, J. and T. Sellers. “Epidemiology of ovarian cancer.” Methods Molecular Biology 472(2009): 413-37. Print

Peter, M. “Let-7 and miR – 200 microRNAs: Guardians against pluripotency and cancer progression.” Cell Cycle 8(2009): 843-852. Print.

Pike, M., C. Pearce, R. Peters, W. Cozen, P. Wan, and A. Wu. “Hormonal factors and the risk of invasive ovarian cancer: a population-based case-control study.” Fertility and Sterility Journal 82.1(2004): 186-195. Print.

Riman, T., P. Dickman, S. Nilsson, H. Nordlinder, C. Magnusson, and I. Persson. “Some lifestyle factors and the risk of invasive epithelial ovarian cancer in Swedish women.” European Journal of Epidemiology 19(2004):1011-1019. Print.

Rossing, M., J. Daling, N. Weiss, D. Moore, and S. Self. “Ovarian tumors in a cohort of infertile women.” New England Journal of Medicine 331(1994):771-776. Print.

Runnebaum , I. and E. Stickeler. “Epidemiological and molecular aspects of ovarian cancer risk.” Journal of Cancer Research in Clinical Oncology 127(2001): 73-79. Print.

Russo, A., V. Calo, L. Bruno, S. Rizzon, V. Bazan, G. Di Fede. “Hereditary ovarian cancer.” Critical Review Oncology Haematology 69.1(2009): 28-44. Print.

Quinn, Mark, N. Cooper, and S. Rowan. Cancer Atlas of the United Kingdom and Ireland 1991-2000. London: Palgrave Macmillan, 2005. Print.

UK Association of Cancer Registries. Library of recommendations on cancer coding and classification policy and practice. 2010. Web.

Zhang, L., S. Volinia, T. Bonome, G. Calin, J. Greshock, N. Yang, C. Liu, A. Giannakakis, P. Alexiou, K. Hasegawa. “Genomic and epigenetic alterations deregulate microRNA expression in human epithelial ovarian cancer.” PNAS 105(2008): 7004–7009. Print.

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