Ovarian Carcinoma
Ovarian carcinoma refers to a group of cancers that originate in the ovaries, the female reproductive glands responsible for producing eggs and hormones. It is a significant health concern, often challenging to diagnose early due to a lack of distinct symptoms in its initial stages.
Biological Basis
Section titled “Biological Basis”Like other cancers, ovarian carcinoma is characterized by the uncontrolled growth and division of abnormal cells. The development of ovarian cancer is a complex process influenced by a combination of genetic and environmental factors. Genetic predisposition plays a role, with research identifying specific loci associated with increased susceptibility. For instance, a genome-wide association study identified a new ovarian cancer susceptibility locus on chromosome 9p22.2[1]. Further studies, including the pooling of data from multiple genome-wide association studies (GWAS), are expected to uncover additional susceptibility alleles for both general invasive ovarian cancer and its specific histological or molecular subtypes[1].
Clinical Relevance
Section titled “Clinical Relevance”Ovarian carcinoma is known for its poor survival rates, largely because approximately 70% of patients are diagnosed at a late stage[1]. For these late-stage diagnoses, less than 40% of cases survive more than five years after diagnosis [1]. Current multi-modal approaches for early detection have limited efficacy. However, the identification of common ovarian cancer susceptibility variants could have future clinical implications by enabling genetic risk profiling. This profiling could help identify a subset of the population at highest risk, who might benefit most from earlier disease detection strategies[1].
Social Importance
Section titled “Social Importance”The high mortality rate and the challenge of early diagnosis underscore the significant social importance of ovarian carcinoma. It profoundly impacts the lives of affected individuals and their families, often leading to aggressive treatments and reduced quality of life. From a public health perspective, understanding the genetic underpinnings of ovarian cancer is crucial for developing improved screening methods, targeted therapies, and more effective prevention strategies, ultimately aiming to reduce the burden of this disease on women globally.
Limitations
Section titled “Limitations”Understanding the genetic underpinnings of ovarian carcinoma is a complex endeavor, and current research, while transformative, is subject to several limitations that impact the comprehensiveness and generalizability of findings. These limitations span methodological challenges, phenotypic complexities, and a remaining gap in fully elucidating disease etiology.
Methodological and Statistical Considerations
Section titled “Methodological and Statistical Considerations”Initial genome-wide association studies (GWAS) often face constraints related to sample size, which can limit their statistical power to detect all common genetic variants influencing ovarian cancer risk. This is particularly evident when investigating rarer histological subtypes of ovarian cancer, such as endometrioid, mucinous, or clear cell cancers, where the number of cases available for study may be insufficient to identify specific susceptibility alleles[1]. Consequently, important genetic contributions unique to these less prevalent forms of the disease might remain undiscovered, leading to an incomplete picture of their genetic architecture. Furthermore, early discovery cohorts in genetic studies can sometimes report inflated effect sizes for newly identified loci, meaning the initial estimate of risk associated with a variant might be higher than its true population effect. For instance, breast cancer susceptibility loci identified in some studies showed higher odds ratios compared to those estimated from larger, more robust population-based collaborative analyses[2]. This underscores the critical need for extensive replication studies and large-scale meta-analyses to refine risk estimates and ensure the reliability and generalizability of genetic findings across diverse populations [3].
Phenotypic Heterogeneity and Generalizability
Section titled “Phenotypic Heterogeneity and Generalizability”Ovarian carcinoma is not a singular disease but rather a heterogeneous group of malignancies comprising various histological and molecular subtypes, each potentially possessing distinct biological characteristics and genetic risk factors. Studies that analyze all ovarian cancer cases collectively may inadvertently dilute the statistical power to identify genetic associations specific to individual subtypes[1]. This approach can obscure unique genetic signals, meaning that identified susceptibility loci might primarily reflect risk for the most common ovarian cancer types, leaving the genetic basis of rarer yet clinically significant subtypes less well understood. Additionally, a significant proportion of large-scale genetic research, particularly early GWAS, has predominantly involved participants of European ancestry. While not always explicitly detailed for all ovarian cancer studies, this demographic skew in genetic research can limit the applicability and generalizability of findings to other ancestral populations. Genetic risk profiles, including allele frequencies and effect sizes of variants, can differ considerably across diverse ancestral groups, potentially hindering a universal understanding of ovarian carcinoma risk and the development of equitable risk prediction tools.
Incomplete Understanding of Disease Etiology
Section titled “Incomplete Understanding of Disease Etiology”Despite the identification of common genetic variants associated with ovarian cancer, these discovered loci often explain only a fraction of the total heritable risk, a phenomenon commonly referred to as “missing heritability.” This suggests that a substantial portion of genetic predisposition remains unaccounted for, potentially due to the influence of rarer genetic variants, structural variations, or complex epistatic interactions that are not easily captured by standard GWAS methodologies. Moreover, the intricate interplay between genetic susceptibility and environmental factors is frequently not fully elucidated in initial genetic studies. Environmental exposures, lifestyle choices, and their interactions with an individual’s genetic makeup can significantly modify disease risk. The current limitations in comprehensively accounting for these gene-environment interactions leave substantial gaps in our understanding of the complete etiology of ovarian carcinoma and impede the development of holistic risk prediction and prevention strategies.
Variants
Section titled “Variants”Genetic variations play a crucial role in an individual’s susceptibility to various diseases, including ovarian carcinoma. Understanding specific single nucleotide polymorphisms (SNPs) and their associated genes can shed light on the underlying biological mechanisms of cancer development and progression. The variants discussed below highlight regions of the genome that have been implicated in cell growth regulation, immune responses, metabolic pathways, and gene expression, all of which are pertinent to cancer risk.
Variants within the FGFR2 gene, such as rs1219648 and rs11200014 , are particularly notable for their strong association with cancer susceptibility.FGFR2 encodes a fibroblast growth factor receptor 2, a receptor tyrosine kinase that is critical for cell growth, differentiation, and tissue repair. Alterations in FGFR2 signaling can lead to uncontrolled cell proliferation, making it a significant player in various cancers. Studies have shown that FGFR2is amplified and overexpressed in a notable percentage of breast tumors, and somatic missense mutations are implicated in cancer development[4]. The variants rs1219648 and rs11200014 are located in intron 2 of FGFR2, a region highly conserved across mammals and containing putative transcription-factor binding sites, suggesting they may influence gene expression or alternative splicing patterns [4]. These SNPs, often found in strong linkage disequilibrium, have been linked to an elevated risk of breast cancer, withrs1219648 showing a significant association with increased risk [5]. Specifically, homozygote variants of rs1219648 have been associated with a significantly increased risk, demonstrating a population attributable risk of 16% for breast cancer[6]. While primarily studied in breast cancer, dysregulation of FGFR2 signaling is also a recognized factor in the pathogenesis of ovarian carcinoma, where it can promote tumor growth and resistance to therapy.
The ABO blood group system, defined by variants like rs554833 , rs657152 , and rs4962116 , encodes glycosyltransferases that determine A, B, and O blood types by modifying carbohydrate antigens on cell surfaces. Beyond their role in blood transfusions, ABO blood groups have been associated with susceptibility to various diseases, including several cancers. These variants can influence the expression of cell surface antigens, which may impact cell adhesion, immune surveillance, and inflammatory responses, all of which are crucial in cancer development. For instance, specific ABO alleles have been linked to altered risks of gastric, pancreatic, and ovarian cancers, potentially by affecting tumor angiogenesis or modulating the immune response against cancer cells. Similarly, variants inMLLT10, including rs7098100 , rs144962376 , and rs1243180 , are of interest. MLLT10 (also known as AF10) is a gene that encodes a transcription factor often involved in chromosomal translocations in leukemia. Its role in regulating gene expression extends to cellular differentiation and proliferation, making its variants potential modulators of cancer risk, including in solid tumors like ovarian carcinoma, by influencing cell cycle control or DNA repair pathways.
Other genetic regions, such as those involving BNC2 and RN7SL720P (with variants like rs10962692 and rs3814113 ), CHCHD4P2 and RPL36P14 (rs630965 ), and LINC00824 (rs1400482 , rs10088218 ), also contribute to the complex genetic landscape of cancer.BNC2 is a transcription factor involved in epidermal differentiation and hair follicle development, and its variants might influence cell growth and tissue remodeling. RN7SL720P is a pseudogene whose RNA product could potentially regulate gene expression through microRNA pathways. The CHCHD4P2 and RPL36P14 loci represent pseudogenes or regions associated with genes involved in mitochondrial function or ribosomal protein synthesis, respectively. Variations in these regions could subtly alter cellular metabolism, protein production, or stress responses, thereby influencing cellular resilience or vulnerability to oncogenic transformation. LINC00824is a long intergenic non-coding RNA (lincRNA), a class of RNA molecules increasingly recognized for their regulatory roles in gene expression, chromatin remodeling, and cell cycle control. Variants in lincRNAs can affect their stability or function, potentially leading to dysregulation of critical cellular processes that contribute to the initiation or progression of ovarian carcinoma.
Furthermore, variants in TIPARP-AS1 (rs62274041 ), TIPARP and TIPARP-AS1 (rs7651446 ), STXBP4 (rs244353 , rs2628317 ), and ADAM29 (rs6826366 ) represent additional avenues for understanding ovarian cancer susceptibility.TIPARP (TCDD-inducible poly(ADP-ribose) polymerase) is involved in cellular response to environmental toxins and DNA damage, playing a role in poly(ADP-ribosylation), a post-translational modification crucial for DNA repair and genome stability. TIPARP-AS1 is an antisense RNA that can regulate TIPARPexpression, so variants in either gene or their interaction can impact the cell’s ability to repair DNA damage, a key mechanism in cancer prevention.STXBP4(syntaxin-binding protein 4) is involved in intracellular vesicle trafficking, which is essential for cell signaling, nutrient uptake, and secretion of growth factors or cytokines. Dysregulation of these processes can contribute to uncontrolled cell growth and metastasis in ovarian carcinoma. Lastly,ADAM29 belongs to the ADAM (A Disintegrin And Metalloproteinase) family, which are cell surface proteins involved in processes like cell adhesion, migration, and proteolysis of extracellular matrix components. Variants in ADAM29could alter these functions, potentially promoting tumor invasiveness or modulating the tumor microenvironment, thereby influencing ovarian cancer progression.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs1219648 rs11200014 | FGFR2 | breast carcinoma ovarian carcinoma |
| rs554833 rs657152 rs4962116 | ABO | type 2 diabetes mellitus ovarian carcinoma endometrial cancer, COVID-19 |
| rs10962692 rs3814113 | BNC2 - RN7SL720P | ovarian carcinoma ovarian serous carcinoma |
| rs630965 | CHCHD4P2 - RPL36P14 | breast carcinoma ovarian carcinoma |
| rs62274041 | TIPARP-AS1 | ovarian carcinoma ovarian serous carcinoma |
| rs7651446 | TIPARP, TIPARP-AS1 | ovarian carcinoma malignant epithelial tumor of ovary |
| rs244353 rs2628317 | STXBP4 | ovarian carcinoma |
| rs6826366 | ADAM29 | ovarian carcinoma |
| rs7098100 rs144962376 rs1243180 | MLLT10 | breast carcinoma ovarian carcinoma diet measurement PHF-tau measurement endometriosis |
| rs1400482 rs10088218 | LINC00824 | ovarian carcinoma ovarian serous carcinoma |
Classification, Definition, and Terminology
Section titled “Classification, Definition, and Terminology”Defining Ovarian Carcinoma and its Genetic Basis
Section titled “Defining Ovarian Carcinoma and its Genetic Basis”Ovarian carcinoma refers to a malignant tumor primarily originating in the ovary. It is clinically characterized by a challenging prognosis, largely due to the fact that approximately 70% of patients receive a diagnosis at a late stage of the disease[1]. Consequently, less than 40% of these cases survive more than five years after their initial diagnosis, highlighting the critical need for improved understanding and early detection [1].
The conceptual framework for ovarian carcinoma includes both sporadic and heritable forms, with a significant emphasis on familial risk. Mutations in genes such asBRCA2are known to confer a high risk for ovarian cancer and are responsible for a substantial proportion of families with multiple affected individuals[1]. However, BRCA2 mutations do not account for all instances of familial risk, indicating that the remaining susceptibility likely stems from a complex interplay of common and/or rare alleles that confer moderate to low penetrance [1]. This understanding points to a multifaceted genetic architecture underlying an individual’s predisposition to the disease.
Classification and Subtyping of Ovarian Carcinoma
Section titled “Classification and Subtyping of Ovarian Carcinoma”Ovarian carcinoma is not a singular disease entity but rather a group of distinct cancers categorized by various classification systems, primarily based on their histological and molecular characteristics[1]. These precise classifications are essential for guiding clinical management, predicting prognosis, and developing targeted therapies. Research has identified specific histological subtypes, including endometrioid, mucinous, and clear cell ovarian cancers, which are often considered rarer and may have unique biological profiles [1].
Beyond histological classifications, the severity of ovarian carcinoma is typically assessed through staging systems, though specific details are not provided in all research contexts. The term “late stage disease” is a critical classification, indicating advanced progression and a significantly poorer prognosis[1]. Ongoing research, including large-scale genomic studies, aims to identify additional susceptibility alleles not only for invasive ovarian cancer generally but also for these specific histological and molecular subtypes[1].
Diagnostic and Risk Assessment Approaches
Section titled “Diagnostic and Risk Assessment Approaches”The diagnostic criteria for ovarian carcinoma are complex, and effective early detection remains a significant clinical challenge. Current multi-modal approaches for early disease detection have shown limited efficacy, underscoring the need for more sensitive and specific methods[1]. However, advancements in identifying genetic susceptibility loci offer promising avenues for enhancing risk assessment strategies.
The identification of common ovarian cancer susceptibility variants, such as a new locus discovered on chromosome 9p22.2, holds future clinical implications for identifying individuals at the highest risk[1]. This concept of “genetic risk profiling” could enable the identification of a specific subset of the population that would most benefit from intensified early detection efforts [1]. Such targeted screening has the potential to improve survival rates by facilitating diagnosis and intervention before the disease progresses to its more advanced, late stages[1].
Signs and Symptoms
Section titled “Signs and Symptoms”Insidious Onset and Late-Stage Diagnosis
Section titled “Insidious Onset and Late-Stage Diagnosis”Ovarian carcinoma is frequently characterized by an insidious onset, where early signs and symptoms are often vague or non-specific, leading to significant diagnostic delays. A substantial majority of patients, approximately 70%, are diagnosed at a late stage of the disease[1]. This late presentation is a critical factor contributing to the poor prognosis associated with this cancer, as the disease has often progressed beyond localized treatment options by the time it is identified. The subtlety of early indicators makes ovarian carcinoma a considerable diagnostic challenge, often necessitating a high index of suspicion in individuals with risk factors.
The high rate of late-stage diagnosis directly impacts survival rates, with less than 40% of these advanced cases surviving more than five years after their diagnosis [1]. The clinical presentation patterns, therefore, are often those of advanced disease, rather than early-stage manifestations. Objective assessment methods for early detection have shown limited efficacy, highlighting the need for improved diagnostic tools that can identify the disease before widespread dissemination[1].
Heterogeneity in Clinical Phenotypes and Presentation Variability
Section titled “Heterogeneity in Clinical Phenotypes and Presentation Variability”The clinical presentation of ovarian carcinoma can exhibit considerable heterogeneity, influenced by various histological and molecular subtypes, such as endometrioid, mucinous, and clear cell ovarian cancers[1]. The existence of these distinct subtypes implies potential differences in how the disease manifests and progresses across individuals, contributing to the diversity in observed clinical phenotypes. While specific symptom patterns for each subtype are not detailed, this phenotypic diversity suggests that a uniform approach to symptom-based diagnosis may overlook atypical presentations.
Inter-individual variation in symptom experience and severity ranges can further complicate early diagnosis, as subjective measures of discomfort or changes in bodily function may vary widely. The limited efficacy of current multi-modal approaches for early detection underscores the challenge in accurately measuring and interpreting these varied presentations [1]. Understanding the variability across these subtypes is crucial for developing more targeted diagnostic strategies that account for the disease’s diverse biological underpinnings.
Diagnostic Significance and Future Screening Approaches
Section titled “Diagnostic Significance and Future Screening Approaches”The significant diagnostic challenge in identifying ovarian carcinoma early stems from the non-specific nature of initial symptoms and the limited effectiveness of existing multi-modal early detection methods[1]. This difficulty results in stark survival rates, with less than half of late-stage diagnoses leading to a five-year survival [1]. Therefore, identifying individuals at an elevated risk before the onset of symptomatic disease is paramount for improving prognostic outcomes and reducing mortality.
Genetic risk profiling presents a promising avenue to identify a subset of the population who might benefit most from earlier disease detection efforts[1]. The identification of common ovarian cancer susceptibility variants could have future clinical implications for stratifying patients by risk, thereby potentially improving the effectiveness of early detection strategies by focusing resources on those most likely to develop the disease[1]. Such an approach aims to address the inherent variability in individual risk, providing a more objective measure for targeted screening rather than relying solely on the often late and non-specific clinical signs and symptoms.
Causes
Section titled “Causes”Ovarian carcinoma development is a complex process primarily influenced by a combination of genetic factors, which dictate an individual’s predisposition to the disease.
Genetic Predisposition
Section titled “Genetic Predisposition”Ovarian carcinoma is influenced significantly by genetic factors, ranging from highly penetrant inherited mutations to a combination of common, lower-risk genetic variants. Mutations in genes such asBRCA1 and BRCA2are well-established high-risk factors, considerably increasing an individual’s susceptibility to ovarian cancer. These specific mutations are found in a substantial proportion of families that exhibit multiple cases of ovarian cancer, underscoring their critical role in Mendelian forms of the disease . This discovery indicates that common genetic variants within this particular region are associated with a higher probability of an individual developing ovarian carcinoma. These inherited genetic mechanisms contribute significantly to the overall risk profile, highlighting the importance of an individual’s genetic makeup in the predisposition to this malignancy.
Pathophysiological Characteristics and Tissue-Level Impact
Section titled “Pathophysiological Characteristics and Tissue-Level Impact”Ovarian carcinoma involves the uncontrolled growth and proliferation of abnormal cells within the ovarian tissue, leading to tumor formation. The genetic susceptibilities, such as those identified at the 9p22.2 locus, are thought to contribute to the initiation or progression of these pathophysiological processes. While the precise molecular and cellular pathways influenced by these specific genetic variants in ovarian carcinoma are still being elucidated, their presence suggests a disruption in normal cellular functions and regulatory networks within the ovarian environment. Ultimately, these disruptions can lead to the characteristic hallmarks of cancer, including sustained proliferative signaling and resistance to cell death, thereby impacting the organ-specific biology of the ovaries[1].
Clinical Relevance of Ovarian Carcinoma
Section titled “Clinical Relevance of Ovarian Carcinoma”Ovarian carcinoma presents significant clinical challenges due to its typically late diagnosis and aggressive nature. Recent research, particularly genome-wide association studies, has begun to uncover genetic predispositions that may impact risk assessment, early detection strategies, and understanding of disease heterogeneity, offering potential avenues for improved patient care.
Risk Stratification and Early Detection
Section titled “Risk Stratification and Early Detection”The identification of common genetic susceptibility variants, such as a newly discovered locus on 9p22.2, holds promise for future clinical applications in identifying individuals at the highest risk for developing ovarian carcinoma[1]. This genetic profiling could serve as a valuable tool to enhance the efficacy of existing multi-modal approaches to early disease detection, which currently have limited success[1]. By focusing screening and surveillance efforts on a genetically predisposed subset of the population, there is a potential to diagnose ovarian carcinoma at earlier, more treatable stages, thereby improving overall patient outcomes[1].
Prognostic Implications and Disease Progression
Section titled “Prognostic Implications and Disease Progression”The prognosis for ovarian carcinoma remains poor, largely due to the high proportion of patients diagnosed with advanced-stage disease[1]. Approximately 70% of individuals receive a diagnosis when the cancer is already in a late stage, profoundly impacting their long-term outlook[1]. For these late-stage cases, fewer than 40% of patients survive beyond five years after their diagnosis [1]. These grim statistics highlight the critical need for advancements in early detection and risk stratification to enable earlier intervention, which could significantly alter the trajectory of disease progression and improve survival rates.
Genetic Susceptibility and Disease Heterogeneity
Section titled “Genetic Susceptibility and Disease Heterogeneity”Research continues to elucidate the genetic landscape of ovarian carcinoma, identifying specific susceptibility loci that contribute to disease risk[1]. Beyond general invasive ovarian cancer, there is increasing recognition of distinct histological and molecular subtypes, including endometrioid, mucinous, and clear cell ovarian cancers, which may each possess unique genetic susceptibility alleles[1]. While current studies have faced limitations in power to identify alleles for these rarer subtypes, the pooling of data from multiple genome-wide association studies is expected to enable the discovery of additional susceptibility alleles relevant to these specific forms of ovarian cancer[1]. Such discoveries are crucial for developing more personalized risk assessments and tailored prevention strategies that account for the inherent heterogeneity of the disease.
Frequently Asked Questions About Ovarian Carcinoma
Section titled “Frequently Asked Questions About Ovarian Carcinoma”These questions address the most important and specific aspects of ovarian carcinoma based on current genetic research.
1. My mom had ovarian cancer; will I definitely get it too?
Section titled “1. My mom had ovarian cancer; will I definitely get it too?”Not necessarily, but your risk is higher. While a strong family history suggests a genetic predisposition, it doesn’t mean you’ll definitely develop it. Many factors, including specific genetic variations you inherit and environmental influences, contribute to your overall risk.
2. Should I get a DNA test if I’m worried about ovarian cancer?
Section titled “2. Should I get a DNA test if I’m worried about ovarian cancer?”Genetic testing can be valuable, especially with a family history. Identifying common ovarian cancer susceptibility variants, like those on chromosome 9p22.2, can help determine if you’re in a higher-risk group. This information can then guide discussions with your doctor about personalized screening strategies.
3. Can my diet or exercise habits change my ovarian cancer risk?
Section titled “3. Can my diet or exercise habits change my ovarian cancer risk?”Yes, lifestyle can play a role. While genetic predisposition is significant, the intricate interplay between your genes and environmental factors, including diet and exercise, can modify your overall disease risk. Research is still working to fully understand these complex gene-environment interactions for ovarian carcinoma.
4. Does my ethnic background affect my ovarian cancer risk?
Section titled “4. Does my ethnic background affect my ovarian cancer risk?”It can. Much of the large-scale genetic research has predominantly involved people of European ancestry, and genetic risk profiles can differ across diverse ancestral groups. This means your specific background might influence your risk and how applicable current research findings are to you.
5. Why do doctors sometimes struggle to understand rarer ovarian cancers?
Section titled “5. Why do doctors sometimes struggle to understand rarer ovarian cancers?”Ovarian carcinoma isn’t just one disease; it has many distinct subtypes, like endometrioid or mucinous cancers. Studying these rarer types is harder because there are fewer cases available for large genetic studies, making it difficult to identify their unique genetic risk factors.
6. Why do some women get ovarian cancer with no family history?
Section titled “6. Why do some women get ovarian cancer with no family history?”Even without a clear family history, genetic factors still play a role. While some cases are linked to strong inherited predispositions, other women may have common genetic susceptibility variants that increase their risk, or their cancer might arise from entirely new genetic changes or environmental influences.
7. If a test says I’m high risk, does that mean I’ll definitely get a specific type?
Section titled “7. If a test says I’m high risk, does that mean I’ll definitely get a specific type?”Not necessarily. Current genetic findings often identify risk for ovarian cancer generally, or for the most common types. Because ovarian carcinoma is so diverse, a general high-risk finding doesn’t always pinpoint the exact subtype you might be susceptible to.
8. If my genes are checked, are there still hidden risks for ovarian cancer?
Section titled “8. If my genes are checked, are there still hidden risks for ovarian cancer?”Yes, there can be. Even with identified genetic variants, a significant portion of the total inherited risk, known as “missing heritability,” remains unexplained. This could be due to rarer genetic variants or complex interactions not yet fully understood by current testing methods.
9. Why do so many women find out they have ovarian cancer so late?
Section titled “9. Why do so many women find out they have ovarian cancer so late?”It’s a major challenge because early ovarian cancer often has no distinct symptoms, making it hard to diagnose. Approximately 70% of diagnoses happen at a late stage, which unfortunately leads to poorer survival rates for patients.
10. Could genetic testing help me prevent ovarian cancer in the future?
Section titled “10. Could genetic testing help me prevent ovarian cancer in the future?”While it can’t prevent it directly, genetic risk profiling can be a powerful tool. By identifying if you’re in a high-risk group, it can help your doctor suggest earlier or more frequent screening strategies, which could lead to earlier detection if cancer does develop.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Song, H et al. “A genome-wide association study identifies a new ovarian cancer susceptibility locus on 9p22.2.”Nat Genet, 2009.
[2] Turnbull, C., et al. “Genome-wide association study identifies five new breast cancer susceptibility loci.”Nat Genet, 2010.
[3] Wang, Y., et al. “Common 5p15.33 and 6p21.33 variants influence lung cancer risk.”Nat Genet, 2008.
[4] Easton DF et al. “Genome-wide association study identifies novel breast cancer susceptibility loci.”Nature, 2007.
[5] Zheng W et al. “Genome-wide association study identifies a new breast cancer susceptibility locus at 6q25.1.”Nat Genet, 2009.
[6] Hunter DJ et al. “A genome-wide association study identifies alleles in FGFR2 associated with risk of sporadic postmenopausal breast cancer.”Nat Genet, 2007.