Digestive System Cancer
Digestive system cancer refers to a group of malignancies that originate in any part of the gastrointestinal tract, including the esophagus, stomach, small intestine, large intestine (colon and rectum), liver, gallbladder, and pancreas. These cancers represent a significant global health challenge due to their high incidence and mortality rates. Understanding the underlying mechanisms and risk factors is crucial for effective prevention, diagnosis, and treatment.
The biological basis of digestive system cancers involves a complex interplay of genetic predispositions and environmental factors. At a cellular level, cancer arises from uncontrolled cell growth and division, often driven by accumulated mutations in genes that regulate cell cycle, DNA repair, and apoptosis. Genetic variations, such as single nucleotide polymorphisms (SNPs), can influence an individual’s susceptibility to developing these cancers. For instance, genome-wide association studies (GWAS) have identified specific susceptibility loci associated with increased risk for pancreatic cancer on chromosomes 13q22.1, 1q32.1, and 5p15.33[1]. Similarly, research has uncovered several new susceptibility loci for colorectal cancer, including those on 11q23, 8q24, and 18q21, and four additional loci identified through meta-analysis[2]. These genetic insights highlight the polygenic nature of cancer risk and the role of common genetic variants.
Clinically, digestive system cancers present diverse challenges. Early detection is often difficult because symptoms may be subtle or non-specific, leading to diagnosis at advanced stages. Advances in screening methods, such as colonoscopies for colorectal cancer, and imaging techniques are vital for improving patient outcomes. Treatment options vary widely depending on the cancer type, stage, and location, and may include surgery, chemotherapy, radiation therapy, and targeted therapies. Genetic profiling of tumors and germline DNA is increasingly used to guide personalized treatment strategies, predict response to therapies, and assess inherited risk.
The social importance of addressing digestive system cancer is profound. These diseases impose a substantial burden on healthcare systems, economies, and individuals globally. They affect quality of life, often requiring extensive and debilitating treatments, and can lead to significant psychological and financial strain for patients and their families. Public health initiatives focused on promoting healthy lifestyles, improving access to screening programs, and educating the public about risk factors are essential for reducing incidence and mortality. Further research into genetic susceptibility and molecular pathways holds promise for developing more effective preventive strategies and novel therapeutic interventions.
Limitations
Section titled “Limitations”Methodological and Statistical ConsiderationsResearch into the genetic basis of digestive system cancers, such as colorectal and pancreatic cancer, often relies on genome-wide association studies (GWAS) and subsequent meta-analyses to identify susceptibility loci[3], [1]. While meta-analyses are crucial for increasing sample size and SNP coverage, they can still be limited by the statistical power required to robustly detect genetic variants with small effect sizes, a common characteristic of complex diseases[4]. Furthermore, initial findings from discovery cohorts necessitate rigorous large-scale replication studies to confirm associations and minimize the risk of false positives, with successful replication efforts often identifying additional risk variants [5], [6].
The application of stringent statistical thresholds, such as the widely accepted p < 5 × 10[7] for genome-wide significance, ensures a high level of confidence in reported associations but may inadvertently cause genuine, yet weaker, signals to be overlooked, particularly in studies with more modest sample sizes [8]. The process of systematically taking forward promising single nucleotide polymorphisms (SNPs) to large-scale replication is essential for validating initial signals and enhancing the overall confidence in the identified risk variants[4]. Without such comprehensive validation across independent datasets, the broader applicability and robustness of genetic associations remain subject to further investigation.
Population and Phenotypic Heterogeneity The generalizability of genetic findings for digestive system cancers can be significantly influenced by the ancestral background and demographic composition of the study populations. Although many genetic studies involve extensive international collaborations and diverse cohorts spanning various regions, including Europe and North America [3], [1], [6], potential population-specific biases may still exist. These biases can limit the direct applicability of findings to all global ancestries, given the differences in genetic architecture, linkage disequilibrium patterns, and allele frequencies across distinct human populations.
Moreover, the precise definition of the “digestive system cancer” phenotype itself introduces a degree of heterogeneity. The research often focuses on specific cancer types, such as colorectal cancer or pancreatic cancer, each possessing unique biological characteristics and etiological pathways[3], [1]. While some genetic variants may confer general cancer susceptibility, the context primarily highlights studies investigating individual cancer types. This specificity means that findings are highly pertinent to the particular cancer under investigation rather than representing a generalized genetic predisposition across the broad spectrum of digestive system malignancies.
Complex Etiology and Unexplained VariationThe development of digestive system cancers is a multifaceted process driven by an intricate interplay of genetic and environmental factors, many of which are still not fully elucidated. While genome-wide association studies have been successful in identifying common genetic variants associated with cancer risk, these variants frequently explain only a small fraction of the observed heritability for these complex diseases, pointing to a substantial amount of “missing heritability”[4]. This gap suggests that numerous other genetic contributors, including rare variants, structural variations, or complex epistatic interactions between genes, have yet to be discovered.
Furthermore, environmental exposures and gene-environment interactions play a critical, yet often underestimated and unquantified, role in cancer etiology. While some studies meticulously control for prominent environmental confounders, such as smoking status in lung cancer research[9], the complex interplay between genetic predispositions and factors like diet, lifestyle choices, microbial environment, and other environmental exposures for digestive system cancers remains challenging to comprehensively capture and model. Deciphering how common regulatory variations functionally impact gene expression in a cell-type dependent manner is crucial for translating identified genetic loci into biological mechanisms, representing an ongoing and significant knowledge gap[9].
Variants
Section titled “Variants”Genetic variations, such as rs116864126 , located in or near the EDIL3 gene or its associated divergent transcript (EDIL3-DT), can influence the activity of the EDIL3 protein. EDIL3, also known as DEL1, is an extracellular matrix protein crucial for cell adhesion, migration, and angiogenesis (the formation of new blood vessels), processes that are often co-opted by cancer cells for growth and spread. Alterations in EDIL3 function or expression due to such variants can promote key aspects of tumor progression, including increased blood supply to tumors and enhanced metastatic potential, as observed in various cancers. Studies have highlighted numerous genetic loci that contribute to cancer risk, including those for colorectal cancer[6]and prostate cancer[10], illustrating the broad impact of genetic variations on disease susceptibility.
Beyond general mechanisms, specific genetic variants have been directly implicated in the susceptibility to digestive system cancers, particularly colorectal cancer. For instance, a meta-analysis identified several single nucleotide polymorphisms (SNPs) associated with altered colorectal cancer risk. The minor allele ofrs961253 was linked to an increased risk of colorectal cancer in a dose-dependent manner, with homozygous carriers facing a higher risk[3]. Similarly, rs4444235 also showed an increased risk, with homozygous carriers having an even higher odds ratio [3]. These findings underscore the complex genetic architecture underlying colorectal cancer susceptibility.
Conversely, some variants may offer a protective effect; the minor allele of rs10411210 was associated with a decreased risk of colorectal cancer in a dose-dependent fashion[3]. Another variant, rs9929218 , was also identified in association with colorectal cancer risk[3]. The presence of these specific genetic markers highlights varied roles in influencing an individual’s predisposition to developing this common digestive malignancy. Furthermore, defects in base-excision repair genes, a fundamental DNA repair pathway, have also been identified as germline susceptibility factors for colorectal cancer, emphasizing the importance of genomic integrity in preventing digestive system cancers[7].
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs116864126 | EDIL3-DT | digestive system cancer |
Classification, Definition, and Terminology of Digestive System Cancer
Section titled “Classification, Definition, and Terminology of Digestive System Cancer”Digestive system cancer encompasses various malignancies that originate in the organs of the gastrointestinal tract, including the esophagus, stomach, liver, pancreas, small intestine, and large intestine (colon and rectum). Understanding these cancers requires precise definitions, a robust classification system, and standardized terminology to facilitate diagnosis, treatment, and research.
Defining Digestive System Cancer and its Epidemiological Context
Section titled “Defining Digestive System Cancer and its Epidemiological Context”Digestive system cancer refers to the uncontrolled growth and spread of abnormal cells within any part of the digestive tract. The conceptual framework for understanding these diseases often relies on epidemiological studies that track their incidence, mortality, and prevalence worldwide[11] [12]. For instance, pancreatic cancer, a significant digestive system malignancy, is extensively studied within the broader field of cancer epidemiology and prevention, which examines its occurrence and factors influencing its development[13]. Operational definitions for tracking these diseases often involve large-scale cohort studies that establish baseline characteristics and monitor long-term outcomes to assess risk factors and disease progression[14].
Genetic Classifications and Subtypes
Section titled “Genetic Classifications and Subtypes”Classification systems for digestive system cancers often include subtypes based on their genetic underpinnings, which can influence susceptibility and prognosis. For pancreatic cancer, specific susceptibility loci have been identified on chromosomes 13q22.1, 1q32.1, and 5p15.33[1], alongside variants in the ABO locus that are associated with increased risk [15]. This genetic categorization highlights the molecular diversity of the disease. Furthermore, certain forms of pancreatic cancer are recognized as hereditary, such as those linked to hereditary pancreatitis, while others are classified as familial pancreatic cancer based on their occurrence within kindreds[16] [17]. Similarly, colorectal cancer can be subtyped by genetic susceptibility, with identified loci on 11q23, 8q24, and 18q21, and additional susceptibility loci recognized through comprehensive genetic analyses[6] [3].
Research Criteria for Genetic Association Studies
Section titled “Research Criteria for Genetic Association Studies”In the scientific investigation of digestive system cancers, particularly in identifying genetic risk factors, specific diagnostic and measurement criteria are employed in research settings. Genome-wide association studies (GWAS) utilize rigorous statistical thresholds to define significant associations between genetic variants and cancer susceptibility. For instance, a conservative p-value threshold of 5 × 10[7] is often used to establish genome-wide significance, ensuring a high degree of confidence in identified associations [8]. This operational definition for statistical significance is crucial for identifying potential biomarkers and contributes to the understanding of the genetic landscape of digestive system cancers, informing future clinical criteria and prevention strategies.
There is no information about the signs and symptoms of digestive system cancer in the provided context.
Causes of Digestive System Cancer
Section titled “Causes of Digestive System Cancer”Digestive system cancers, encompassing conditions such as colorectal and pancreatic cancer, arise from a complex interplay of various factors that influence cellular integrity and proliferation within the gastrointestinal tract. While the precise mechanisms can differ between specific cancer types, a significant component of risk is rooted in an individual’s genetic makeup.
Inherited Genetic Predisposition
Section titled “Inherited Genetic Predisposition”Genetic factors play a significant role in determining an individual’s susceptibility to digestive system cancers. Inherited variants, passed down through generations, can increase the risk of developing conditions such as colorectal and pancreatic cancer. These predispositions are often linked to alterations in genes that regulate cell growth, DNA repair, or other fundamental cellular processes, leading to an elevated lifetime risk. While some forms of cancer involve highly penetrant single gene mutations, a substantial portion of inherited risk arises from the cumulative effect of many common genetic variations.
Polygenic Risk and Susceptibility Loci
Section titled “Polygenic Risk and Susceptibility Loci”Genome-wide association studies (GWAS) have been instrumental in identifying numerous common genetic variants that collectively contribute to the polygenic risk of digestive system cancers. For colorectal cancer, meta-analyses of GWAS data have pinpointed several new susceptibility loci[3]. Similarly, research has identified specific susceptibility loci for pancreatic cancer on chromosomes 13q22.1, 1q32.1, and 5p15.33[1]. These loci represent regions of the genome where variations are more common in individuals who develop these cancers, suggesting their involvement in disease pathogenesis by influencing gene expression or function.
Specific Genetic Markers and Risk Modulation
Section titled “Specific Genetic Markers and Risk Modulation”Beyond broad chromosomal regions, specific genetic markers have been linked to an altered risk of digestive system cancers. For instance, variants within the ABO locus have been associated with susceptibility to pancreatic cancer[15]. The presence of these specific alleles can modulate an individual’s risk profile, potentially by influencing cellular interactions, immune responses, or other biological pathways relevant to cancer development. While the precise mechanisms for all identified variants are still under investigation, these findings highlight the intricate genetic architecture underlying digestive system cancer risk.
Biological Background
Section titled “Biological Background”Genetic Predisposition to Digestive System Cancers
Section titled “Genetic Predisposition to Digestive System Cancers”Digestive system cancers, such as pancreatic and colorectal cancer, are complex diseases influenced by a combination of environmental and genetic factors. Genome-wide association studies (GWAS) have been pivotal in uncovering specific genetic variations that increase an individual’s susceptibility to these malignancies. By analyzing large populations, researchers can identify common genetic markers, often single nucleotide polymorphisms (SNPs), that are more frequently observed in individuals diagnosed with digestive system cancers[3]. These findings highlight the inherent genetic component contributing to the risk of developing these life-threatening conditions.
Chromosomal Susceptibility Loci
Section titled “Chromosomal Susceptibility Loci”Research has pinpointed several specific chromosomal regions associated with the risk of developing digestive system cancers. For pancreatic cancer, genome-wide association studies have identified susceptibility loci on chromosomes 13q22.1, 1q32.1, and 5p15.33[1]. These regions likely harbor genes or regulatory elements whose variations contribute to the disease’s etiology. Similarly, for colorectal cancer, comprehensive meta-analyses of genome-wide association data have led to the identification of four new susceptibility loci, expanding the known genetic landscape of this disease[3]. The discovery of these distinct genetic markers underscores the organ-specific genetic predispositions within the digestive system.
The ABO Locus and Pancreatic Cancer
Section titled “The ABO Locus and Pancreatic Cancer”Among the notable genetic findings for digestive system cancers is the association between variants in the ABO locus and susceptibility to pancreatic cancer. The ABO blood group system is defined by specific antigens present on the surface of red blood cells and other cell types throughout the body, including digestive tissues. Variations within the ABO gene can influence the expression or structure of these antigens, potentially altering cellular interactions or signaling pathways relevant to pancreatic cell growth and differentiation[15]. This specific genetic link suggests that fundamental biological processes related to blood group determination may play an unexpected role in pancreatic carcinogenesis.
Genetic Variation and Cellular Impact
Section titled “Genetic Variation and Cellular Impact”The presence of specific genetic variants, such as those identified for digestive system cancers, suggests an underlying impact on cellular functions and regulatory networks. While the precise molecular and cellular pathways affected by each identified locus require further elucidation, these variations are understood to influence the biological processes within affected tissues. Such alterations can disrupt the delicate homeostatic balance, potentially initiating or promoting the uncontrolled cell growth characteristic of cancer. Understanding how these genetic variations translate into functional changes at the cellular level is crucial for comprehending the overall pathophysiological mechanisms of digestive system cancers.
Genetic Predisposition and Regulatory Variation
Section titled “Genetic Predisposition and Regulatory Variation”The development of digestive system cancer is significantly influenced by genetic predisposition, where specific sequence variants identified through genome-wide association studies (GWAS) increase an individual’s susceptibility. These identified loci often involve common regulatory variations that impact gene expression in a cell type-dependent manner[9]. This mechanism highlights how subtle changes in non-coding regions or within genes can alter the transcription or translation of critical proteins, thereby modulating cellular pathways and contributing to an elevated risk of cancer. Such genetic alterations can disrupt the delicate balance of normal cellular processes, setting the stage for disease progression.
Pathway Dysregulation in Digestive System Cancers
Section titled “Pathway Dysregulation in Digestive System Cancers”The genetic variants associated with digestive system cancer susceptibility are implicated in the dysregulation of essential cellular pathways. While the specific molecular details of these pathways, including receptor activation, intracellular signaling cascades, or metabolic flux control, are complex and multifactorial, the presence of susceptibility loci suggests altered functionality in processes critical for cell growth, differentiation, and survival. This dysregulation represents a fundamental disease-relevant mechanism, where genetic predispositions can lead to an environment that favors uncontrolled cell proliferation and impaired cell death, key hallmarks of cancer development. The cumulative effect of these genetic influences can shift cellular states towards a cancerous phenotype.
Locus-Specific Genetic Associations
Section titled “Locus-Specific Genetic Associations”Specific chromosomal regions have been identified as susceptibility loci for various digestive system cancers. For pancreatic cancer, genome-wide association studies have pinpointed significant variants on chromosomes 13q22.1, 1q32.1, and 5p15.33[1]. Additionally, variants within the ABO locus have been associated with an increased susceptibility to pancreatic cancer[15]. In the context of colorectal cancer, studies have identified susceptibility loci on chromosomes 11q23, 8q24, and 18q21, underscoring the genetic complexity underlying this disease[2]. These distinct genetic regions serve as crucial indicators of inherited risk, highlighting specific genomic areas where variations contribute to the overall genetic architecture of digestive system cancer.
Systems-Level Genetic Interactions
Section titled “Systems-Level Genetic Interactions”The identification of multiple, distinct susceptibility loci across the genome for both pancreatic and colorectal cancers points towards a complex, polygenic basis for disease risk. This systems-level integration suggests that the overall etiology of digestive system cancers may arise from the cumulative effects and potential interactions among these various genetic variants, rather than being driven by a single dominant mutation. Such network interactions and hierarchical regulation, where multiple genetic contributions collectively influence cellular behavior, represent an emergent property of disease susceptibility. Understanding these broader genetic interactions is critical for comprehending how inherited factors collectively contribute to cancer development and progression.
Clinical Relevance
Section titled “Clinical Relevance”Understanding the genetic underpinnings of digestive system cancers is pivotal for advancing clinical practice, enabling more precise risk assessment, and informing tailored patient management strategies. Research has identified specific genetic variants that contribute to the susceptibility of various digestive system malignancies, including pancreatic and colorectal cancers. These discoveries pave the way for a more stratified approach to prevention, surveillance, and potentially treatment, moving towards personalized medicine.
Genetic Risk Stratification and Early Surveillance
Section titled “Genetic Risk Stratification and Early Surveillance”The identification of specific genetic susceptibility loci for digestive system cancers plays a crucial role in risk stratification. For instance, studies have identified susceptibility loci for pancreatic cancer on chromosomes 13q22.1, 1q32.1, and 5p15.33, as well as variants within the ABO locus[15]. Similarly, meta-analyses have uncovered new susceptibility loci for colorectal cancer[3]. These findings allow clinicians to identify individuals at an elevated genetic risk for developing these cancers, even in the absence of a strong family history.
By stratifying individuals based on their genetic risk profiles, healthcare providers can implement more targeted and effective early surveillance programs. Individuals identified as high-risk through genetic screening could benefit from more frequent or intensive screening modalities, potentially leading to earlier detection of precancerous lesions or early-stage cancers. This proactive approach aims to improve patient outcomes by allowing for timely interventions when the disease is most treatable, ultimately shifting the paradigm from reactive treatment to preventative and early diagnostic strategies.
Informing Personalized Prevention and Management
Section titled “Informing Personalized Prevention and Management”Knowledge of genetic susceptibility to digestive system cancers holds significant implications for personalized prevention and management strategies. Beyond identifying high-risk individuals, understanding the specific genetic variants involved can illuminate underlying biological pathways that contribute to carcinogenesis. For example, the association of ABO blood group variants with pancreatic cancer susceptibility may point to novel mechanisms or interactions that could be targeted for prevention or therapeutic development[15].
This genetic information can guide the development of personalized medicine approaches, where prevention strategies are tailored to an individual’s unique genetic makeup. For those at increased risk, specific lifestyle modifications, dietary recommendations, or chemopreventive agents might be considered. While the provided studies primarily focus on susceptibility, the long-term implications of these genetic findings extend to predicting disease progression in at-risk populations and potentially influencing future treatment selection by identifying molecular targets, thereby offering a more nuanced approach to patient care that goes beyond population-level recommendations.
Molecular Insights and Disease Associations
Section titled “Molecular Insights and Disease Associations”The discovery of specific genetic variants associated with digestive system cancers provides valuable molecular insights into disease etiology and can highlight potential associations with other biological functions. The identification of susceptibility loci for pancreatic cancer on chromosomes 13q22.1, 1q32.1, and 5p15.33[1], alongside the association of ABO locus variants with pancreatic cancer risk[15], underscores the complex genetic architecture of these malignancies. These findings not only serve as markers for risk but also offer critical clues into the genes and pathways that, when dysregulated, contribute to cancer development.
While the research primarily focuses on susceptibility, these genetic associations can imply broader biological connections and potential overlapping phenotypes, which warrant further investigation. Understanding these molecular underpinnings can contribute to a more comprehensive view of digestive system cancers, potentially revealing shared mechanisms with other conditions or identifying targets for novel therapeutic interventions. This deeper molecular understanding is essential for advancing basic science and translating these discoveries into tangible improvements in long-term patient care and prognostic understanding.
Frequently Asked Questions About Digestive System Cancer
Section titled “Frequently Asked Questions About Digestive System Cancer”These questions address the most important and specific aspects of digestive system cancer based on current genetic research.
1. My parent had digestive cancer. Will I get it too?
Section titled “1. My parent had digestive cancer. Will I get it too?”Having a parent with digestive cancer can increase your susceptibility, as genetic predispositions play a role. While it doesn’t mean you’ll definitely get it, you might have common genetic variations that elevate your risk. For example, specific gene regions linked to colorectal or pancreatic cancer can be inherited. It’s important to discuss your family history with your doctor to understand your personal risk.
2. Can a healthy diet overcome my family’s cancer history?
Section titled “2. Can a healthy diet overcome my family’s cancer history?”Yes, a healthy lifestyle, including diet, is crucial even if you have a family history. Cancer arises from a complex interplay of genetic factors and environmental influences. While you can’t change your inherited genetic variations, maintaining healthy habits can help mitigate the environmental factors that contribute to cancer development. Public health initiatives emphasize healthy lifestyles as essential for reducing incidence.
3. Is getting a DNA test useful for my cancer risk?
Section titled “3. Is getting a DNA test useful for my cancer risk?”Yes, genetic profiling of your germline DNA is increasingly used to assess inherited risk for various cancers, including those of the digestive system. A DNA test can identify specific genetic variations that influence your susceptibility. This information can help guide personalized prevention strategies and inform your doctor about potential monitoring needs. It provides a more precise understanding of your individual risk profile.
4. What subtle signs should I look out for?
Section titled “4. What subtle signs should I look out for?”Digestive system cancers often present with subtle or non-specific symptoms, making early detection challenging. The article emphasizes that symptoms can be vague, and it doesn’t list specific signs. This highlights the importance of regular check-ups and open communication with your doctor about any persistent or unusual changes in your body, rather than looking for specific “subtle signs” yourself.
5. Does my family background affect my personal risk?
Section titled “5. Does my family background affect my personal risk?”Yes, your ancestral background can influence your genetic risk for digestive system cancers. Genetic studies show that findings can be affected by the demographic and ancestral composition of populations, due to differences in genetic architecture and allele frequencies. This means certain genetic variations that increase risk might be more common or have different effects in specific ethnic groups, making your background a relevant factor.
6. What can I do daily to lower my chances?
Section titled “6. What can I do daily to lower my chances?”Focusing on a healthy lifestyle is key to lowering your chances of developing digestive system cancer. This includes adopting habits that promote overall well-being and reduce environmental risk factors. While the article doesn’t detail specific daily actions, it stresses that public health initiatives promoting healthy lifestyles are essential for reducing incidence and mortality.
7. Why do some people get cancer but others with similar habits don’t?
Section titled “7. Why do some people get cancer but others with similar habits don’t?”This difference often comes down to the complex interplay of genetic predispositions and environmental factors. Even with similar habits, individuals have unique genetic makeups, including different inherited genetic variations (SNPs) that influence susceptibility. This polygenic nature of cancer risk means some people are genetically more vulnerable, even if their lifestyle seems comparable to someone who doesn’t develop cancer.
8. Could I pass on a higher risk to my kids?
Section titled “8. Could I pass on a higher risk to my kids?”Yes, if you carry certain genetic predispositions, you could potentially pass on a higher inherited risk to your children. Genetic variations that influence susceptibility to digestive system cancers, like those identified for colorectal or pancreatic cancer, can be inherited. Understanding your own genetic profile can help assess this potential risk for future generations.
9. When should I start screening for these cancers?
Section titled “9. When should I start screening for these cancers?”The appropriate age to start screening for digestive system cancers depends on several factors, including your specific cancer risk and family history. For example, advances in screening methods like colonoscopies are vital for improving outcomes in colorectal cancer. Discuss your personal and family history with your doctor, as they can recommend the most suitable screening schedule for you.
10. Does regular exercise help reduce my genetic risk?
Section titled “10. Does regular exercise help reduce my genetic risk?”While regular exercise can’t change your inherited genetic makeup, it absolutely contributes to a healthy lifestyle that helps reduce youroverallrisk. The article emphasizes that public health initiatives promoting healthy lifestyles are crucial for reducing cancer incidence. Exercise helps mitigate environmental factors that interact with your genes, making it a powerful tool in prevention.
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
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