Prostate Cancer In Family

Anderson Quillan Syndrome (AMS) is a rare disease with a prevalence rate of 300/100,000 as determined by a recent ecological study. There is speculation that AMS is a consequence of certain exposures, namely increased tea or chocolate consumption and smoking. There is a possible genetic link, but not all AMS patients exhibit this genetic risk. A case-control study (CCS) is proposed in which AMS cases are compared to two control groups. Control group C1 are living genetically related family members of AMS patients and control group C2 is a more diverse cohort of non-AMS subjects without known family history of AMS. The primary goal is to determine whether there is an association between the named exposures and AMS. The secondary goal is to determine whether the presence of a known family history of AMS is a confounder.

Women who are at the greatest risk are over the age over the age of fifty years of age. Patients with a family history of cancer, especially in their first degree relatives, may have inherited mutations of BRCA1 and/or BRCA2. BRCA1 and BRCA2 are genetic mutations that put patients are risk for cancer. Patients that have a history of breast cancer are five times more likely of developing cancer in the opposite breast. Patients with dense breast are at risk for developing breast cancer due to the fact dense breast contains more glandular and connective tissue. Patients who are exposed to high doses of ionizing radiation to the thorax, early menarche, tobacco use, nulliparity, late menopause, and first child birth after thirty years of age put the patient at risk for breast cancer (Ignatavicius, 2013, p.

Hereditary breast and ovarian cancer is mostly due to a mutation in the Breast cancer susceptibility gene 1(BRCA1) and breast cancer susceptibility gene 2 (BRCA 2) genes and is the most common cause of both forms of breast and ovarian cancers due to hereditary (Weitzel, Blazer, MacDonald, Culver, & Offit, 2011). Although the overall prevalence of the BRCA 1/2 genes is estimated 1 in 400 to 1 in 800 with a higher occurrence in the Ashkenazi Jewish population which is 1 in 40 that have the BRCA genes. According to Weitzel, Blazer, MacDonald, Culver, & Offit (2011), the likelihood of having the BRCA1 or BRCA2 mutation is dependent on one’s personal and/or family history of cancer and can be assessed by using several mutation probability models. After a BRCA1 or BRCA2 gene has been identified in the family, testing of all of at-risk relatives can identify those family members who may also have the BRCA gene and therefore will need to have an increased in following and early intervention when a cancer is diagnosed. There are several options that a person who has been diagnosed with having

In trying to understand the differentials based on genetic factors, studies of the polymorphism Cyp3A4, which is important in androgen metabolism in prostate cancer, would have suggested that the presence of this polymorphism is a factor; however, the reality is that there wasn’t correlation with disease outcomes. In reality, the preponderance of all data suggests that there are no differences in outcomes based on race.

But when I inquired about the genetics of cancer, I learned something astonishing. “... Most cancer is NOT inherited. Only about 5-10% of cancer is related to a mutation in a single gene that is being passed on through the family causing significantly increased risks for certain types of cancer” (Schenck). To me, this was a shocking revelation.

The propensity for specific disease processes are found when analyzing a client’s family tree history. Typically, completing a genogram with at least three generations can show which disease processes show a pattern in a specific family tree. As figure 1 shows, the current generation has a predisposition for cardiovascular disease, diabetes, and cancer. The history complied spans four generations, with three generations on the paternal side, father, grandfather, grandmother, and great-grandfather, contracting heart disease, either suffering from a heart attack, having high blood pressure, or high cholesterol. On the maternal side, there is little information past the second generation. However,

The purpose of this paper is to complete a Genetic and Genomic Nursing Assessment to analyze family genetic health risks. Genomics is the study of genes in the human genome and their interactions with each other and the environment and genetics is the study of individual genes and their effect on clinical disorders (Kaakinen, Coehlo, Steele, Tabacco, & Hanson, 2015). Nurses should be able to perform an assessment of a family 's genetic health risks by using a three-generation family pedigree to obtain information regarding possible genetic inheritance pattern and recurrence risks. The family chosen for this paper has a history of chromosome balanced and unbalanced translocation. A balanced translocation is a chromosomal abnormality that if unbalanced (too much or too little genetic material) can lead to infertility, multiple miscarriages, or a child with congenital abnormalities, developmental issues, etc. A balanced translocation does not have a straightforward inheritance pattern. It depends on the chromosomes involved, if the carrier is a male versus female and how much genetic material is involved in the translocation itself.

While there are several biological factors that have the ability to lead to cancer, genetics is the most currently researched. A study done by Bharaj, Scorilas, Giai and

For example, age is the biggest factor. We all know that as men age and get older they run a higher chance of their prostate enlarging and developing cancer. Family history and race are also the other two big ones. If people in your immediate family have had the cancer, then you run a higher risk of contraction because you’re already genetically predisposed to getting prostate cancer. Also, African American men are more likely to be diagnosed with the cancer, with white and Hispanic men following behind. According to the CDC, from the years 1999-2013, black men had higher mortality and contraction rates than men of other races and ethnicities.1 Hormones are also a risk factor; should the male be producing a lot of testosterone could put him at risk.

Lynch syndrome, previously known as hereditary nonpolyposis colorectal cancer (HNPCC) is a parental inherited condition that exposes a person to the risks of cancers, but most commonly colon cancer1-9. It is a heterozygous autosomal dominant genetic condition, which means that if only one parent carries the gene for Lynch syndrome (LS), then a 50 percent chance of passing on the mutation will be passed to each child1-9. LS is limited to families with a known pathogenic germline mutation2. A germline mutation is when mutations occur in the germ line, which is a group of cells that contribute to the improvement of gametes2,3,10. To find out how individuals are to contract this disease, the family medical history must be taken into account. Early

Meanwhile, in addition to the male's occupation, radiation exposure and age can lead to breast cancer developments ( National Cancer Institute, 2007). When these risk factors are revealed in a diagnoses of breast cancer, men have more advanced cancerous growths than women (Giordano, 2004). So men may think, how do I get breast cancer? Is it inherited?

Heredity also plays a role in the development of cancer. If a person’s relatives have a history of cancer, then that person has a higher risk of developing cancer. Genetic variations, particularly those influencing how the body responds to carcinogens, may create a greater vulnerability to cancer.

Aim: To calculate meta-analytic estimates of heritability in liability and shared an individual – specific environmental effects from the pooled twin data.

Researchers have associated mutations in specific genes with more than 50 hereditary cancer syndromes, which are disorders that may predispose individuals to developing certain cancers. Genetic tests can tell whether a person

Impact Statement: The potential impact of our research study on the reduction or elimination of the disproportionate effects of prostate cancer in AA population is on several grounds. Using our innovative molecular screening approaches it is for the first time we are evaluating the prevalence of prostate cancer specific molecular markers using the whole-mount prostate tissue of AA population on a large cohort of 500 AA men with prostate cancer. So far, no study has included such a large number of cases to interrogate the prevalence of known molecular markers, particularly using whole-mount tissue. Given the unique tumor resources available at the Henry Ford Health system we will be able to accomplish the proposed goal within the stipulated time. Conventional approaches using dominant/index nodule and decisions made on single marker screening may not provide the actual incidence of the molecular markers and attempts to make clinical correlations often fail to establish meaningful associations. In our study we will be evaluating all tumor foci, including atypical foci, high grade prostatic intraepithelial neoplasia (HGPIN), HGPIN mimics, and variant morphological forms irrespective of size and Gleason grade on whole-mount tissue to estimate the overall prevalence of molecular markers in AA prostate cancer compared with EA prostate cancer. Our approach preserves the spatial architecture and distribution of each tumor foci, which will provide meaningful observations on clonal