For some time I have been searching for a book similar to , which a number of review suggested was just as good. Because it was on the shelves of my local library, I picked it up immediately. Jeff Wheelwright's book examines the population genetics of a particular BRCA1 mutation. The BRCA1 and BRCA2 (breast cancer 1 and 2) genes were first linked to heritable breast and ovarian cancer (HBOC) in the early nineties. Since the initial discovery of the genes, scientists have identified many mutations in BRCA1 and 2 that are linked with HBOC as well as other cancers. Rebecca Skloot's book about Henrie tta Lack s . After some searching on Amazon, I found The Wandering Gene and the Indian Princess: Race, Religion, and DNA which a number of review suggested was just as good. Because it was on the shelves of my local library, I picked it up immediately. Jeff Wheelwright's book examines the population genetics of a particular BRCA1 mutation. The BRCA1 and BRCA2 (breast cancer 1 and 2) genes were first linked to heritable breast and ovarian cancer (HBOC) in the early nineties. Since the initial discovery of the genes, scientists have identified many mutations in BRCA1 and 2 that are linked with HBOC as well as other cancers.





When functioning properly, the BRCA tumor suppressor genes produce proteins (breast cancer type 1/2 susceptibility protein) that are primarily involved in DNA repair. These proteins ensure that cells with errors in their DNA sequence either fix the mistakes or are destroyed. When a BRCA mutation is present, there is still a wild type ("normal") copy of the BRCA gene on the matching chromosome. Thus, the presence of a BRCA mutation is not necessarily an assurance of getting cancer (cancer risk rates for BRCA mutation carriers range from 35-80%, depending on the stud y and the type of cancer). If something occur s to alter the function of th e wild typ e copy of the gene, then the cell is left with no functional BRCA1 or 2. Thus, DNA errors become more prevalent, which makes it more likely that a healthy cell will become a cancer cell. BRCA mutations account for only 10% of breast cancer s ; the majority of cancers are sporadic , caus ed by random rather than inherited mutations.





The Wandering Gene focuses on the BRCA1 185delAG mutation; this mutation is due to the deletion (del) of two DNA residues (A and G, or adenine and guanine) at position 185, which results in a **. This particular BRCA1 mutation has been linked to Ashkenazi or Eastern European Jews. Here, the author meets the Medinas, an Hispano family from New Mexico, as they receive genetic counseling and testing for the 185delAG mutation. The family is descendants of Native Americans and Spanish Catholics; thus, they were surprised to learn that they carry a mutation that has been linked to Ashkenazim. Geneticists and historians think that the focuses on the BRCA1 185delAG mutation; this mutation is due to the deletion (del) of two DNA residues (A and G, orand guanine) at position 185, which results in a frame shift (or misreading) in the DNA sequence and ultimately the sequence of the protein that the DNA encodes**. This particular BRCA1 mutation has been linked to Ashkenazi or Eastern European Jews. Here, the author meets the Medinas, an Hispano family from New Mexico,they receive genetic counseling and testing for the 185delAG mutation. The family is descendants of Native Americans and Spanish Catholics; thus, they were surprised to learn that they carry a mutation that has been linked to Ashkenazim. Geneticists and historians think that the 185delAG mutation in this group likely arose from a population of Jews from Spain, who were persecuted during the inquisition, converted to Catholicism, and then established themselves in the Americas.





arose and how it became fixed in one particular population. There is evidence that a 2500-year-old Jewish ics of Jewish history (the cultural isolation and the large losses of population, such as from pogroms, forced relocation, and mass murders) led to frequent Jews are not more sus ceptible to genetic mutations; it is simply t hat, for a variety of re asons, they have been studied more th oroughly than other population groups. The most interesting element of the book examines where the 185delAG mutationand how it became fixed in one particular population. There is evidence that a 2500-year-old Jewish founder could be the source of the mutation. Two particular characteristof Jewish history (the cultural isolation and the large losses of population, such as from pogroms, forced relocation, and mass murders) led to frequent genetic bottlenecks . Bottlenecks occur due to the loss of genetic variability in a population; dramatic losses of population size can cause deleterious mutations (such as the BRCA1 mutation) to become fixed in a group. The founder effect can also explain the presence of other heritable diseases that are linked to the Jewish population, such as Tay-Sachs disease (carried by one in 25 Ashkenazim) and more than forty other genetic disorders . It is important to note here that

There are other examples of founder effects in small, isolated populations, including the Amish and fundamentalist Mormons.





d isease as early as the 1980s. A group called x Jew s for the most common genetic disorders and informs couples looking to wed whether or not they are a good genetic match. This approach has decreased the incidence of Tay-Sachs disease. The blood samples from Dor Yeshorim were useful for determin ing the prevalence of the 185delAG mutation in the Jewish population (1%). A recent story in the The book also discusses the rise in genetic screening in certain populations where BRCA mutations are more common. Interestingly, such large-scale screening programs began in an effort to control Tay-Sachsisease as early as the 1980s. Agroup called Dor Yeshorim screens Orthodofor the most common genetic disorders andcouples looking to wed whether or not they are a good genetic match. This approach has decreased the incidence of Tay-Sachs disease. The blood samples from Dor Yeshorim were useful for determinthe prevalence of the 185delAG mutation in the Jewish population (1%). A recent story in the New York Times highlights the efforts in Israel, where one in 40 women carry a mutation in BRCA (compared to one in 100 women in the population as a whole), to begin universal screening for the mutations. The June 2013 BRCA1 and 2, which led to high costs ( more t Supreme Court decision, which ruled that naturally occurring human genes and mutations cannot be patented, should decrease the cost of the test in the United States. Prior to that decision, Myriad Genetics held patents on

han $3000) for the test.





The subtitle of the book is definitely a good representation of what is inside; each of these topics seemed to get equal treatment. When the focus was on the DNA or race, the book held my interest. However, when the focus was more on religion, I found myself skipping pages. I didn't see how the history and beliefs of the Jehovah's witnesses helped the reader understan d the genetics of this mutation. There were some surface similarities with Rebecca Skloot's book, as both hav e a ve ry strong human angle . T he book was a quick read, it taught me some new things about population genetics and BRCA mutations, and it served as an excellent jumping - off point for me to learn more.







