The drug tamoxifen has been used to treat some types of breast cancer. Suppose even among female patients with the same tumor grade there is variation in responsiveness to tamoxifen. It is also found that this variation is at least partly genetic; his variation is at least partly genetic; women with a relative who had a low responsiveness to the drug are at higher risk of low responsiveness to the drug The target of tamoxifen is a protein called the estrogen receptor. A. Outline how a “candidate gene approach” could be conducted to investigate whether variation in the gene for estrogen receptor affects tamoxifen responsiveness

Another blood disease, hemophilia, is caused by the failure of blood to clot.  The genetic basis for the disease is due to one of two dysfunctional clotting factor genes, recessive alleles that lead to the disorders hemophilia A and hemophilia B. Due to the long history of arranged European royal marriages within a relatively small sample population, the prevalence of both hemophilia and G6PD-deficiency disorder are both high. In fact, in certain family lines sons, but not daughters, are nearly always either born with both G6PD-deficiency and hemophilia A-disease or are born completely healthy. In other family lines sons, but not daughters, are born about a quarter of the time with both G6PD-deficiency and hemophilia B. (G = G6PD gene, A = Hemophilia A, and B = Hemophilia B, X = X chromosome, Y = Y chromosome) Which of the following arrangement of loci on chromosomes best explains these observations?  A B C D or E

There is a protein called neurogenin that stimulates neuronal cells to differentiate. In order to determine what kind of receptor neurogenin binds to, you add a general phosphatase (one that can remove phosphates from any substrate) to neural cells when you add neurogenin, and you discover that this inhibits differentiation. Furthermore, in the presence of this phosphatase, you find that not even a G protein is activated in response to neurogenin. 1.  With this information, what kind of receptor does neurogenin bind to? 2.  In a normal cell, how does the G protein in this pathway get activated? 3.  In a normal cell, why does the response to neurogenin cease over time?

Please answer question 8

If a genetic female fetus is exposed to testosterone in the uterus, would this fetus (baby) will develop a complete male phenotypic sex, partial male phenotypic sex, or a normal female phenotypic sex? Explain your answer, describing the sex phenotype of the gonads, internal genital ducts and external genitalia. What would the developmental outcome be if the fetus were instead exposed to dihydrotestosterone in the uterus?

In Metastatic Breast Cancer [such as in Breast Invasive Ductal Carcinoma; Breast Invasive Carcinoma, NOS; Breast Invasive Cancer, NOS; Invasive Breast Carcinoma; Breast Invasive Lobular Carcinoma; Breast Mixed Ductal and Lobular Carcinoma] what role does the genes Tp53 and Tp63 have?  Would one of them affect the other (i.e. mutation, etc) or there is not relationship among the two genes at all.