Retinoblastoma can be seen as a familial cancer, inherited in an autosomal recessive manner (RB-/RB-), individuals heterozygous for the RB+ and RB- alleles can develop tumor as a result of…A mitotic crossover that leads to homozygosity for RB+ in some cells and RB- in other cellsA meiotic mutation in the RB+ allele that leads to homozygosity for RB+A somatic mutation in the RB- allele that leads to homozygosity for RB+The fact that RB- is dominant to RB+

Name: Retinoblastoma can be seen as a familial cancer, inherited in an autos
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Description: Retinoblastoma can be seen as a familial cancer, inherited in an autosomal recessive manner (RB-/RB-), individuals heterozygous for the RB+ and RB- alleles can develop tumor as a result of…A mitotic crossover that leads to homozygosity for RB+ in som

The Rb gene is an archetypal tumor suppressor gene. Mutations in this gene result into…

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Biology

Retinoblastoma can be seen as a familial cancer, inherited in an autosomal recessive manner (RB-/RB-), individuals heterozygous for the RB+ and RB- alleles can develop tumor as a result of… A mitotic crossover that leads to homozygosity for RB

Retinoblastoma can be seen as a familial cancer, inherited in an autosomal recessive manner (RB-/RB-), individuals heterozygous for the RB+ and RB- alleles can develop tumor as a result of… A mitotic crossover that leads to homozygosity for RB

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter12: Genes And Cancer

Section: Chapter Questions

Problem 12QP

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A couple was referred for genetic counseling because they wanted to know the chances of having a child with dwarfism. Both the man and the woman had achondroplasia (MIM 100800), the most common form of short-limbed dwarfism. The couple knew that this condition is inherited as an autosomal dominant trait, but they were unsure what kind of physical manifestations a child would have if it inherited both mutant alleles. They were each heterozygous for the FGFR3 (MIM 134934) allele that causes achondroplasia. Normally, the protein encoded by this gene interacts with growth factors outside the cell and receives signals that control growth and development. In achrodroplasia, a mutation alters the activity of the receptor, resulting in a characteristic form of dwarfism. Because both the normal and mutant forms of the FGFR3 protein act before birth, no treatment for achrondroplasia is available. The parents each carry one normal allele and one mutant allele of FGRF3, and they wanted information on their chances of having a homozygous child. The counsellor briefly reviewed the phenotypic features of individuals with achondroplasia. These include facial features (large head with prominent forehead; small, flat nasal bridge; and prominent jaw), very short stature, and shortening of the arms and legs. Physical examination and skeletal X-ray films are used to diagnose this condition. Final adult height is approximately 4 feet. Because achondroplasia is an autosomal dominant condition, a heterozygote has a 1-in-2, or 50%, chance of passing this trait to his or her offspring. However, about 75% of those with achondroplasia have parents of average size who do not carry the mutant allele. In these cases, achondroplasia is due to a new mutation. In the couple being counseled, each individual is heterozygous, and they are at risk for having a homozygous child with two copies of the mutated gene. Infants with homozygous achondroplasia are either stillborn or die shortly after birth. The counselor recommended prenatal diagnosis via ultrasounds at various stages of development. In addition, a DNA test is available to detect the homozygous condition prenatally. What is the chance that this couple will have a child with two copies of the dominant mutant gene? What is the chance that the child will have normal height?
A couple was referred for genetic counseling because they wanted to know the chances of having a child with dwarfism. Both the man and the woman had achondroplasia (MIM 100800), the most common form of short-limbed dwarfism. The couple knew that this condition is inherited as an autosomal dominant trait, but they were unsure what kind of physical manifestations a child would have if it inherited both mutant alleles. They were each heterozygous for the FGFR3 (MIM 134934) allele that causes achondroplasia. Normally, the protein encoded by this gene interacts with growth factors outside the cell and receives signals that control growth and development. In achrodroplasia, a mutation alters the activity of the receptor, resulting in a characteristic form of dwarfism. Because both the normal and mutant forms of the FGFR3 protein act before birth, no treatment for achrondroplasia is available. The parents each carry one normal allele and one mutant allele of FGRF3, and they wanted information on their chances of having a homozygous child. The counsellor briefly reviewed the phenotypic features of individuals with achondroplasia. These include facial features (large head with prominent forehead; small, flat nasal bridge; and prominent jaw), very short stature, and shortening of the arms and legs. Physical examination and skeletal X-ray films are used to diagnose this condition. Final adult height is approximately 4 feet. Because achondroplasia is an autosomal dominant condition, a heterozygote has a 1-in-2, or 50%, chance of passing this trait to his or her offspring. However, about 75% of those with achondroplasia have parents of average size who do not carry the mutant allele. In these cases, achondroplasia is due to a new mutation. In the couple being counseled, each individual is heterozygous, and they are at risk for having a homozygous child with two copies of the mutated gene. Infants with homozygous achondroplasia are either stillborn or die shortly after birth. The counselor recommended prenatal diagnosis via ultrasounds at various stages of development. In addition, a DNA test is available to detect the homozygous condition prenatally. Should the parents be concerned about the heterozygous condition as well as the homozygous mutant condition?
A couple was referred for genetic counseling because they wanted to know the chances of having a child with dwarfism. Both the man and the woman had achondroplasia (MIM 100800), the most common form of short-limbed dwarfism. The couple knew that this condition is inherited as an autosomal dominant trait, but they were unsure what kind of physical manifestations a child would have if it inherited both mutant alleles. They were each heterozygous for the FGFR3 (MIM 134934) allele that causes achondroplasia. Normally, the protein encoded by this gene interacts with growth factors outside the cell and receives signals that control growth and development. In achrodroplasia, a mutation alters the activity of the receptor, resulting in a characteristic form of dwarfism. Because both the normal and mutant forms of the FGFR3 protein act before birth, no treatment for achrondroplasia is available. The parents each carry one normal allele and one mutant allele of FGRF3, and they wanted information on their chances of having a homozygous child. The counsellor briefly reviewed the phenotypic features of individuals with achondroplasia. These include facial features (large head with prominent forehead; small, flat nasal bridge; and prominent jaw), very short stature, and shortening of the arms and legs. Physical examination and skeletal X-ray films are used to diagnose this condition. Final adult height is approximately 4 feet. Because achondroplasia is an autosomal dominant condition, a heterozygote has a 1-in-2, or 50%, chance of passing this trait to his or her offspring. However, about 75% of those with achondroplasia have parents of average size who do not carry the mutant allele. In these cases, achondroplasia is due to a new mutation. In the couple being counseled, each individual is heterozygous, and they are at risk for having a homozygous child with two copies of the mutated gene. Infants with homozygous achondroplasia are either stillborn or die shortly after birth. The counselor recommended prenatal diagnosis via ultrasounds at various stages of development. In addition, a DNA test is available to detect the homozygous condition prenatally. What if the couple wanted prenatal testing so that a normal fetus could be aborted?
The Xg cell-surface antigen is coded for by a gene located on the X chromosome. No equivalent gene exists on the Y chromosome. Two codominant alleles of this gene have been identified: Xg1 and Xg2. A woman of genotype Xg2/Xg2 bears children with a man of genotype Xg1/Y, and they produce a son with Klinefelter syndrome of genotype Xg1/Xg2Y. Using proper genetic terminology, briefly explain how this individual was generated. In which parent and in which meiotic division did the mistake occur?
Hemophilia A is caused by a recessive X-linked allele that encodes a defective form of a clotting protein. If a affected father and a mother who is known to not be a carrier have children, what percentage of female offspring will have hemophilia?
How can the retinoblastoma trait be inherited in a dominant fashion if the deletion of the RB gene is recessive to the wild-type RB+ allele?
Nondisjunction which can affect sex chromosomes as well as autosomal chromosomes as a common cause of genetic disorders. Use the space provided to illustrate the process of nondisjunction with the end result being that one cell exhibits in the monopsony me while other one exhibits trisomy. Hint: a sperm will fertilize the egg and add it’s chromosome in the last step)
Assuming no other abnormalities, classify each of the following human sex chromosome complements as to whether or not individuals with that complement will be morphologically male or female. Three human sex chromosome complements will be classified as male and three will be classified as female. XXY XYY XXX XO XY XX
Draw and label the mitotic phases (prophase, metaphase, anaphase & telophase) and meiotic phases (prophase I, metaphase I, anaphase I, telophase I, prophase II, metaphase II, anaphase II, & telophase II) for 2N=6. Be sure to indicate the chromosomal complement at each stage and whether the chromosomes are duplicated (consisting of sister chromatids) or not. For the meiotic phases, please add the following labels to your diagrams: In prophase I: tetradIn metaphase I: nonsister chromatidsIn anaphase I: homologous chromosomes, kinetochore microtubule In telophase I: sister chromatidsIn prophase II: centriolesIn metaphase II: centromereIn anaphase II: nonkinetochore microtubule, astral raysIn telophase II: cleavage furrow
Pancreatic cancer is clearly inherited as an autosomal dominant trait in the family illustrated in Figure 23.1. Yet most cases of pancreatic cancer are sporadic, appearing as isolated cases in families with no obvious inheritance. How can a trait be strongly inherited in one family and not inherited in another?
Is the following true or false AND EXPLAIN: Cells with one functional copy of a proto-oncogene will usually proliferate faster than normal cells.
An individual is heterozygous for a reciprocal translocation, with the following chromosomes: A • B C D E F A • B C V W X R ST • U D E F R ST • U V W X Q. Explain why the fertility of this individual is likely to be less than the fertility of an individual without a translocation.