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Cancer, Tumor suppressor, Gene Mutation, Mitosis, Cell, Allele, Oncogene.

The key terms of this Biology chapter include Cancer, Tumor suppressor, Gene Mutation, Mitosis, Cell, Allele, Oncogene, Breast Cancer, Growth Factor, Abdominal Pain, Disease, Gene Expression, Brca1 And Brca2, Diagnosis, Epigenetic, Telomerase, Genes, translocation, apoptosis, cytokine, proto-oncogene


A cancer cell is injected into a healthy mouse. The mouse develops tumors. This experiment indicates that cancer is

A. contact inhibited.
B. transplantable.
C. benign.
D. invasive.
E. malignant.


Loss of tumor suppression in a cell usually results from

A. cytokine activation of a tumor suppressor gene.
B. a translocation of a tumor suppressor gene.
C. an inversion involving a tumor suppressor gene.
D. a deletion of a tumor suppressor gene.
E. activation of a proto-oncogene by a virus.


The term used to describe the fact that cancer cells have lost the specializations of the cells from which they descend is

A. heritable.
B. angiogenic.
C. oncogenic.
D. dedifferentiated.
E. apoptotic.


Growth of new blood vessels in and around tumors is called

A. invasiveness.
B. angiogenesis.
C. metastasis.
D. dedifferentiation.
E. apoptosis.


After mutations begin a cancer, other factors that influence whether the disease proceeds include

A. how old the person is and whether he or she smokes.
B. whether the person has had cancer before, and where in the body it was.
C. location of the cancerous cell in the tissue, and how specialized the cell is.
D. whether or not relatives have cancer.
E. the type of exercise that the person does and whether the diet includes enough fruits and vegetables.


A cancer stem cell can divide to give rise to

A. tumor cells, abnormal daughter cells, normal cells, and more cancer stem cells.
B. more cancer stem cells only.
C. healthy stem cells and normally differentiated cells.
D. nothing. It cannot divide further.
E. invasive cells and metastatic malignant cells.


People were trying to treat cancer as long ago as

A. a million years ago.
B. 5,000 years ago.
C. 1600 B.C.
D. 1900 A.D.
E. since the discovery of the genetic code in the 1960s.


A cancer’s spread is called

A. metastasis.
B. malignancy.
C. carcinogenesis.
D. microstasis.
E. oncogenesis.


Cancer does not typically follow a Mendelian pattern of inheritance because it is usually caused by

A. two gene variants, one dominant and one recessive, and no environmental input.
B. specific combinations of alleles and an environmental factor.
C. specific combinations of an environmental factor and one dominant gene variant.
D. environmental insults and no genes at all.
E. genes that cause death before birth.


In 1971, cancer was thought to be caused by

A. too little exercise.
B. too much chocolate and other sweets.
C. radiation, viruses, and chemical exposures.
D. oncogenes and tumor suppressor gene mutations.
E. a bacterial infection.


All cancers reflect, at the most general level, a defect in

A. DNA replication.
B. the formation of mitochondria.
C. cell membrane structure.
D. the cell’s ability to extract energy from nutrients.
E. the cell cycle.


Genes that normally prevent cell division are

A. tumor suppressors.
B. transcription factors.
C. proto-oncogenes.
D. growth factors.
E. oncogenes.


Loss of tumor suppression in a cell usually results from

A. cytokine activation of a tumor suppressor gene.
B. a translocation of a tumor suppressor gene.
C. an inversion involving a tumor suppressor gene.
D. a deletion of a tumor suppressor gene.
E. activation of a proto-oncogene by a virus.


Matthew has the inherited form of the eye cancer retinoblastoma. His disease is caused by

A. a germinal mutation in one RB allele, and no mutation in the other allele.
B. a somatic mutation in each copy of the RB gene in the same cell.
C. a germinal mutation in one RB allele, then a somatic mutation in the other allele.
D. a somatic mutation in the one of the RB genes in the same area of the retina of one eye.
E. activation of the X-linked oncogene RB.


Tanisha was just diagnosed with an aggressive form of breast cancer called Her-2/neu. The cancer started because

A. she has a deletion in the BRCA1 gene that is found in African-American and Ashkenazi Jewish women.
B. her affected breast cells have many extra receptors for epidermal growth factor, and so they receive too many signals to divide.
C. her affected cells have extra genes for epidermal growth factor, sending signals for the cells to divide too frequently.
D. a translocation occurred between chromosomes 7 and 8, generating and activating a breast-specific oncogene.
E. fusion proteins dot the surfaces of her affected breast cells, which attract carcinogens.


In Wilms’ tumor,

A. heart cells divide as frequently as do cells in the skin.
B. being exposed to cigarette smoke in the uterus causes lung cancer in the infant.
C. cells in a child’s kidney divide as frequently as if they were still in a fetus.
D. deletion of the retinoblastoma gene causes an eye tumor.
E. cancer develops in the breast when cells have too many growth factor receptors.


A gatekeeper gene

A. regulates mitosis and meiosis.
B. regulates its own mutation rate.
C. can destabilize the genome when mutant.
D. releases microRNAs that trigger parts of the cell membrane to open.
E. regulates apoptosis and mitosis.


When tumor cell DNA is examined from people at different stages of the same cancer type, mutations that are common to all of them

A. act early in the disease.B. act late in the disease.
C. acted on an initial cell and then reverted to wild type.
D. entered the cells on the same type of virus.
E. are there by coincidence and do not mean anything about the disease.


The first mutation typically detected in FAP colon cancer is

A. APC.
B. TGF.
C. P53.
D. PRL-3.
E. RB.


Loss of tumor suppression in a cell usually results from

A. cytokine activation of a tumor suppressor gene.
B. a translocation of a tumor suppressor gene.
C. an inversion involving a tumor suppressor gene.
D. a deletion of a tumor suppressor gene.
E. activation of a proto-oncogene by a virus.


Types of genetic information in a cancer “atlas” include

A. the types of foods a person eats and how he or she exercises.
B. lists of where people have lived and what environmental toxins they have been exposed to.
C. the numbers of each type of nitrogenous base in the genome.
D. mutations, gene expression, SNPs, microRNAs, and copy number variants. E. the number of macroRNAs that are activated in a particular tumor type.


A more recently developed cancer treatment is

A. releasing control over apoptosis.
B. stimulating telomerase activity.
C. stimulating cells to return to a stem-like state of specialization.
D. inhibiting angiogenesis.
E. replacing the nuclei in cancer cells.


A breast cancer test for HER2 considers

A. genotype.
B. phenotype.
C. gene expression.
D. mutation rate.
E. receptor diversity.


In addition to activated oncogenes and inactivated tumor suppressor genes, epigenetic changes in gene expression are seen in cancer.

TRUE


Mitosis in a cancer cell can be compared to a runaway train that is racing along without signals and control points.

TRUE


Pancreatic cancer typically begins 10 to 15 years before it causes abdominal pain and by the time diagnosis usually occurs, it has usually to the point where it is lethal within two years.

TRUE