g protein D. Growth factor receptor ng Tool 0 Q ing C. Growth factor-binding protein D. Growth factor receptor E. Transcription activator A child with retinoblastoma is found to have a 13q14 deletion. The Rb gene, which resides at this locus, produces which kind of tumor-associated protein? A. Cell cycle regulator B. Growth factor ㅂ분 요 9 12 W □ @ 2 C Edit in Paint 8 60 8 Focus

g protein D. Growth factor receptor ng Tool 0 Q ing C. Growth factor-binding protein D. Growth factor receptor E. Transcription activator A child with retinoblastoma is found to have a 13q14 deletion. The Rb gene, which resides at this locus, produces which kind of tumor-associated protein? A. Cell cycle regulator B. Growth factor ㅂ분 요 9 12 W □ @ 2 C Edit in Paint 8 60 8 Focus

Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

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4). p53 (sometimes called TP53 for “tumor protein 53") is a human tumor suppressor gene that is mutated in the majority of human cancers (many tumor types). a. For each of the mutations described below (i-iv): is this a mutation you would expect to find when sequencing p53 alleles from tumor cells? Why or why not? i. A missense mutation encoding a hyperactive form of the protein. ii. A deletion of the gene. iii. An insertion in the promoter that increases transcription 10-fold. iv. A nonsense mutation. b. When sequencing the p53 gene in tumor cells, would you expect to find only mutant version(s) of the gene or a mix of mutant and wild type versions? c. For any of the mutations you said you would expect to find in tumor cells, would you expect tumor cells to be homozygous (same mutation on both chromosomes)? Why or why not? d. Individuals with Li-Fraumeni syndrome have a very high risk of tumors originating in various tissues due to inheritance of a loss-of-function mutant allele of…
Can you please answer 10, and 11
1. One of the following sentences is NOT correct A. P53 is an example of tumour suppressor gene B. Wright's stain is sued to visualize a peripheral blood smear C. leukotrienes are derived from arachidonic acid by cyclooxygenase D. effective bacteriocidal enzymes are contained in lysosome of the neutrophils E. H&E stain is the most commonly used tissue stain for routine histological examination F. proteoglycans are located in the ECM but not in the ground substance of connective tissue 2. Which of the following sentences is NOI correct? A Microvilli increase the surface area of the epithelial cells B. Desmosomes are an effective barrier to the diffusion of substances across an epithelium C. Epithelial tissues are classified by the shape of the epithelial cells in the basal layer D. Release of lipid droplets from cells is a type of merocrine secretion E. Epithelial tissues are classified by the number of cell layers F. None of the above G. Both A and E H B. C and D 3. Which of the…
F. Written Response 1. If gene transcription is inhibited after fertilization, development past the two-cell stage does not take place in the mouse. However, in frog embryos, this treatment does not disrupt development until late cleavage. Explain this difference. 2. Twist transcription factors (TF) play key roles in embryonic development and are largely undetectable in normal adult tissues; however, their expression is reactivated during tumor progression and correlates with invasive and metastatic lesions. Transcription of the Twist gene is activated by Wnt signals and the Twist TF represses the gene for E-cadherin. Answer the following questions as briefly as possible, based on what was presented in class, not an internet search (complex answers that go beyond class material may lose points) a. Outline the steps from the Wnt signal to the E-cadherin gene (inclusive); e.g., A → B → C (with some clarifications such as "binds to", "activates", "represses") b. What are the normal…
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Please answer question 8
I’m having trouble with this fill in the blank. Could you please let me know if I need to change any of my answers.
A mutation in the Ras protein could directly affect improper _____ Select one: a. cell signaling leading to alterations in cell division b. cell signaling leading to alterations proteasome activity c. microtubule assembly leading to faulty cell division d. protein degradation during the cell cycle e. protein phosphorylation in the cell cycle
Can you match the type of mutations that can occur from the selected below? a. either proto-oncogene or tumor suppressor gene b. proto-oncogene c. tumor suppressor gen 1. Frameshift mutation 2. Missense mutation 3. Nonsense mutation
19: What are 3 phenotypes of GA, or BR, or ABA, or CK over-producing mutants. 20: Think about a hormone receptor, specifically the structure of the receptor. Describe ONE why a mutation would cause insensitivity to the hormone, AND ONE way it could cause hypersensitivity to the hormone. Explain your answer to each. 22: Not all cells in tissues are the same. They differentiate from stem cells. Describe how ONE cell type acquires cell identity. (Pick any cell in the plant)
Hi, can you elaborate about the relationships between Non-small-cell lung carcinoma and mutations in p53 and RAS protein?
Lung cancer mitotic index: 0.25 Breast cancer mitotic index: 0.35 Skin cancer mitotic index: 0.4 Looking at the mitotic index for all 3 cancer types, which one is likely to be the most resistant (least affected) to the growth-inhibiting effects of traditional chemotherapy drugs that target rapidly dividing cells?