• Wrong document? Swap it for free
  • Written by students who passed
  • Immediately available after payment
  • Read online or as PDF
Sell
Where do you study
Your language
Document preview thumbnail
Preview 3 out of 23 pages
Exam (elaborations)

Cancer Genetics Exam Questions with Verified Answers Latest Update (Rated A+)

Document preview thumbnail
Preview 3 out of 23 pages

Cancer Genetics Exam Questions with Verified Answers Latest Update (Rated A+) What is Cancer? - Answers Tumorigenesis Metastasis Carcinogenesis Tumorigenesis - Answers Loss of control of cell division Induce genes that promote cell division Repress genes that inhibit cell division Deregulation of apoptosis Angiogenesis Metastasis - Answers Nodal involvement Organ involvement Carcinogenesis - Answers the production, development, or origin of cancer Environmental carcinogens - Answers Mutate somatic cell DNA Interrupt normal cell cycle Tumor formation Inherited Cancer: The Two-Hit Model - Answers Retinoblastoma Inherited: Affected parent Affected offspring 50% Bilateral Non-inherited: no familial pattern Unilateral Two-Hit Model: Inherited form already has one copy of abnormal gene Non-inherited form has acquired two mutations in somatic cells Tumor Suppressor Genes - Answers Normally block uncontrolled cellular proliferation Therefore, suppress tumor formation Usually involved in regulating cell cycle Recessive at the cellular level Require two copies of mutant allele to form tumor Somatic (non-tumor) cells will still be heterozygous Proto-oncogenes - Answers Produce 4 basic regulators of cell growth Growth factors Growth factor receptors Signal transduction molecules Nuclear transcription factors Mutation in proto-oncogene Oncogene Unregulated cell growth and differentiation Dominant at the cellular level -gain-of-function mutation Very rarely present in the germline Senescence - Answers Telomeres at ends of chromosomes shorten with each cell division After 50 -70 cell mitotic events, telomeres depleted --senescence--apoptosis Tumor cells activate gene for telomerase Adds telomeres to newly divided cells Allows for continued cell division Rarely found in normal cells Telomerase present in up to 90% of tumor cells TP53 - Answers -Mutations in TP53occur in half of all human tumor types (50 types isolated so far) -TP53codes for p53 -1st function of p53: Halt cell cycle for DNA repair to occur prior to S phase 2ndFunction of p53: - Answers -Induce apoptosis if DNA damage is beyond repair -If problems with normal function of pRbpathway of repair, then apoptosis induced by p53 If problems with TP53(i.e. mutation): - Answers -Can not repair damage prior to replication -Can not induce apoptosis of cells with DNA damag TP53 and Clinical Prognosis - Answers Tumor tissue analysis to determine prognosis TP53mutations carry particularly poor prognosis Associated with aggressive form of cancer Therapeutic potential Insertion of "normal" TP53into tumors with TP53mutation Induces apoptosis in transfectedcells Results in tumor regression Fraught with typical problems of gene therapy TP53and Li FraumeniSyndrome (LFS) - Answers Autosomal dominant (at the organismallevel) Early onset ½ develop invasive cancer by age 30 90% have primary tumor by age 70 Often multiple primary tumors Breast, Colon, Soft tissue sarcoma, Osteosarcoma, Brain tumors, Leukemia, Adrenocorticalcarcinoma 75% have mutations in p53 (two-hit model) Remainder have mutation in CHEK2which activates p53 TP53 and Toxins - Answers AflatoxinB1 Present in Aspergillussp.

Content preview

Cancer Genetics Exam Questions with Verified Answers Latest Update 2024-2025 (Rated A+)



What is Cancer? - Answers Tumorigenesis


Metastasis


Carcinogenesis

Tumorigenesis - Answers Loss of control of cell division


Induce genes that promote cell division


Repress genes that inhibit cell division


Deregulation of apoptosis


Angiogenesis

Metastasis - Answers Nodal involvement


Organ involvement

Carcinogenesis - Answers the production, development, or origin of cancer

Environmental carcinogens - Answers Mutate somatic cell DNA


Interrupt normal cell cycle


Tumor formation

Inherited Cancer: The Two-Hit Model - Answers Retinoblastoma


Inherited: Affected parent Affected offspring 50%

,Bilateral


Non-inherited: no familial pattern


Unilateral


Two-Hit Model:


Inherited form already has one copy of abnormal gene


Non-inherited form has acquired two mutations in somatic cells

Tumor Suppressor Genes - Answers Normally block uncontrolled cellular proliferation


Therefore, suppress tumor formation


Usually involved in regulating cell cycle


Recessive at the cellular level


Require two copies of mutant allele to form tumor


Somatic (non-tumor) cells will still be heterozygous

Proto-oncogenes - Answers Produce 4 basic regulators of cell growth


Growth factors


Growth factor receptors


Signal transduction molecules

, Nuclear transcription factors


Mutation in proto-oncogene Oncogene


Unregulated cell growth and differentiation


Dominant at the cellular level -gain-of-function mutation


Very rarely present in the germline

Senescence - Answers Telomeres at ends of chromosomes shorten with each cell division


After 50 -70 cell mitotic events, telomeres depleted -->senescence-->apoptosis


Tumor cells activate gene for telomerase


Adds telomeres to newly divided cells


Allows for continued cell division


Rarely found in normal cells


Telomerase present in up to 90% of tumor cells

TP53 - Answers -Mutations in TP53occur in > half of all human tumor types (>50 types isolated so far)


-TP53codes for p53


-1st function of p53: Halt cell cycle for DNA repair to occur prior to S phase

2ndFunction of p53: - Answers -Induce apoptosis if DNA damage is beyond repair


-If problems with normal function of pRbpathway of repair, then apoptosis induced by p53

Document information

Uploaded on
December 9, 2024
Number of pages
23
Written in
2024/2025
Type
Exam (elaborations)
Contains
Questions & answers
$8.79

Wrong document? Swap it for free Within 14 days of purchase and before downloading, you can choose a different document. You can simply spend the amount again.
Written by students who passed
Immediately available after payment
Read online or as PDF

Seller avatar
Reputation scores are based on the amount of documents a seller has sold for a fee and the reviews they have received for those documents. There are three levels: Bronze, Silver and Gold. The better the reputation, the more your can rely on the quality of the sellers work.
TutorJosh
3.5
(76)
Sold
497
Followers
16
Items
32941
Last sold
1 day ago




Why students choose Stuvia

Created by fellow students, verified by reviews

Quality you can trust: written by students who passed their tests and reviewed by others who've used these notes.

Didn't get what you expected? Choose another document

No worries! You can instantly pick a different document that better fits what you're looking for.

Pay as you like, start learning right away

No subscription, no commitments. Pay the way you're used to via credit card and download your PDF document instantly.

Student with book image

“Bought, downloaded, and aced it. It really can be that simple.”

Alisha Student

Working on your references?

Create accurate citations in APA, MLA and Harvard with our free citation generator.

Working on your references?

Frequently asked questions