Cancer Flashcards
Repeated sequences not used to make cell proteins
Telomeres -as cells divide, more and more telomeres are lost -there is an association between telomere loss and cell death
How do cancer cells affect telomeres
They replace telomeres by activating telomerase, thus can divide indefinitely or are “immortalized”
Changes in both oncogenes and tumor suppressor genes are typically required for FAP to develop. T/F
True
Cells that can no longer divide are ______
terminally differentiated
An example of how multiple genetic changes are often required for cancer to arrise
Familial Adenomatous Polyposis (FAP)
Cancer is genetic, but not necessarily inherited. T/F
True. Cancer always involves mutations, we don’t always get those mutations from our parents, usually from being exposed to an environment.
Examples of chromosomal changes
- aneuploid- loss of diploid state
- translocations and other rearrangements
- chromosomal instability
Characteristics of benign neoplasms ‘tumors’
Well differentiated and are localized
3 phases of tumor growth
- Initiation
- DNA mutation, irreversible
- must occur first
- Promotion
- Stimulates cell proliferation
- reversible in early stages
- must follow initation for tumors to form
- Progression
- malignant phenotype
- invasiveness, metastasis
- autonomous growth
- genomic instability
A well localized tumor with no evidence of metastasis would most likely be treated with?
Surgery
Which of the following indications are related to blood loss in our patient? -Dark stools -Low hemoglobin levels -Fatigue -All of the above
All of the above are related to blood loss.
mutations in ____ are assosociated with many types of cancer
p53
if DNA is not repaired, new mutations will be passed on to cell progeny, and if these mutations alter growth signals, cancer may result
mutations in p53 are associated with many types of cancer
Diagnosising and staging of tumor growth
- TNM
- Tumor
- Nodes
- Metastasis
A type of cancer due to mutations in DNA repair genes
HNPCC- Hereditary nonpolyposis colon cancer
- This decrease in DNA repair leads to an increase in genome instability
- Damaged DNA repair gene cannot correct the errors within newly replicated DNA
- ‘mutator phenotype’ increases the likelihood that an individual will develop cancer
A cell protein that has a number of anti-cancer functions centered around DNA repair
p53
- activation of DNA repair proteins
- arrest of the cell cycle to allow DNA repair proteins time to fix mutations
- initiation of apoptosis if DNA damage cannot be reversed
The ability of a cell to divide and requires growth signals including growth factors that stimulate the cell to divide by mitotic division
Proliferation
Normally restrain cell growth, if mutated may form proteins that do not work (loss of function)
Tumor Suppressor Genes examples: -transcription factors (pRB and p53) -Cell adhesion proteins (APC and DCC)
mutate BOTH copies
Mutations in both alleles of _____, which normally prevent tumors, are required in order to see changes related to cancer.
Tumor suppressor genes
when lose both alleles due to mutation you lose the function of that gene to suppress the tumor growth
The more undifferentiated, the greater the capacity to proliferate, and the more _____ the cancer
malignant
Elevated levels of ____ are associated with certain cancers and can be used clinically to assess responses to treatment
carcinoembryonic antigen (CEA)
Cells become more _____ as they mature
specialized
Acts as a brake to the cell as this protein governs cell cycle commitment
pRB
- -its activity is governed by phosphorylation (adding or removing a phosphate group)
- disruption of pRB leads to increased cell proliferation
- commonly found in cancer cells
The cell cycle in cancer cells is affected by 3 underlying causes of growth and maturity abnormalities…
- The ability to produce the enzyme telomerase
- Changes in the pRB gene, which governs the cell cycle rate
- Changes in the p53 gene, which slows the cell cycle to allow for repair of DNA mutations before cell division
Most people diagnosed with colorectal cancer have a primary relative who also has colorectal cancer. T/F
False. Many of these mutations are acquired from their environment.
Definition of interphase and what it includes
- the time between cell divisions
- G1 (gap) phase
- S (synthesis) phase
- G2 phase
Mitotic phase includes
mitosis and cytokinesis
Characteristics of malignant tumors
Less differentiated Grow rapidly Invade neighboring tissues Have the capacity to spread to other body sites
____ is genetic but not necessarily inherited
cancer genetic - ‘mutation’ inherited - from parent
The process of tumor formation and a series of mutatiions is required for cancer
Carcinogenesis
The degree of specialization of a given cell in terms of structure and function
Differentiation Cells will normally become more specialized as they mature.
Which of the following types of hereditary or familial colon cancer are associated with mutations in DNA repair genes? -FAP -HNPCC
-HNPCC Hereditary Non Polyposis Colon Cancer
Basis of cell cycle include…
- DNA replication/synthesis
- Mitosis (nucleus divides)
- Cytokinesis (cell divides)
Means “new growth” and may be malignant or benign
Neoplasia
Examples of tumor markers in cancer cells
- prostate-specific antigen (PSA)
- CA-125
- carcinoembryonic antigen (CEA)
Markers are not diagnostic but changes in levels are often consistent with changes in tumor growth or responsiveness to treatment, and therefore are sometimes clinically useful.
Malabsorption can occur with colon cancer and contribute to weight loss. T/F
True changes in GI tract may lead to reduction of absorbtion of crucial nutrients
Normally correct damage or mutations in the cellular DNA
DNA repair genes
- failure to fix these mutations increases the likelihood that cancer will arise
a rare childhood cancer of the eye that involves mutations in both alleles of the tumor suppressor gene called pRB
Retinoblastoma
- mutations may be inherited or aquired
- persons born with a mutated allele predisposes them to this form of cancer
- loss of pRB function leads to unregulated growth or cancer
How does proliferation change in cancer
All cells have alimited number of cell divisions before that cell will die, but cancer cells have become immortalized (keep dividing without undergoing cell death) Cancer cells ignore normal growth restraints and have a high proliferative capacity. Divides more rapidly than their normal cellular counterparts
There is a/an ______ relationship between differentiation and the ability of a cell to proliferate
Inverse relationship
Common symptoms in cancer
Distinct diseases with similar underlying cellular changes and common manifestations:
- Pain - common, more so in progressive disease;
- Cachexia - severe form of malnutrition, associated with anorexia, tumor necrosis factor (TNF);
- Declining hematopoiesis - anemia often observed, tumors in bone or bone marrow suppression can contribute.
Screening tests that measure the presence of blood in the stool include -Colonoscopy -FOBT -CEA -All of the above
- FOBT Fecal test for evidence of blood in stool (hemacult)
Aneuploid
loss of diploid state
Normally promote growth as protooncogenes within cells (growth factors, receptors)
Oncogenes
- mutate ONE copy
- can be aquired through viruses
Protooncogenes form gowth factors, enzymes, receptors within the cell that generally promote cell growth
Conversion of a normal cell into a cancer requires ____ mutations
multiple may be point mutations or chromosomal rearrangements
Mutations in only one allele of these genes listed below, which normally promote cell growth, is associated with changes associated with cancer.
- Tumor suppressor genes
- Protooncogenes
- DNA repair genes
- Genes encoding telomerase
- Protooncogenes
Mutation from protooncogenes to oncogene which now has altered growth factor which is a result of that mutation.
Promotes growth, secretes growth factors/hormones and promotes spread, scretes proteases
Altered biochemical properties
what are aberrant adherence properties
loss of contact inhibition, anchorage independence, promotes invasion and metastais
