Genomic final exam 9-12 Flashcards
What are the Cancer Stats discussed
Can be inherited as a Mendelian form or as a complex, multifactorial disorder • 10,000,000 new cases of cancer are diagnosed annually worldwide • 1.7 million in US alone • Lifetime incidence of developing cancer: –Nearly 1 out of 2 for men –1 out of every 3 for women
What are the main causes of cancer
Chemicals Radiation Heredity Viruses Some types of cancer can be avoided through lifestyle choices
Broadly speaking, cancer has 2 key abilities:
Ability of cells to proliferate uncontrollably 2. Ability to invade and to spread to other tissues
A tumor grows from a single cancer cell.
Cancer cells spread through lymph and blood vessels to other parts of the body.
Cancer cells invade neighboring tissue.
What is the most common cancer in america and what is the estimated cases
prostate cancer men 19% and breast womane 30 percent
lung and bronchous 14% men and 12% women
Colon and rectum 9% men and 8% women
urinary bladder 7% men uterine and corpeus 7% women
melonoma on skin 6% and thyroid 5%
Neoplasia
Disorganized tissue growth • Net increase in number of dividing cell • A proliferating mass of abnormal cells is a neoplasmor a tumor • Lose the balance between cell proliferation and cell differentiation
What Tumor cell lose the ability that normal cellss have the ability to do
Tumors lose the balance between cell proliferation and cell differentiation
cancer cells are dedifferntiated
what are the 2 types of tumors
Benign= tumors that grow in a confined area –Usually self-contained with clear borders –Can be removed without affecting other tissues • Malignant= can invade surrounding tissues and spread via metastasis • The term CANCER generally refers to a malignant tumor
What are the classification of cancer orgin
Carcinomasarise in external or internal body coverings (skin) – Sarcomasarise in supportive and connective tissue (bone) – Leukemiasand lymphomasarise from bloodforming tissues
General classes of surgery
Surgery –suitable for benign tumors, selfcontained – *Chemotherapy –metastatic tumors, leukemiasand lymphomas – *Radiation – Precision Medicine Approaches: – Hormone therapy – Immunotherapy–may soon become one of the primary treatments – Oncogene specific inhibitors
*Target actively dividing cells
Main causes of cancer ultimately lead to mutations in genes*
Chemicals 2. Radiation 3. Infectious Agents 4. Heredity *Genes that coordinate entry and exit of the cell cycle or DNA repair are particularly affected by cancer causing factors
Review of Cellular Control
Most cells in the Go phase
A set of molecules, including growth factors,
that triggers and coordinates events of the cell
cycle
– Checkpoints
– Control points where signals regulate the cell
cycle
– G1 checkpoint allows entry into the S phase or
causes the cell to leave the cycle, entering a
nondividing G0 phase
– G2 checkpoint
– M checkpoint
what cellular control
Effects of a growth factor at the G1
checkpoint
– A growth factor is a protein that stimulates growth
and cell division
– Growth factors bind to a receptor in the plasma
membrane
– Within the cell, a signal transduction pathway
propagates the signal through a series of relay
molecules
– The signal reaches the cell cycle control system to
trigger entry into the S phase
cancer cells escape what cycle
cancer cells escape controls on the
cell cycle – Cancer cells divide rapidly, often in the absence of
growth factors
– They spread to other tissues through the
circulatory system
– Growth is not inhibited by other cells, and tumors
form
– Benign tumors remain at the original site
– Malignant tumors spread to other locations by metastasis
what are the 3 main classes of cancer
Oncogenes*
2. Tumor Suppressor Genes*
3. DNA Repair (or Genomic Stability)
Genes
what is proto oncogenes and oncogene
Proto-oncogenes – normally trigger cell division
When activated, they become oncogenes
Oncogene = cancer causing gene ”driver” or “initiator”
alteration of pro-protoncogenes gain of function
what is a tumor suppressor gene
normally control or block
cell division. When mutated, they lose their function* and
cannot prevent cancer. Mutations to TSGs are typically
recessive.
-normal growth inhibiting protein under control control cell division
cell division nonfunctional protein> not under control
DNA repair genes
These genes function mismatch repair (fixing spontaneous errors made normally during the DNA replication proces
3. DNA Repair Genes - These genes function mismatch repair (fixing spontaneous errors made normally during the DNA replication process) Some of these mutations occur in proto-oncogenes or tumor suppressor genes Thus, mutations in DNA repair genes lead to an accumulation of mutations in other genes and drastically increases likelihood of cancer
True or false cancer is more likely in younger people
False its in older patients
Multiple genetic changes are necessary to develop cancer. Cancer results from the gradual accumulation of mutations in somatic cells. This is why our risk of cancer increases as we age - we are accumulating mutations
what differniate cancer cell and normal cells when it comes to growth signals
Most normal cells require an external
growth signal to replicate
• Cancer cells make their own external growth
factors
• Cancer cells stimulate their division by
activating their signal pathways without an
external signal
• 25 - 50% of all cancer types have a mutation
in the Ras proto-oncogene that turns on a
signal that tells the cell to divide
why does cancer grow uncontrollable
Cancer cells grow even in the absence of
growth signals
– Even without growth factors to initiate the cell
cycle and mitosis, cancer cells will go right
through that checkpoint
What is
ras and how it correlate to cancer
Ras Family of Oncogenes
Mutations in Ras cause the protein to become locked in its
activated form - always signaling to initiate cell growth and
division
Only 1 mutation is so its dominant
Inactive Ras GDPRas»»> to convert to active GEF»»> GTP RAS active
To convert inactive again GAP convert GTP to GDP
Give and example of a Tumor suppressor gene
• pRB - retinoblastoma protein
– tumor suppressor protein that inhibits progression
through the cell cycle
– Mutations in Rb prevent Rb protein from inhibiting the
growth cycle: Mutant Rb means a loss of function*
– It takes two mutant Rbs to knock out its function
– Rb is a classic tumor suppressor gene
Test Question what is retinoblastoma
Rare childhood cancer of the eye that occurs in hereditary
and spontaneous forms
• Now, 90% of children with Rb are cured
• In families of Rb survivors, their children have 50% chance
of developing the cancer
• In Rb patients, doctors noticed that they were missing a
portion of Chr. 13
• Later, the Rb gene was identified on Chr. 13
• Two “hits” to the Rb gene are needed to deactivate it
• First tumor suppressor gene to be identified
Rare childhood cancer of the eye that occurs in hereditary
and spontaneous forms
• Now, 90% of children with Rb are cured
• In families of Rb survivors, their children have 50% chance
of developing the cancer
• In Rb patients, doctors noticed that they were missing a
portion of Chr. 13
• Later, the Rb gene was identified on Chr. 13
• Two “hits” to the Rb gene are needed to deactivate it
• First tumor suppressor gene to be identified
Rare childhood cancer of the eye that occurs in hereditary
and spontaneous forms
• Now, 90% of children with Rb are cured
• In families of Rb survivors, their children have 50% chance
of developing the cancer
• In Rb patients, doctors noticed that they were missing a
portion of Chr. 13
• Later, the Rb gene was identified on Chr. 13
• Two “hits” to the Rb gene are needed to deactivate it
• First tumor suppressor gene to be identified
test question 2 two hit model of tumor formation
A “hit” is a point mutation or a deletion that takes out the function of the “good” allele
If a baby is born with an inherited hit in their Rb gene, then they are half way to the two hits
In 90% of babies born with one hit, the other Rb copy develops a hit in a cell and leads to a tumo
what is mechanism of loss of heterzygosity
mutation deltetion rescue of trisomy and mitotic recobination
