202 Intro To Oncology Flashcards
Oncology refers to the study of?
Many abnormal cells are needed for cancers to occur. True or false
Cancer refers to diseases caused by cells that do what?
What is molecular oncology?
What two heritable properties define cancer cells?
Study of tumors is oncology. Only once abnormal cell is needed to start dividing uncontrollably and they saana don’t serve any function in the body. They’re called neoplasticism or cancer cells.
So it needs only one cell to divide uncontrollably and that one cell must have a competitive or selective advantage over other cells and the body’s defenses.
Oncology is the study of tumours. A tumour arises when a single abnormal cell divides uncontrollably to eventually form a mass of new abnormal cells.
2.These abnormal cells which serve no useful function in the body are described as neoplastic cells or cancer cells.
3.Cancer is the term applied to a group of diseases in which the abnormal cells of the body no longer responds to the normal restraints on growth. Cancer is the uncontrolled growth of abnormal cells anywhere in a body.
4.Molecular oncology is the study of cancer at the DNA level, using techniques that allow detection of genetic alterations down to single base pair changes.
Cancer cells thus break the basic rules of cell behaviour and are defined by two heritable properties:
●Continuous reproduction of the abnormal cells in defiance on the normal restraints on cell division,
●These abnormal cells invading and colonizing other areas of the body and interfering and preventing the function of normal cells in these areas.
So in my own words, the cancer isn’t listening to the body’s signals or restraints for it to stop dividing anyhow. On top of everything else, it saana invades other parts of the body and prevents those parts from functioning the way they should normally.
3.The combination of these two properties makes cancer very dangerous.
An abnormal cell with disagreeable properties will cause significant damage even if its proliferation is under control. It can easily be handled by the body.
True or false
A tumor is only considered a cancer if it is malignant. What does the term malignant mean?
How is it different from metastases
What is anaplasia and dysplasia
False.
An abnormal cell with disagreeable properties will cause no significant
damage if its proliferation is under control. It can easily be handled by the body.
The out-of-control proliferation is what gives rise to a tumour or neoplasm, which is the relentless growing mass of abnormal cells. So keyword is it must not only be abnormal but must also be dividing abnormally or have out of control proliferation.
A tumour is considered a cancer only if it is malignant - acquired the ability to invade surrounding tissue. (So if it’s cancer of the liver, it invades the liver and stays within that confines. Once it moves out of the liver through the bloodstream and to another part of the body, it has metastasized)
These have one purpose - to eventually kill you.
Invasiveness implies the ability to break lose, enter the bloodstream of lymphatic vessels and form secondary tumours called metastases at other sites in the body. This increases the difficulty of treatment.
Malignant tumours therefore have rapid growth rate, loss of differentiation and absence of normal tissue organization. This results in irregularity of size and shape of the nucleus and other structures.
So with malignancy, it’s staying in one tissue and invading structures close to the tissue so in the case of the liver, maybe the bile ducts and blood vessels near the liver
But once it moves from the liver and surrounding tissues via the blood vessels or lymphatic vessels to another part of the body that is distant, it has
Metastasized
Anaplasia is absence of differentiation recognized by loss of organization and increase in nuclear size
Here’s a simple and clear explanation:
Dysplasia means abnormal development or growth of cells, but the cells are still somewhat organized.
• It often looks like cells are starting to behave badly — changing size, shape, or arrangement.
• It can be mild, moderate, or severe.
• Dysplasia can sometimes go back to normal if the cause (like irritation) is removed — but if it gets worse, it can lead to cancer.
Anaplasia means complete loss of cell structure and function — cells become very primitive, ugly, and chaotic.
• It is a hallmark of malignant cancer.
• The cells look nothing like the normal cells they came from.
• They grow uncontrollably and are very aggressive.
In short:
• Dysplasia = early, disorganized changes that might still be reversible.
• Anaplasia = full loss of normal features, not reversible, and always linked to malignancy.
Would you also like a few very short bullet points to memorize them even faster?
Uncontrolled growth of normal cells is cancer. True or false.
Cancer can be solid or liquid (or hematological) tumors. What is a carcinoma? Il what is a sarcoma
What is leukemia
What is a lymphoma
Solid tumors
What does it mean to say a carcinoma is in situ and how is it different from an invasive carcinoma
False. Uncontrolled growth of normal cells is benign. We don’t say benign cancer. We say benign cells. Cancer is uncontrolled growth of abnormal cells.
Solid tumours are designated according to the issue of origin
a)Carcinoma – epithelial cells for interior and exterior parts of the body e.g. breast –ductal carcinoma, lung, colon
b)Sarcoma – bone, cartilage, muscle, connective tissues e.g. skeletal muscle malignant cancers are rhabdomyosarcomas
c)Leukemia – begin in bone marrow and accumulate in blood stream
d)Lymphoma – in lymphocytes and immune system
e)Malignant melanoma – melanocytes
f)Blastoma – neuroblastoma or retinoblastoma
Classification of benign cells
1.For any name of a malignant tumour there is a corresponding name for the benign.
2.The adenoma, papilloma, chrondroma etc. as used to describe the benign cells.
3.For example, adenoma is benign epithelial whilst adenocarcinoma is malignant. For example, hepatocellular adenoma and hepatocellular carcinoma
4.Also, chondroma and chondrosarcoma are benign and malignant for the cartilage.
5.Benign and malignant for smooth muscles of the uterus are leiomyoma and leiomyosarcoma and for fat cells lipoma and liposarcoma.
6.About 90% of human cancers are carcinomas perhaps because most cell proliferation occurs in the epithelia or because epithelia tissues are most frequently exposed to physical and chemical damag
For the haematological malignancies, tumours arising from the white blood cells are either leukemias or lymphomas.
●Leukemia is a neoplastic disease of blood or blood forming tissue (bone marrow) in which large numbers of white blood cells populate the bone marrow and peripheral blood.
●Lymphoma is a neoplasm of lymphocytes where the B and T lymphocytes divide faster or survive longer than normal to form discrete tissue masses
3.Carcinoma in situ (CIS) is pre-invasive epithelial malignant tumours. These cancers have not broken through or invaded the surrounding tissue.
4.CIS is found in a number of sites including cervix, breast, stomach, endometrium and are readily treatable with sparing surgery.
5.Alternatively is the invasive or infiltrating carcinoma (IC). Which means the cancer has gone out of the organ while in situ means restricted to the organ and haven’t broken into surrounding tissue but for malignancy, it moves into surrounding tissue.
Metastases, it moves to distant parts of the body far away from the tissue
Why is cancer called the disease of the aged?
Tumour progression involves mutation and natural selection. The abnormal cell must have a selective advantage over its neighbours so it can better thrive. Sometimes we may even die before the cancer has time to develop.
True or false
Most human cancers are as a result of. Genetic instability.
State four defects fhat human cancer cells have.
What cancer enzymes make cancer cells immoral?
Tumors are hereditary tthe or false?
Cuz you’ll need at least six mutations before you can get cancer and the mutations happen as the years go by.
Most human cancers are as a result of. Genetic instability.
Most human cancers are as a result of genetically unstability. The defect may be in the inability to (i) repair DNA damage, (ii) correct replication errors, (iii) control cell differentiation or (iv) maintaining chromosome integrity.
This together with the availability of the cancer enzyme telomerase makes cancer cells immortal and will continue to divide forever under favourable conditions.
Yes, telomerase can be considered a “cancer enzyme” because it is often reactivated in many types of cancer cells. Here’s how:
1. Normal cells: In normal somatic (body) cells, telomerase activity is low or absent, which leads to gradual telomere shortening with each cell division. This shortening eventually leads to cell death or senescence (when a cell stops dividing).
2. Cancer cells: In most cancer cells, telomerase is reactivated, which allows the cells to maintain or even lengthen their telomeres. This enables the cells to continue dividing indefinitely, essentially bypassing the normal cellular aging process. This contributes to the uncontrolled growth characteristic of cancer.
Why it’s important in cancer:
• Telomerase reactivation helps cancer cells maintain their immortality, allowing them to evade the normal aging process and keep proliferating.
• Targeting telomerase activity is being explored as a potential anti-cancer therapy, with the aim of inducing telomere shortening in cancer cells to limit their ability to divide and survive.
Would you like more details on how telomerase reactivation contributes to cancer?
5.Thus, while several human cancers have a strong tendency to run in families, tumours themselves are not passed from parents to offspring. It is therefore not heritable. However, a predisposition toward cancer may be inherited if one or more mutations is already present at conception.
False. Tumors aren’t hereditary but the predisposition to tumors is. This predisposition is most through a defect in the DNA repair mechanism that allows them to accumulate mutations.
Why do cancer cells grow anyhow
The growth may be due to mutations in genes that regulate which three key cell processes?
Carcinogenesis (generation of cancer) appears to be linked with mutagenesis. Chemical carcinogens changes the DNA sequence; ionization radiations causes chromosomal breaks and translocations and viruses introduce foreign DNA into the cells.
They result from somatic mutations and a vast majority of cancers are initiated by genetic changes. There is therefore an abnormality in their DNA sequence that distinguishes them from the normal cells.
Cancer cells don’t need anything to make them start dividing. They also don’t respond to growth inhibitory signals.
They are also resistant to apoptosis
They can grow independent of structural support such as extracellular matrix (loss of anchorage dependence) and can grow indefinitely (immortalized).
The tumours can develop angiogenic potential i.e. have the capacity to form new blood vessels and capillaries to bring in oxygen and nutrients. Malignant tumours can induce formation of blood vessels which serve as routes for the transport of nutrients into the tumour using the vascular endothelial growth factor (VEGF)
Note: This aberrant growth pattern may result from mutations in genes that regulate proliferation, differentiation and cell survival (three processes). It is this genetic changes that prevent the cancer cells from responding to signals that govern the growth of normal cells.
Why can benign cells cause serious health complications?
Can those cells become malignant?
Benign cells
The uncontrolled growth of the normal cells are termed benign cells as they are not cancers
They are encapsulated and well differentiated and retain some normal tissue structure.
These do not invade other tissues and more often than not are not life threatening, but can still cause serious health complications by compressing other structures.
Cells initially described as benign can progress to cancer and become malignant.
1.What are the names of genes that cause cancer?
2.What are the names of the normal forms of these cancer genes before they become cancer genes?
What are the functions of these normal forms of cancer genes?
The genes that cause cancer are dominant and normally produce what two things?
Explain gain of function mutation and loss of function mutation.
1.Oncogenes
2. Proto oncogenes
For every gene that mutates to cause a cancer (oncogene) there was a corresponding cellular gene (proto-oncogene), which is the normal form of the oncogene.
Mutated versions of proto-oncogenes that increase the risk of cancer are oncogenes. Oncogenes are dominant and normally produce either an active protein or an increase in protein number.
The proto oncogenes encode proteins that control l cell proliferation and normal cell growth e.g. growth factors, growth factor receptors, signal transduction proteins, transcription factors, cell cycle and apoptosis regulators.
Under normal circumstances, proto oncogenes need to be activated by certain signals and should only occur in cells that need to undergo cell division.
Any mutations that causes these genes to be over expressed or their protein products to be over active can result in uncontrolled proliferation. These mutations that causes the proto-oncogene to become an oncogene and drive the cancer forward is a gain-of-function mutations.
Gain of function mutations means the mutation causes over expression of the normal function while loss of function mutation means mutation causes under expression of the normal function or prevent them from doing their normal function kraa. Example of loss of function mutation is mutation in p53.
How do oncogenes work?
What is the most common oncogene? Explain the model action for this gene.
Not every gene mutates for you to get cancer. Only proto oncogenes are the ones that if they mutate p3, you’ll definitely get cancer and these mutations are gain of function mutations cuz they’ll be over working.
Oncogenes include cell membrane receptors that are bound by growth factors, hormones and other extracellular signals.
●These receptors transduce signals through the cell membrane, cytoplasm and then nucleus, where they activate factors that initiate DNA synthesis (G1 to S) or mitosis (G2 to M).
●Unlike proto-oncogenes, these signals can be transduced in the absence of growth promoting indications
●The first experiments to show that oncogenes were mutant forms of proto-oncogene involved cells cultured from human bladder carcinoma. The DNA sequence of the ras oncogene differed from the normal ras proto-oncogene. Similar mutations were found in the ras gene of lung and colon tumours.
Ras oncogene is the most common oncogene.
Model action:
Alright, let’s build it step-by-step, starting from the growth factor:
1. Growth factor binds to a growth factor receptor on the cell surface. 2. This activates the receptor’s tyrosine kinase activity (it adds phosphate groups inside the cell). 3. Adaptor proteins link the activated receptor to Ras (a small GTPase). 4. Ras switches from inactive (Ras-GDP) to active (Ras-GTP). 5. Active Ras triggers the MAP kinase cascade (Raf → MEK → ERK). 6. This cascade activates transcription factors inside the nucleus. 7. The transcription factors promote gene expression that leads to cell growth and division.
In the case of Ras oncogene:
• Ras is permanently active (stuck with GTP), even without growth factor signals.
• This causes continuous cell proliferation → cancer risk.
So in conclusion, growth factor bonds to growth receptor to activate K ras(k ras is the most common type of ras that affects humans). When the K ras is activated, it starts the MAP kinase pathway and this leads to constant transcription occurring and this leads to cell cycle progression.
But if ras is mutated, it cannot hydrolyse GTP to GDP to turn its activation off. So ras stays active even in the absence of growth factors.
Okay, here’s a simple explanation:
Normally, Ras works like a switch:
• When Ras binds GTP, it is ON (active) — it sends signals for cell growth.
• Then it quickly hydrolyzes GTP to GDP (GTP → GDP), which turns it OFF.
BUT — if Ras is mutated (e.g., in cancers), it cannot hydrolyze GTP properly.
So it stays stuck with GTP and remains permanently ON.
Result:
• Constant signals for cell growth, even when there’s no growth factor.
• Cells keep dividing uncontrollably → Cancer.
State the classes of oncogenes, their respective pro oncogenes, how they become cancerous , their locations and the disease they cause
- Growth Factors(oncogene)
• Example:fibroblast Growth Factors (FGF),
proto oncogenes: int-2
• How they become cancerous: Amplification (too many copies) → too much growth signal
• Where they act: Secreted (they leave the cell to tell other cells to grow)
• Cancer examples: Breast cancer, bladder cancer - Growth Factor Receptors
• Example: Epidermal Growth Factor Receptor (EGFR family)
Proto-oncogenes-
• erb-B1
• erb-B2 (also called HER2)
• How they become cancerous:
• erb-B1: Overexpression (too much) → Lung cancer
• erb-B2: Amplification (too many copies) → Breast, ovarian, stomach cancers
• Where they act: On the cell membrane (receiving signals) - Signal Transduction Proteins (Middle messengers inside the cell)
• Examples(oncogene first and beside it is the proto oncogene)
• G proteins(oncogene): ras(proto oncogene)
• Serine/threonine kinases: akt-1
• Tyrosine kinase: abl
• How they become cancerous:
• ras: Point mutation → multiple cancers
• akt-1: Amplification → ovarian cancer
• abl: Translocation → leukemia
• Where they act: Cytoplasm - Transcription Factors (Proteins that tell the cell which genes to turn on)
• Examples:
• proto oncogenes-
Hox-11: translocation → T-cell leukemia
Myc: translocation → Burkitt’s lymphoma
• Where they act: In the nucleus - Apoptosis Regulators (Control cell death)
• Example: proto oncogene is Bcl-2
• How it becomes cancerous: Translocation → prevents cells from dying
• Where it acts: Mitochondria
• Cancer example: Follicular B-cell lymphoma - Cell Cycle Regulators (Control when a cell divides)(cyclins and cyclin dependent kinases)
• Examples:
• proto oncogenes;
Cyclin D: Translocation → lymphoma
• CDK4 (Cyclin-dependent kinase 4): Amplification or point mutation → breast, liver, esophageal cancers
• Where they act: In the nucleus
Simple Summary:
• Growth factors and their receptors tell the cell to grow.
• Signal transducers pass on the message.
• Transcription factors tell the DNA what to do.
• Apoptosis regulators decide if the cell should die.
• Cell cycle regulators control when cells divide.
Mutations in any of these can cause cancer.
Would you like me to also draw you a super short memory map for this? (to cram it faster?)
How are proto oncogenes converted to oncogenes
Note: correction genes prevent conversion of proto oncogenes to an oncogene.
Chemical mutagens or radiation can (a) cause a mutation in the regulatory region of the gene increasing rate of production of oncogene or (b) mutate a coding portion to synthesize a different protein.
2.The entire proto-oncogene may be translocated and be under a different more active promoter to produce excess protein. If a portion is translocated, a truncated protein may be synthesized or fusing with another gene may produced a combined protein.
3.The proto-oncogene may be amplified resulting in multiple copies of the gene in a single cell.
4.If an oncogenic virus infects the cell, its oncogene may integrate into the host genome producing abnormal oncogene protein product.
The structure of a gene at the simple level is made up of the promoter region and the coding region. The promoter region tells the gene to be on or off and the coding region makes the protein or is where the instructions to make the protein are found or is the part that gets translated or transcribed.
So using this, there are six ways proto oncogenes can be converted to oncogenes:(1,2 can be due to radiation or chemical carcinogens and 1,2,3,4,5 are point mutations)
1. Mutation in promoter region causing excessive expression
2. Mutation in coding region causing production of hyperactive protein
3: amplification of coding region leading to expression of multiple copies of the proto oncogene (gene amplification)
4. Fusion of a coding region: You’re thinking well — let me explain it slowly:
When they say
“Proto-oncogene or a portion of it is fused with another gene,” it usually means the coding region (or sometimes part of the coding region plus part of a regulatory region) gets joined to another gene by accident.
This happens by chromosomal translocation — two parts of different chromosomes break and wrongly join together.
What happens after fusion?
• The new fused gene can make a fusion protein.
• This fusion protein can behave abnormally — either
• Overproduced (made too much) or
• Hyperactive (too strong activity).
Simple example:
• In chronic myeloid leukemia (CML), a fusion happens between the BCR gene and the ABL gene (from two different chromosomes).
• They form a fusion called BCR-ABL.
• BCR-ABL is a hyperactive tyrosine kinase — it signals too much, leading to cancer.
Answer to your specific question:
Is this fusion of a coding region? Yes, usually coding regions are involved in the fusion. • Sometimes it’s only coding regions. • Sometimes it’s coding + regulatory region.
Would you like me to give you a super quick 1-line to memorize this? It will make it stick easier!
- Translocation of promoter region to a different stronger coding region.
- Translocation of coding region to a stronger promoter region making the proto oncogene under the control of a strong promoter or influencer.
What’s the function of tumor suppressor genes like p53
How do they work?
These encode proteins whose function is to correct the mutation, repress protein synthesis and cell proliferation in response to certain signals such as DNA damage. A common example is p53.
●They thus stop replication, transcription and translation, repair damaged DNA and promoting programmed cell death or apoptosis
●They act by counteracting the movement of the cell from either G1 to S or G2 to M phases.
●They include factors that control replication, transcription or translation of genes required for cell division.
●In most cancers, both copies of the tumour suppressor gene must be inactivated, resulting in loss-of-function mutations before cancer can occur. That’s why if your p53 is mutated or damaged, you’ll get loss of function mutation where the gene can’t protect you anymore by correcting the mutations in oncogene
●In contrast, only one allele of a proto-oncogene needs to be converted to an oncogene to initiate transformation
So while both copies of the tumor suppressor gene need to be inactivated for cancer to occur, only one allele of a proto oncogene must be converted to an oncogene to initiate transformation to an oncogene.
What family of proteins control progression of cell cycle by activating key proteins by phosphorylation
What two amino acids really help in phosphorylation
The complexes rhat form to allow the cell to progress in the cell cycle are activated by what factors?
What inhibit them?
Remember tumor suppressor genes control apoptosis of dna damaged cells
Molecular control of cell proliferation
1.Cell proliferation is linked to the control of the cell cycle where two growth phases G1 and G2 separate DNA replication (S phase) and mitosis (M phase).
2.Cyclins and cyclin-dependent kinases (CDKs) family of proteins control progression of cell cycle by activating key proteins by phosphorylation.
3.The cycin-CDK complexes are activated by external growth factors (proto-oncogenes) through signaling pathways.
4.They are also inhibited by internal signals including CDK inhibitors e.g. ckl that prevent DNA replication and mitosis from proceeding if there is DNA damage and incomplete replication respectively.
5.Cell division is arrested for DNA repair. If the DNA damage is un-repairable, the arrested cell is programmed to die via apoptosis, and tumour suppressor genes control this process.
6.The most important tumour suppressor gene is p53 as loss of p53 function has been implicated in many cancers and is nicknamed the guardian of the genome.
Serine and threonine. Sometimes tyrosine but for tyrosine kinases
Explain how G1/S transition in the cell cycle is controlled
So when a growth factor binds to the receptor, it initiates the ras/raf signaling pathway
Note that ras is a small Gtpase and the raf is a serine threonine kinase. Raf activates MEK which is another kinase and MEK activates ERK which is another kinase. The ERK moves into the nucleus and turns on genes that lead to cell division and growth.
So this ras/raf signaling leads to activation of transcription factors and these factors increase production of cyclin D.
Cyclin D binds to cyclin dependent kinase 4 or cyclin dependent kinase 6 to form the active cyclin D/CDK 4 or 6 complex.
This complex phosphorylates Rb protein(retinoblastoma protein).
This phosphorylated protein releases E2F transcription factors and this activates the genes for DNA replication meaning the cell can now enter the S phase.
You’re very close! Let’s clean it up slightly and walk through it clearly:
Correct understanding:
• Cyclin D binds to CDK4/6 → forms an active Cyclin D–CDK4/6 dimer (yes, it’s a complex/dimer).
• CDK4/6 are serine/threonine kinases — they phosphorylate the Rb protein because serine and threonine have –OH groups.
• When Rb is phosphorylated, it releases E2F transcription factors → E2F then activates genes needed for S phase.
About inhibition:
• p53 works through p21, not directly CKI-1.
• p21 is a CDK inhibitor (CKI) — it binds to and inhibits CDK4/6, blocking Rb phosphorylation.
• When Rb remains unphosphorylated, it keeps holding E2F, so the cell can’t enter S phase — this is important if there’s DNA damage!
Simple corrected flow:
Cyclin D + CDK4/6 → phosphorylates Rb → E2F released → S phase entry. p53 → increases p21 → inhibits Cyclin D–CDK4/6 → stops Rb phosphorylation → cell cycle arrest.
Quick notes:
Term Meaning
Cyclin D–CDK4/6 Pushes G1 → S
p53 → p21 Blocks G1 → S if DNA is damaged
Phosphorylation of Rb Frees E2F
No phosphorylation E2F stays trapped
Would you like a one-sentence way to remember this whole G1/S regulation? (It really helps in MCQs!)
Absolutely! Here are refined MCQs that specifically cover everything you sent about p53—including its role as a transcription factor, its response to DNA damage, its regulation of the cell cycle via p21, stimulation of DNA repair enzymes, and activation of apoptosis genes like bax and IGF-BP3.
- What is the function of the p53 protein in the cell?
A. Promotes mitosis
B. Regulates the cell cycle and apoptosis
C. Stimulates DNA replication
D. Inhibits tumor suppressor genes
Answer: B. Regulates the cell cycle and apoptosis
Explanation: p53 acts as a transcription factor that regulates the cell cycle, halts replication in damaged cells, and initiates apoptosis when necessary.
- Why is p53 known as the “guardian of the genome”?
A. It ensures rapid DNA replication
B. It activates oncogenes
C. It stops damaged cells from dividing and promotes repair or apoptosis
D. It accelerates the G1/S transition
Answer: C. It stops damaged cells from dividing and promotes repair or apoptosis
Explanation: p53 halts the cell cycle in response to DNA damage and directs the cell to either repair or undergo programmed death.
- Which gene does p53 activate to inhibit the cyclin/CDK complex?
A. bax
B. IGF-BP3
C. p21
D. p16
Answer: C. p21
Explanation: p21 inhibits cyclin/CDK activity, preventing the cell from entering the S-phase of the cell cycle.
- What happens to p53 levels in response to DNA-damaging mutagens?
A. They decrease to allow repair
B. They stay the same
C. They rise to halt the cell cycle and trigger DNA repair
D. They are immediately degraded
Answer: C. They rise to halt the cell cycle and trigger DNA repair
Explanation: Upon DNA damage, p53 levels increase to prevent cell cycle progression and to initiate repair mechanisms.
- If DNA repair fails after p53 activation, which of the following happens next?
A. p53 activates cell division
B. p53 deactivates itself
C. p53 activates apoptosis genes like bax and IGF-BP3
D. The cell returns to mitosis
Answer: C. p53 activates apoptosis genes like bax and IGF-BP3
Explanation: When DNA repair is unsuccessful, p53 initiates programmed cell death via pro-apoptotic genes.
- Where does p53 operate within the cell?
A. Cytoplasm
B. Mitochondria
C. Cell membrane
D. Nucleus
Answer: D. Nucleus
Explanation: As a transcription factor, p53 functions in the nucleus to regulate gene expression.
Abnormality in the colon signifies inactivation of which gene ?
What is the role of this gene?
Remember; when you see loss, it means tumor suppressor cuz the tumor suppressor has to be lost before cancer proceeds and if you see activate, it means it’s an oncogene cuz that has to be activated for cancer to occur
So p53 functions include activated ion of p21,GADD45(this helps arrest the cell cycle especially at G2/M checkpoint and it facilitates DNa repair) and apoptotic enzymes to destroy cells.
If DNa is repaired, p53 and GADD45 levels drop but if not, p53 promotes apoptosis instead
Colorectal cancer from epithelium lining the colon and rectum shows (i) how a tumour suppressor gene can be identified and (ii) how its identification leads us to understand the molecular mechanism of a common type of tumour.
●Abnormality starts with the deletion or inactivation of a gene called adenomatous polyposis coli (APC).
●For individuals that inherited one mutant copy, cancers arise from cells where the normal copy has mutated. For individuals that had two normal copies, tumour cells only were again found to have lost both copies.
●This identifies APC as a tumour suppressor gene. APC inhibits the pathway of cell proliferation in crypts of the gut, hence the generation of polyps.
Absolutely! Here are refined MCQs that specifically cover everything you sent about p53—including its role as a transcription factor, its response to DNA damage, its regulation of the cell cycle via p21, stimulation of DNA repair enzymes, and activation of apoptosis genes like bax and IGF-BP3.
- What is the function of the p53 protein in the cell?
A. Promotes mitosis
B. Regulates the cell cycle and apoptosis
C. Stimulates DNA replication
D. Inhibits tumor suppressor genes
Answer: B. Regulates the cell cycle and apoptosis
Explanation: p53 acts as a transcription factor that regulates the cell cycle, halts replication in damaged cells, and initiates apoptosis when necessary.
- Why is p53 known as the “guardian of the genome”?
A. It ensures rapid DNA replication
B. It activates oncogenes
C. It stops damaged cells from dividing and promotes repair or apoptosis
D. It accelerates the G1/S transition
Answer: C. It stops damaged cells from dividing and promotes repair or apoptosis
Explanation: p53 halts the cell cycle in response to DNA damage and directs the cell to either repair or undergo programmed death.
- Which gene does p53 activate to inhibit the cyclin/CDK complex?
A. bax
B. IGF-BP3
C. p21
D. p16
Answer: C. p21
Explanation: p21 inhibits cyclin/CDK activity, preventing the cell from entering the S-phase of the cell cycle.
- What happens to p53 levels in response to DNA-damaging mutagens?
A. They decrease to allow repair
B. They stay the same
C. They rise to halt the cell cycle and trigger DNA repair
D. They are immediately degraded
Answer: C. They rise to halt the cell cycle and trigger DNA repair
Explanation: Upon DNA damage, p53 levels increase to prevent cell cycle progression and to initiate repair mechanisms.
- If DNA repair fails after p53 activation, which of the following happens next?
A. p53 activates cell division
B. p53 deactivates itself
C. p53 activates apoptosis genes like bax and IGF-BP3
D. The cell returns to mitosis
Answer: C. p53 activates apoptosis genes like bax and IGF-BP3
Explanation: When DNA repair is unsuccessful, p53 initiates programmed cell death via pro-apoptotic genes.
- Where does p53 operate within the cell?
A. Cytoplasm
B. Mitochondria
C. Cell membrane
D. Nucleus
Answer: D. Nucleus
Explanation: As a transcription factor, p53 functions in the nucleus to regulate gene expression.
Abnormality in the colon signifies inactivation of which gene ?
What is the role of this gene?
Remember; when you see loss, it means tumor suppressor cuz the tumor suppressor has to be lost before cancer proceeds and if you see activate, it means it’s an oncogene cuz that has to be activated for cancer to occur
So p53 functions include activation of p21,GADD45(this helps arrest the cell cycle especially at G2/M checkpoint and it facilitates DNa repair) and apoptotic enzymes to destroy cells.
If DNa is repaired, p53 and GADD45 levels drop but if not, p53 promotes apoptosis instead
Colorectal cancer from epithelium lining the colon and rectum shows (i) how a tumour suppressor gene can be identified and (ii) how its identification leads us to understand the molecular mechanism of a common type of tumour.
●Abnormality starts with the deletion or inactivation of a gene called adenomatous polyposis coli (APC).
●For individuals that inherited one mutant copy, cancers arise from cells where the normal copy has mutated. For individuals that had two normal copies, tumour cells only were again found to have lost both copies.
●This identifies APC as a tumour suppressor gene. APC inhibits the pathway of cell proliferation in crypts of the gut, hence the generation of polyps.
- Which of the following statements about nitrosoamines is TRUE?
a. They are found only in synthetic preservatives.
b. They interact with proteins in the blood.
c. They can be formed in the stomach from nitrates and amines.
d. They have no known link to cancer in humans.
High consumption of preserved fish has been linked to increased gastric cancer risk due to the formation of:
a. Polyamines
b. Nitrogen oxides
c. Nitrosoamines
d. Nitrates
Which of the following BEST explains how some chemotherapeutic agents may unintentionally contribute to cancer development?
a. They suppress immune cells that normally kill cancer cells.
b. They only target healthy cells and ignore cancer cells.
c. They stimulate growth of all cells including cancer cells.
d. They cause mutations while targeting DNA in proliferating cells.
Why are DNA bases vulnerable to chemical carcinogens like nitrosoamines?
a. They have double bonds that attract oxygen.
b. Their oxygen and nitrogen atoms are electron-rich and react with electron-seeking groups.
c. They are always exposed in the nucleus.
d. DNA bases are unstable under physiological pH.
- Which of the following statements about nitrosoamines is TRUE?
a. They are found only in synthetic preservatives.
b. They interact with proteins in the blood.
c. They can be formed in the stomach from nitrates and amines.
d. They have no known link to cancer in humans.
Answer: c. They can be formed in the stomach from nitrates and amines.
Explanation: Nitrosoamines can be formed from nitriles (preservatives) and secondary amines in food, especially in the acidic environment of the stomach.
- High consumption of preserved fish has been linked to increased gastric cancer risk due to the formation of:
a. Polyamines
b. Nitrogen oxides
c. Nitrosoamines
d. Nitrates
Answer: c. Nitrosoamines
Explanation: Preserved fish contains secondary amines and nitrates which can combine to form nitrosoamines, linked to stomach cancer.
- Which of the following BEST explains how some chemotherapeutic agents may unintentionally contribute to cancer development?
a. They suppress immune cells that normally kill cancer cells.
b. They only target healthy cells and ignore cancer cells.
c. They stimulate growth of all cells including cancer cells.
d. They cause mutations while targeting DNA in proliferating cells.
Answer: d. They cause mutations while targeting DNA in proliferating cells.
Explanation: While aiming to destroy rapidly dividing cells, chemotherapy can sometimes introduce new mutations, acting as carcinogens themselves.
- Why are DNA bases vulnerable to chemical carcinogens like nitrosoamines?
a. They have double bonds that attract oxygen.
b. Their oxygen and nitrogen atoms are electron-rich and react with electron-seeking groups.
c. They are always exposed in the nucleus.
d. DNA bases are unstable under physiological pH.
Answer: b. Their oxygen and nitrogen atoms are electron-rich and react with electron-seeking groups.
Explanation: Many carcinogens are electrophilic and attack electron-dense sites like oxygen and nitrogen atoms in DNA bases.
- For genetic pre disposition as a factor contributing to cancer, certain rare mutations make particular cancers likely that they are said to cause the disease. A mutation in the RB1 gene is strongly associated with which type of cancer?
A. Breast cancer
B. Retinoblastoma
C. Lung cancer
D. Leukemia - Which environmental exposure is most likely to cause DNA damage leading to cancer?
A. Fresh air
B. Asbestos,benzene,smoking,radiations
C. Filtered water
D. Organic vegetables - Which virus is most commonly linked to cervical cancer?
A. Hepatitis C
B. Epstein-Barr virus
C. Papilloma virus
D. Influenza virus - BPA (Bisphenol A), suspected to contribute to cancer, is commonly found in:
A. Bottled water
B. Feeding bottles and can linings
C. Cooked rice
D. Clothing dyes - Oestrogen replacement therapy has been associated with increased risk of which cancer(s) cuz they stimulate cell proliferation?
A. Colon and stomach
B. Prostate and liver
C. Breast and ovarian
D. Lung and pancreatic - Helicobacter pylori infection is most strongly associated with which type of cancer?
A. Pancreatic
B. Gastric (stomach)
C. Liver
D. Lung - Sodium nitrate in food preservatives may be metabolized into:
A. Amino acids
B. Simple sugars
C. Potent carcinogens
D. Water-soluble vitamins - Which of the following is considered a xenobiotic carcinogen in the local diet?
A. Plantain
B. Kanzo (overcooked rice crust)
C. Yam
D. Tomatoes
Note that stress can also cause cancer but the mechanism isn’t certain.
- Which substance is linked to bladder cancer?
A. Aflatoxin B
B. Asbestos
C. Aniline dyes
D. Radon - Which cancer is associated with exposure to asbestos?
A. Mesotheliomas
B. Skin cancer
C. Lung cancer
D. Liver cancer - Exposure to radon is most commonly linked to which type of cancer?
A. Bladder cancer
B. Lung cancer
C. Cervical cancer
D. Stomach cancer - Arsenic exposure is associated with which type of cancer?
A. Skin cancer
B. Stomach cancer
C. Liver cancer
D. Lung cancer - Chromium and nickel exposure increase the risk of which cancer?
A. Lung cancer
B. Liver cancer
C. Skin cancer
D. Bladder cancer - Vinyl chloride exposure is strongly linked to which cancer?
A. Bladder cancer
B. Liver angiosarcoma
C. Lung cancer
D. Vaginal cancer - Which cancer is linked to diethylstilbestrol (DES) exposure?
A. Vaginal cancer
B. Lung cancer
C. Bladder cancer
D. Cervical cancer - Nitrosamines, commonly found in food preservatives, are associated with which cancer?
A. Liver cancer
B. Stomach cancer
C. Bladder cancer
D. Skin cancer - Aflatoxin B exposure increases the risk of which cancer?
A. Hepatocellular carcinoma
B. Lung cancer
C. Skin cancer
D. Cervical cancer - Cigarette smoke is linked to which types of cancer?
A. Lung, bladder, head and neck cancers
B. Liver cancer
C. Stomach cancer
D. Skin cancer - Human papillomavirus (HPV) is strongly associated with which cancer?
A. Cervical cancer
B. Lung cancer
C. Liver cancer
D. Bladder cancer - Epstein-Barr virus (EBV) is linked to which cancers?
A. Burkitt’s and Hodgkin lymphomas
B. Cervical cancer
C. Stomach cancer
D. Skin cancer - Hepatitis B virus (HBV) is associated with which type of cancer?
A. Hepatocellular carcinoma
B. Lung cancer
C. Bladder cancer
D. Cervical cancer
- A mutation in the RB1 gene is strongly associated with which type of cancer?
Correct answer: B. Retinoblastoma - Which environmental exposure is most likely to cause DNA damage leading to cancer?
Correct answer: B. Asbestos - Which virus is most commonly linked to cervical cancer?
Correct answer: C. Papilloma virus - BPA (Bisphenol A), suspected to contribute to cancer, is commonly found in:
Correct answer: B. Feeding bottles and can linings - Oestrogen replacement therapy has been associated with increased risk of which cancer(s)?
Correct answer: C. Breast and ovarian - Helicobacter pylori infection is most strongly associated with which type of cancer?
Correct answer: B. Gastric (stomach) - Sodium nitrate in food preservatives may be metabolized into:
Correct answer: C. Potent carcinogens - Which of the following is considered a xenobiotic carcinogen in the local diet?
Correct answer: B. Kanzo (overcooked rice crust) - Which substance is linked to bladder cancer?
Correct answer: C. Aniline dyes - Which cancer is associated with exposure to asbestos?
Correct answer: A. Mesotheliomas - Exposure to radon is most commonly linked to which type of cancer?
Correct answer: B. Lung cancer - Arsenic exposure is associated with which type of cancer?
Correct answer: A. Skin cancer - Chromium and nickel exposure increase the risk of which cancer?
Correct answer: A. Lung cancer - Vinyl chloride exposure is strongly linked to which cancer?
Correct answer: B. Liver angiosarcoma - Which cancer is linked to diethylstilbestrol (DES) exposure?
Correct answer: A. Vaginal cancer - Nitrosamines, commonly found in food preservatives, are associated with which cancer?
Correct answer: B. Stomach cancer - Aflatoxin B exposure increases the risk of which cancer?
Correct answer: A. Hepatocellular carcinoma - Cigarette smoke is linked to which types of cancer?
Correct answer: A. Lung, bladder, head and neck cancers - Human papillomavirus (HPV) is strongly associated with which cancer?
Correct answer: A. Cervical cancer - Epstein-Barr virus (EBV) is linked to which cancers?
Correct answer: A. Burkitt’s and Hodgkin lymphomas - Hepatitis B virus (HBV) is associated with which type of cancer?
Correct answer: A. Hepatocellular carcinoma
- Which wavelength of UV light is most associated with causing DNA damage and cancer? Note most common radiation exposure is UV light and Currently UVA has been linked to slow repair of DNA damage.
A. UVA (320-400 nm)
B. UVC (100-280 nm)
C. UVB (280-320 nm)
D. Infrared radiation - What type of DNA damage is primarily caused by UVB light?
A. Single strand breaks
B. Thymine dimers
C. Double strand breaks
D. Mismatched base pairs - Which repair pathway is responsible for fixing thymine dimers caused by UV exposure?
A. Homologous recombination
B. Nucleotide excision repair which involves about 20 genes
C. Base excision repair
D. Mismatch repair - What condition results from a lack of enzymes required for thymine dimer repair due to lack of the excinuclease?
A. Xeroderma pigmentosum(genetic condition with extensive mutation and skin cancer.)
B. Retinoblastoma
C. Cystic fibrosis
D. Sickle cell anemia - What is the recommended Sun Protection Factor (SPF) of sunscreen to adequately protect against both UVA and UVB radiation?
A. SPF 10
B. SPF 15
C. SPF 30
D. SPF 50 - Which of the following is a consequence of excessive UV radiation exposure, leading to skin cancer?
A. Overproduction of vitamin D
B. Thymine dimers remaining unrepaired
C. Increased melanin production
D. Cell cycle acceleration - Which tumor marker is associated with colon cancer?
A. Carcinoembryonic antigen (CEA)
B. Human chorionic gonadotropin (HCG)
C. Prostate specific antigen (PSA)
D. α-Fetoprotein (AFP) - What is the tumor marker for testicular cancer?
A. Carcinoembryonic antigen (CEA)
B. Human chorionic gonadotropin (HCG)
C. Prostate specific antigen (PSA)
D. CA 19-9 - Which tumor marker is associated with thyroid cancer?
A. Calcitonin
B. Catecholamines
C. CA 19-9
D. α-Fetoprotein (AFP) - What tumor marker is associated with adrenal cortex cancer?
A. Catecholamines
B. Carcinoembryonic antigen (CEA)
C. Human chorionic gonadotropin (HCG)
D. Prostate specific antigen (PSA) - What tumor marker is used for diagnosing prostate cancer?
A. Prostate specific antigen (PSA)
B. CA 19-9
C. α-Fetoprotein (AFP)
D. Carcinoembryonic antigen (CEA) - Which tumor marker is most commonly associated with ovarian cancer?
A. CA 19-9
B. CA 125
C. α-Fetoprotein (AFP)
D. Carcinoembryonic antigen (CEA) - What is the tumor marker for pancreatic cancer?
A. CA 19-9
B. CA 125
C. Prostate specific antigen (PSA)
D. Human chorionic gonadotropin (HCG) - Which tumor marker is associated with liver cancer?
A. Carcinoembryonic antigen (CEA)
B. α-Fetoprotein (AFP)
C. Prostate specific antigen (PSA)
D. Calcitonin
Remember that p21 (also known as p21^CIP1/WAF1) is a cyclin-dependent kinase inhibitor that plays a crucial role in regulating the cell cycle, particularly the transition from G1 to S phase.
- Which wavelength of UV light is most associated with causing DNA damage and cancer?
Correct answer: C. UVB (280-320 nm) - What type of DNA damage is primarily caused by UVB light?
Correct answer: B. Thymine dimers - Which repair pathway is responsible for fixing thymine dimers caused by UV exposure?
Correct answer: B. Nucleotide excision repair - What condition results from a lack of enzymes required for thymine dimer repair?
Correct answer: A. Xeroderma pigmentosum - What is the recommended Sun Protection Factor (SPF) of sunscreen to adequately protect against both UVA and UVB radiation?
Correct answer: C. SPF 30 - Which of the following is a consequence of excessive UV radiation exposure, leading to skin cancer?
Correct answer: B. Thymine dimers remaining unrepaired - Which tumor marker is associated with colon cancer?
Correct answer: A. Carcinoembryonic antigen (CEA) - What is the tumor marker for testicular cancer?
Correct answer: B. Human chorionic gonadotropin (HCG) - Which tumor marker is associated with thyroid cancer?
Correct answer: A. Calcitonin - What tumor marker is associated with adrenal cortex cancer?
Correct answer: A. Catecholamines - What tumor marker is used for diagnosing prostate cancer?
Correct answer: A. Prostate specific antigen (PSA) - Which tumor marker is most commonly associated with ovarian cancer?
Correct answer: B. CA 125 - What is the tumor marker for pancreatic cancer?
Correct answer: A. CA 19-9 - Which tumor marker is associated with liver cancer?
Correct answer: B. α-Fetoprotein (AFP)
Limits of Immunological methods
However, some tumours could not be detected with this method, it could also not distinguish between some tumours and could not predict accurately the stage, which are necessary for correct prescription and dosage.
DNA microarrays is a collection of short DNA sequences of choice attached to the glass support. In this case they will be mutant sequences of the cancer.
mRNA is obtained from the patient, converted to cDNA and applied to the beads. cDNA (complementary DNA) is a form of DNA that is synthesized from an mRNA (messenger RNA) template through a process called reverse transcription. This process is catalyzed by the enzyme reverse transcriptase. Complementary base pairing will occur under high stringency revealing all possible genes that bind as well as their expression levels simultaneously.
Future of cancer therapy
Gene therapy
In clinical trials, genes are being given to cancer patients to make healthy cells more tolerant/resistant to- or make tumours more sensitive to- chemotherapy e.g. bone marrow cells from 30 women with late-stage ovarian cancer were infected with a virus carrying a gene to make them more tolerant to chemo. With this protection more dosage can be applied.
Retroviruses carrying a normal p53 gene was injected directly into tumours of lung cancer patients. The gene regulates cell cycle and promotes apoptosis. The tumours shrank in three patients and stopped growing in three others. No cures yet.
Adenoviruses are more active and can carry larger inserts. Upon infection, they produce a protein that detects cells with inactivated p53.
Thus the use of adenoviruses will only kill the cancer cells that lack p53.
In the above scenarios, obstacles being worked out are the time, dosage and duration, and mode of entry for the treatment.
Preventing proto-oncogenes to oncogenes, inactivating oncogenes, increased resistant of tumour suppressor genes and apoptosis pathways.
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Future of cancer therapy
Exciting new cancer drug kinder than chemotherapy
Blinatumomab or blina which is licensed to treat only adults is the current option after chemo fails
Tried for children with B-cell acute lymphoblastic leukaemia (B-ALL).
The drug is immunotherapeutic that seeks out cancer cells so the body’s own immune system can recognise and destroy them.
This death hunt is precisely targeted - healthy cells are untouched, unlike with chemo.
Blina comes in a bag of liquid administered through a thin plastic tube that remains running into a vein in the patient’s arm for many months.
A battery-operated pump controls how quickly the drug trickles into the bloodstream - a bag can last days.
All of the kit can be carried in a backpack smaller than an A4 textbook, making it fully portable.
Another targeted immunotherapy drug, chimeric antigen receptor T-cell therapy (CAR-T), has also recently become available.
But it is more expensive than blina and the patient’s own cells must be taken and then altered in the lab before being given back as the medicine, which takes time.
Gleevac (Imatinib)
Gleevac is a tyrosine kinase inhibitor that blocks the tyrosine kinase abl from phosphorylating proteins and initiating the signaling cascade necessary for cancer development. This halts the growth of the cancer cells which are then subject to the programmed cell death pathway. It is used in the treatment of multiple cancers that depend on tyrosine kinase signaling including chronic myelogenous leukemia.
Ganciclovir
This drug, a synthetic analog of 2-deoxyguanosine is an antiviral medication used to treat cytomegalovirus (herpesvirus) infections. The cancer gene therapy strategy involves the introduction of suicide genes that converts a non toxic pro-drug into a toxic derivative. Ganciclovir is converted to the triphosphate and is incorporated into DNA by actively dividing cells. This stalls the DNA polymorso londina to a conlieation block resulting in the cell undergoing apoptosis
Gardasil and HpV
Tumours are classified by
A.Their ability to spread
B.The tissue of origin
C.The person who discovered them
D.Whether they are benign or malignant
Answer is b
