Oncology MCQ 1

Cancer cells divide uncontrollably and can invade nearby tissues and spread to other parts of the body (metastasis).

These agents can damage DNA and increase the risk of cancer. Examples include viruses (like HPV), bacteria (like Helicobacter pylori), and parasites (like Schistosoma haematobium).

This checkpoint checks for sufficient nutrients and undamaged DNA before allowing the cell to enter the S phase (DNA replication).

This repair mechanism is prone to errors, potentially introducing mutations. It joins DNA ends together without the need for a template, making it less precise.

These genes act as 'brakes' to control cell growth. When they are mutated or inactivated, they can contribute to cancer development by allowing cells to grow uncontrolled.

DNA replication occurs in this phase where all the DNA is copied for the two daughter cells.

Rb protein prevents the cell from moving into the S phase (DNA replication) until specific conditions are met. This acts as a control mechanism to prevent uncontrolled cell growth.

The process relies on a homologous strand to serve as a template for accurately repairing damaged DNA. This method ensures that the sequence is corrected precisely.

Apoptosis is a process of programmed cell death. Overexpression of Bcl-2 protein prevents cells from undergoing apoptosis, allowing tumor cells to survive and proliferate.

The MAPK pathway (Mitogen-Activated Protein Kinase) is a signaling cascade involved in cell growth, proliferation, and differentiation. Its activation in cancer promotes uncontrolled cell division and tumor development.

CD8+ T-cells play a vital role in the immune system by directly killing infected or cancerous cells. They recognize and destroy tumor cells through antigen-specific recognition and the release of cytotoxic molecules.

The Warburg effect (aerobic glycolysis) describes the metabolic adaptation of cancer cells where they rely heavily on glucose fermentation for energy even in the presence of oxygen. This allows for rapid growth and nutrient acquisition.

The tumor microenvironment is the surrounding tissue that supports tumor growth. It provides nutrients, growth factors, and signals that promote tumor proliferation, angiogenesis, and evasion from the immune system.

ATM (Ataxia Telangiectasia Mutated) is a checkpoint protein essential for recognizing and responding to DNA damage. It activates DNA repair mechanisms and can trigger cell cycle arrest to prevent the proliferation of damaged cells.

Loss of contact inhibition is a hallmark of cancer characterized by the ability of cells to proliferate even when they are in contact with other cells. This allows for uncontrolled growth and formation of tumors.

Radiation therapy works by inducing DNA damage in cancer cells, causing cell death and halting tumor growth. Targeted radiation delivery aims to damage tumor cells while sparing healthy tissues.

p53 is a tumor suppressor gene that plays a crucial role in regulating cell cycle progression and preventing uncontrolled cell growth. It can induce apoptosis or arrest the cell cycle in response to DNA damage.

Evading immune destruction is a hallmark of cancer that allows tumor cells to avoid detection and elimination by the immune system. This occurs through mechanisms like immune suppression and immune evasion.

Neoantigens are unique tumor-specific proteins not present in normal cells. They are a key target for the immune system to recognize and attack cancerous cells.

Autoimmune diseases happen when the immune system mistakenly attacks healthy cells in the body as if they were foreign invaders.

The escape phase describes the situation where cancer cells successfully evade the immune system's attacks and continue to grow unchecked.

Dendritic cells act like messengers that collect bits of foreign material (antigens) and present them to T-cells to launch a targeted immune response.

The immunosurveillance theory explains how the immune system constantly monitors tissues for cancer cells and eliminates them before they develop into tumors.

The neoantigen-MHC complex is a structure that allows T-cells to recognize and attack cancer cells specifically. It's formed when a neoantigen is displayed on the surface of a cancer cell.

IFN-γ (Interferon gamma) is a key player in tumor immunity. It helps kill cancer cells and attracts other immune cells to join the fight.

The equilibrium phase is a delicate balancing act where the immune system keeps the tumor growth in check, preventing it from spreading too quickly.

Adaptive immunity, unlike innate immunity, is highly specific to a particular invader. It learns and remembers past encounters, mounting a stronger and more effective response upon re-infection.

Darwinian microevolution in cancer refers to the process where the existing tumor cells develop resistance to immune attack due to random mutations that make them less recognizable to the immune system.

Helicase is an enzyme that unwinds the DNA double helix, separating the two strands to prepare them for replication. It breaks the hydrogen bonds holding the base pairs together, creating a replication fork.

Mismatch repair deficiency disrupts the process of correcting errors that occur during DNA replication. Without proper mismatch repair, mutations accumulate leading to genomic instability, which is a hallmark of many cancers.

Anti-PD-1 antibodies block the interaction between the PD-1 protein on T cells and its ligands PD-L1 and PD-L2, which are expressed on tumor cells. By blocking this interaction, the antibodies prevent the tumor from suppressing the immune response.

CAR-T cells are genetically engineered T cells with a chimeric antigen receptor (CAR) that allows them to specifically target and kill cancer cells. Natural T cells rely on MHC-I for activation, while CAR-T cells have a customized receptor to recognize specific antigens.

Hypoxia, or low oxygen levels, promotes angiogenesis, the formation of new blood vessels. This is because tumors need a constant supply of oxygen and nutrients to grow, and hypoxia triggers the release of pro-angiogenic factors.

Cdk1/Cyclin B is a protein complex that plays a central role in regulating the G2/M checkpoint. This checkpoint ensures that the cell has completed DNA replication and is ready for mitosis before proceeding to cell division.

Neoantigens are unique antigens that are presented on the surface of tumor cells. They arise from mutations within the tumor's DNA and are often recognized by the immune system as non-self. This makes them potential targets for immunotherapy.

CAR-T cell therapy directly involves engineered immune cells. T cells are extracted from the patient, genetically modified to express a CAR that targets specific cancer cells, and then infused back into the patient.

Variolation, a practice in 16th century China, involved intentionally infecting individuals with a weak form of smallpox virus to induce immunity. It predates Edward Jenner's vaccination by nearly two centuries.

William Coley observed a spontaneous tumor remission in an osteosarcoma patient after a severe erysipelas infection. This observation led him to hypothesize that infections could be used to treat cancer.

Cancer is characterized by uncontrolled cell division that can invade nearby tissues and potentially spread to other parts of the body (metastasis).

The G1/S checkpoint ensures that a cell has sufficient nutrients and that its DNA is undamaged before being allowed to replicate its DNA (S phase) .

Non-homologous end joining (NHEJ) is a DNA repair mechanism that joins broken DNA ends together without using a template. This process is error-prone, potentially leading to mutations.

Tumor suppressor genes are responsible for controlling cell growth. When they are mutated, they lose their ability to regulate cell division, contributing to cancer development.

The S phase is where a cell replicates its entire DNA content to prepare for division.

The Rb protein acts like a gatekeeper, preventing the cell from entering the S phase until specific conditions are met, effectively preventing uncontrolled cell growth.

Homologous Recombination (HR) repairs broken DNA using an undamaged copy of the same DNA sequence as a template, ensuring accurate repair.

Bcl-2 protein overexpression prevents apoptosis (programmed cell death), allowing tumor cells to survive and proliferate.

Overexpression of growth promoting pathways like MAPK (Mitogen-Activated Protein Kinase) can promote tumor growth and development.

CD8+ T cells are cytotoxic lymphocytes that directly kill cancer cells by recognizing and eliminating them. They are a key part of the immune system's fight against cancer.

The Warburg effect describes a metabolic adaptation of cancer cells where they rely heavily on aerobic glycolysis, even in the presence of oxygen, to quickly obtain energy for growth.

Evading immune destruction is a hallmark of cancer that allows tumor cells to avoid detection and elimination by the immune system. Cancer cells can achieve this by suppressing immune responses or by expressing molecules that help them evade detection and destruction.

A PET scan measures the uptake of a radioactive glucose analog in tissues. This can help detect cancer cells, as they often take up glucose at a higher rate than normal cells.

Anti-PD-1/PD-L1 therapy is a type of immunotherapy that uses antibodies to block the interaction between PD-1 on T cells and its ligands PD-L1 and PD-L2 on tumor cells. This helps to reactivate the immune system's ability to fight cancer.

Angiogenesis is the process of forming new blood vessels. This is important for cancer development, as tumors need a steady supply of blood to grow and survive.

B-cells are a type of white blood cell that are part of the adaptive immune system, playing a role in producing antibodies to target specific pathogens.

The escape phase of immunoediting is when tumor cells have successfully developed mechanisms to evade the immune system's attack, and the tumor continues to grow unchecked.

BRCA1 protein is involved in DNA repair, particularly in homologous recombination, which is vital for repairing double-strand breaks in DNA, preventing mutations.

IL-10 is a cytokine that suppresses immune responses. In the tumor environment, its effect can help suppress immune cell activity, allowing tumors to evade the immune system.

Tumor-associated macrophages (TAMs) reside in the tumor microenvironment, and they can promote tumor growth by suppressing immune responses and releasing pro-angiogenic factors to support tumor vascularization.

Anti-VEGF therapy targets the process of angiogenesis by blocking the activity of vascular endothelial growth factor (VEGF), hindering the formation of new blood vessels and reducing tumor growth.

Dendritic Cells (DCs) act as messengers of the immune system, by picking up antigens (fragments of invaders) and presenting them to T cells, triggering an immune response against cancer cells.

Proton Therapy is a specialized form of radiation therapy that uses protons to deliver radiation precisely to the tumor, minimizing damage to surrounding healthy tissues.

Helicase unwinds the DNA double helix, separating the two strands to prepare them for replication.

Mismatched repair (MMR) deficiency disrupts the process of correcting errors that occur during DNA replication, leading to mutations and genomic instability in cancer cells.

Unique proteins expressed by tumor cells but not by normal cells. They act as targets for the immune system to identify and attack cancerous cells.

The immune system's ability to recognize and destroy cancer cells, preventing them from forming tumors.

Proposed by Paul Ehrlich, it suggests that the immune system patrols the body and eliminates cancerous cells as they develop, acting as a defense mechanism against tumor formation.

The second phase of the Immunoediting theory, where a balance exists between the immune system and the tumor. The immune system controls tumor growth, but it doesn't completely eliminate it. This can lead to a period of dormancy.

During the initial stage of the Immunoediting theory, the immune system tries to completely eliminate tumor cells, primarily through the activity of NK cells and T cells.

Neoantigens are derived from mutations in cancer cells. These mutations can occur in both coding and non-coding regions of the genome, resulting in new proteins or altered sequences that are unique to the tumor cells. These unique proteins allow immune cells to recognize cancer cells as different from normal cells.

Allergies are an immune response caused by an overreaction of the immune system to harmless substances, like pollen or food, triggering the release of histamine and other chemicals.

The tumor cells acquire mutations and mechanisms to evade the immune system's attacks, leading to uncontrolled growth and spread.

Dendritic cells are specialized antigen-presenting cells that engulf and process antigens, then present them to T cells, activating a tailored immune response.

Immunosurveillance theory, while a strong foundation, struggles to fully explain the progression of tumors in individuals with functioning immune systems. Some cancers develop and spread without being completely eliminated by the immune system. The theory's limitations highlight the need for further research into the complex interactions between tumor cells and the immune system.

The neoantigen-MHC complex is a structure formed when a neoantigen (a mutated protein from the cancer cell) binds to an MHC molecule on the surface of the cancer cell. This complex is recognized by T cell receptors (TCRs) on T cells, triggering an immune response against the cancer cell.

IFN-γ (Interferon gamma) is a powerful cytokine that plays a crucial role in activating and directing the immune response against tumors. It induces apoptosis (programmed cell death) in tumor cells and attracts other immune cells to the site of the tumor.

During the equilibrium phase of immunoediting, the immune system maintains a control over tumor growth, preventing it from becoming aggressive and spreading rapidly. This can result in a period of dormant tumor cells.

Adaptive immunity is characterized by its specificity and memory. It learns to recognize specific antigens from pathogens it has encountered before and mounts a more targeted and effective response if it encounters the same antigen again. This makes adaptive immunity more effective in fighting specific invaders, including cancers.

During the equilibrium phase of immunoediting, the immune system acts as a selective pressure on tumor cells. This pressure can drive the evolution of cancer cells, leading to the development of new escape mechanisms to evade immune recognition and grow unchecked.

Heat shock proteins (HSPs) and IFN-γ are danger signals released by stressed or damaged cells, including early tumor cells. These signals attract immune cells to the site of the tumor, triggering an immune response.

Coley's toxin, a mixture of bacterial toxins, was used to treat cancer by stimulating the immune system to fight against the tumor. It demonstrated that infections could boost immune responses, leading to a notable regression in tumor size.

The thymus is a primary lymphoid organ where T cells undergo maturation and selection. During this process, T cells that are self-reactive (those that could attack the body's own cells) are removed. This ensures that only T cells capable of recognizing foreign antigens are allowed to mature.

Innate immunity provides an immediate, non-specific response to a wide range of threats. It's the body's first line of defense, activated by pattern recognition receptors (PRRs) that recognize common pathogen-associated molecular patterns (PAMPs). This rapid response is essential to contain infections and prevent the spread of pathogens.

Downregulation of MHC-I (Major Histocompatibility Complex Class I) molecules is a strategy used by tumor cells to evade the immune system. MHC-I molecules present antigens to CD8+ T cells, triggering their activation. By reducing MHC-I expression, the tumor becomes less visible to T cells.

Cancer-associated fibroblasts (CAFs) are transformed fibroblasts that play a crucial role in creating a tumor-friendly environment. They build a dense collagenous barrier around the tumor, which acts as a physical shield, limiting the ability of immune cells to access the tumor and destroy it.

VEGF (Vascular Endothelial Growth Factor) is a cytokine that promotes angiogenesis ( the formation of new blood vessels). In the context of tumor immunity, VEGF can increase vascular permeability, making it difficult for immune cells to reach the tumor.

Tumors can downregulate the expression of Fas (death receptors) on their cell surface, making them less susceptible to apoptosis induced by Fas ligand (FasL), a protein released by T cells that signals cell death. This resistance to apoptosis allows tumor cells to survive and proliferate.

The Warburg effect is a metabolic adaptation of cancer cells, where they rely heavily on glycolysis (glucose fermentation) for energy production even in the presence of oxygen. This shift from aerobic metabolism to glycolysis is associated with rapid tumor growth and increased glucose consumption.

The tumor microenvironment often lacks sufficient oxygen and glucose due to rapid tumor growth and poor blood supply (hypoxia). This nutrient depletion leads to anergy in T cells, reducing their ability to fight the tumor.

Lactate produced by tumor cells can lower the pH of the tumor microenvironment, creating an acidic environment. This acidity inhibits the function and activity of immune cells, making it harder for the immune system to effectively fight the cancer.

Hypoxia (low oxygen levels) in the tumor microenvironment suppresses the activity of immune cells. This makes it harder for immune cells to perform their functions and effectively target cancer cells.

IL-10 (Interleukin-10) is a cytokine that plays a role in suppressing immune responses. In the context of tumor immunity, IL-10 can increase T-cell sensitivity to apoptosis, promoting their death and limiting the immune response against the tumor.

M1 macrophages are pro-inflammatory, while M2 macrophages are anti-inflammatory and contribute to tumor progression by suppressing anti-tumor immunity. In a tumor-rich environment, M1 macrophages can be reprogrammed to display M2-like phenotypes, contributing to tumor survival and growth.

Tumors can produce non-functional ligands (molecules that bind to receptors) that can block chemokine receptors, such as CXCR3 on immune cells. This disrupts the immune cells' ability to navigate to the tumor, hindering their ability to effectively combat the cancer.

Regulatory T cells (Tregs), a subpopulation of T cells, play a crucial role in suppressing immune responses, preventing autoimmunity. In the context of tumor immunity, Tregs dampen the immune response against tumor cells, allowing the tumor to escape immune attack and grow unchecked.

Fibroblasts, when converted into CAFs (Cancer-associated fibroblasts), contribute to the formation of a dense collagenous barrier around the tumor, acting as a physical barrier that restricts immune cell infiltration and hinders their ability to reach and destroy cancer cells.

In the tumor microenvironment, CD4+ T cells can become reprogrammed to express Treg markers, a key feature of regulatory T cells. This transformation is crucial for tumor immune evasion, as Tregs suppress the immune response, leading to decreased tumor recognition and elimination.

Tumors upregulate the expression of soluble ligands (molecules that interact with receptors) that engage with inhibitory receptors on NK cells. This interaction suppresses the activity of NK cells, allowing the tumor to evade their killing mechanisms.

The tumor microenvironment is characterized by high lactate levels and low oxygen availability, which creates unfavorable conditions for immune cells. This metabolic inhibitory mechanism diminishes immune cell function, making them less effective at fighting the tumor.

T cells are highly sensitive to glucose depletion. In the tumor microenvironment, where glucose is often scarce, T cells are unable to maintain their energy levels and become functionally impaired, hindering their ability to mount a successful attack against the tumor.