Cancer MCQ Quiz in मल्याळम - Objective Question with Answer for Cancer - സൗജന്യ PDF ഡൗൺലോഡ് ചെയ്യുക

Key Points

• All genes whose genetic and epigenetic changes contribute to the causation of cancer is described as cancer-critical genes.
• These genes contribute to the transformation process by driving cell proliferation or reducing sensitivity to cell death and differentiation.
• These genes may be involved in the following processes:

1. Cell cycle progression (e.g. RB1, MYC)
2. Differentiation process (e.g. APC)
3. DNA repair (e.g. ATM, BRCA)
4. Cell death (e.g. BCL2)

• Cancer-critical genes are grouped into two broad classes, according to whether the cancer risk arises from a gain-of-function mutation of a gene, or loss-of-function mutation.
• Genes for which a gain-of-function mutation drives a cell toward cancer, are called proto-oncogenes.
• Whereas genes for which a loss-of-function mutation creates the cancer are called tumor suppressor genes.
• Tumor suppressor genes can directly or indirectly inhibit cell growth.
• Those that directly inhibit cell growth or promote cell death are known as gatekeepers and their activity is rate limiting for tumor cell proliferation.
• Those tumor suppressor genes that do not directly suppress proliferation, but function to promote genetic stability are known as caretakers.
• Caretakers function in DNA repair pathways and elimination of caretakers results in increased mutation rates.
• Five broad classes of genes are generally grouped into tumor-suppressor genes:

• Genes encoding checkpoint-control proteins that arrest the cell cycle, if DNA is damaged (e.g. p53))
• Genes that promote apoptosis.
• Genes that encode enzymes that participate in DNA repair.

Concept:

Retroviruses

• The first cancer-inducing (oncogenic) retrovirus, the avian sarcoma virus, was isolated by Peyton Rous in 1911.
• By the late 1970s, the study of retrovirally induced cancers led to the discovery of oncogenes, cellular genes that induce tumors when they are abnormally expressed.
• Retroviruses also cause serious human diseases such as acquired immune deficiency syndrome (AIDS) and adult T-cell leukemia.

 Explanation:

• Retroviruses cause tumors by a wide variety of mechanisms, but a common theme is the activation of oncogenes.
• Induction of tumors by nonacutely transforming retroviruses is due to retroviral insertion adjacent to cellular proto-oncogenes.
• Retroviral integration is mutagenic since the proviral genome is inserted at random into regions of actively transcribed chromatin.
• When a retrovirus integrates near a cellular proto-oncogene tumors frequently result because the viral LTR acts as a dominant control element that stimulates aberrant expression of the oncogene.
• The central role of proto-oncogenes in cancer and in regulating normal cell growth and differentiation has expanded study of these molecules beyond the bounds of retrovirology.

Correct option: 4) may carry cellular protooncogenes in their genome 

Concept:

• Tumor suppressor proteins play a critical role in inhibiting the proliferation of cells that could lead to tumor development. Their functions involve regulating the cell cycle, repairing DNA damage, and initiating cell death (apoptosis) if damage cannot be repaired. They act as part of the body's defense against uncontrolled cell growth and cancer.
• Cellular oncogene activation is just one of two different genetic changes that contribute to tumor formation; the other is the inactivation of tumor suppressor genes.
• Genetic changes that either boost gene expression or cause uncontrolled activity of the oncogene-encoded proteins cause oncogenes to promote abnormal cell proliferation.
• The opposite side of cell growth control is represented by tumor suppressor genes, which typically work to prevent tumor development and cell proliferation.
• These genes are frequently lost or inactivated in tumors, eliminating any inhibitors of cell growth and promoting the uncontrolled growth of tumor cells.

Explanation:

• A particular class of protein known as a tumor suppressor protein controls cell growth and reproduction to thwart the emergence of cancer.
• Tumor growth may be aided by the loss or reduction of tumor suppressor proteins' function by mutations in the genes that code for those proteins.
• Among their many actions, tumor suppressor proteins can promote cell death, prevent cell division, or fix DNA harm.
• Oncogenes, in comparison, are genes that encourage cell division and growth, and their activation or overexpression can aid in the formation of tumors.
• Tumor suppressor proteins can be rendered inactive by oncogenes, which results in the loss of their tumor-suppressive properties.

Key Pointsa) is one whose action causes a tumor to progress.

• This statement is incorrect. Tumor suppressor proteins act to prevent tumors from developing or progressing, not cause them.

b) is a protein whose loss of function can lead to cancer.

• A genetic link to tumors describe the function or nature of tumor suppressor proteins. The statement is more about the genetic basis of cancer rather than specifically about tumor suppressor proteins.

• Tumor suppressor proteins are encoded by tumor suppressor genes, and the loss of function or inactivation of these genes can contribute to tumor development because the cell loses critical regulatory mechanisms that normally prevent uncontrolled cell growth, evade apoptosis, and maintain genomic stability.

• Tumor suppressor genes, when functioning correctly, help prevent the formation of tumors by controlling cell growth and division, repairing DNA damage, and ensuring cells undergo programmed cell death (apoptosis) when necessary. Mutations or deletions in these genes can remove these controls, leading to cancer development. In this context, the statement highlights the crucial link between genetic factors (specifically mutations or inactivation in tumor suppressor genes) and the ensuing risk of tumor formation.

c) are rendered inactive by oncogenes.

• While there is an interaction between oncogenes and tumor suppressor genes in cancer development, saying that tumor suppressor proteins are "rendered inactive by oncogenes" oversimplifies the relationship. Oncogenes can promote cell growth, while mutations or deletions in tumor suppressor genes can fail to inhibit this growth. However, the inactivation of tumor suppressor genes often happens through mutations or deletions within the tumor suppressor genes themselves, not directly by oncogenes.

d) stops the cell cycle from progressing by phosphorylating cyclins.

• This statement misunderstands the mechanism of action of tumor suppressor proteins. In fact, tumor suppressor proteins, such as pRb (retinoblastoma protein), can inhibit the cell cycle, but they typically do so not by phosphorylating cyclins but rather by other means, such as inhibiting cyclin-dependent kinases (CDKs) or controlling the transcription of genes necessary for cell cycle progression. It's worth noting specifically that pRb inhibits the cell cycle by preventing the phosphorylation of itself by CDKs, thereby halting the progression of the cell cycle from the G1 phase to the S phase.

Concept:

• Four phases are typical for malignancies. The size and location of the tumor are two criteria that affect the precise stage:
• Stage I: Cancer has not progressed to the lymph nodes or other tissues and is contained in a small location.
• Stage II: Cancer has expanded but not yet metastasized.
• Stage III: Cancer has gotten bigger and may have gotten into other tissues, like lymph nodes.
• Stage IV: Additional organs or parts of your body that have been affected by cancer. Additionally known as metastatic or advanced cancer, this stage.

Explanation:

• The correct sequence of tumor development is:
  • Initiation
  • Promotion
  • Progression
  • Metastasis​
• The earliest stage of tumor development is called initiation, and it occurs when a genetic mutation or other change in a cell's DNA triggers the start of uncontrolled cell growth.
• The stage of promotion is when the started cells are encouraged to multiply more and create a preneoplastic lesion.
• The preneoplastic lesion progresses into a malignant tumor at this stage, acquiring additional genetic and epigenetic changes that provide the cancer cells a survival advantage.
• The ultimate stage of tumor development is known as metastasis, in which cancer cells travel from the primary tumor to distant areas in the body through the lymphatic or circulatory systems, causing the creation of secondary tumors that can be fatal.

Therefore, the correct answer is option 2.

The correct answer is B and D only.

Explanation:

• Apoptosis, or programmed cell death, is a tightly regulated biological process crucial for maintaining cellular homeostasis and eliminating damaged or unnecessary cells.
• The intrinsic pathway of apoptosis is mediated by mitochondrial signals and involves the release of cytochrome C, which interacts with apoptotic protease activating factor-1 (Apaf-1) and caspase-9 to form the apoptosome. This complex activates downstream effector caspases, leading to cell death.
• Caspase-9 plays a central role in the intrinsic pathway as the initiator caspase that activates the executioner caspases (e.g., caspase-3).
• A loss-of-function mutation in caspase-9 can impair the apoptotic process, leading to defective cell death mechanisms.

Statement A: Loss of mitochondrial membrane potential and release of cytochrome C

• This statement is incorrect. The loss of mitochondrial membrane potential and the release of cytochrome C occur upstream of caspase-9 activation.
• These events are mediated by pro-apoptotic members of the Bcl-2 family, such as Bax and Bak, and are not directly affected by a caspase-9 mutation.

Statement B: Reduced formation of the apoptosome and defective initiation of apoptosis

• This statement is correct. Caspase-9 is a key component of the apoptosome. A mutation in the caspase-9 gene would impair the assembly or functionality of the apoptosome, leading to defective initiation of apoptosis. This would disrupt the intrinsic pathway of cell death.

Statement C: Inability to activate the death receptors

• This statement is incorrect. Death receptors (such as Fas and TNF receptors) are part of the extrinsic pathway of apoptosis, which is independent of caspase-9.
• Mutations in caspase-9 would not directly affect the activation of death receptors.

Statement D: Become resistant to UV irradiation-induced cell death

• This statement is correct. UV irradiation induces DNA damage, which activates the intrinsic pathway of apoptosis. A loss-of-function mutation in caspase-9 would impair this pathway, making cells resistant to UV-induced apoptosis.

Key Points

• Cystic fibrosis is a genetic disorder caused by mutations in the CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) gene located on chromosome 7.
• The CFTR gene mutation leads to thick mucus production that blocks airways and other ducts in the body.
• Cystic fibrosis primarily affects the lungs, pancreas, and digestive system.
• Common symptoms include chronic respiratory infections, difficulty breathing, digestive issues, and infertility in males.

Important Points

• The CFTR gene mutation involves a deletion of the amino acid phenylalanine at position 508 (ΔF508), which is the most common mutation causing cystic fibrosis.
• Cystic fibrosis is inherited in an autosomal recessive pattern; both parents must pass down a defective gene for the child to develop the disorder.
• Early diagnosis and treatment can help improve the quality of life and life expectancy for individuals with cystic fibrosis.

The correct answer is 2-hydroxyglutarate, α-ketoglutarate

Explanation:

• Glioblastomas, oligodendrogliomas, and astrocytomas are types of gliomas, which are cancers originating in glial cells of the brain or spinal cord.
• These cancers frequently harbor mutations in the enzyme isocitrate dehydrogenase (IDH), specifically IDH1 and IDH2.
• Normally, IDH enzymes are involved in the citric acid (Krebs) cycle, where they catalyze the oxidative decarboxylation of isocitrate to produce α-ketoglutarate (also known as 2-oxoglutarate).
• However, mutations in IDH (commonly R132H in IDH1 and R172K in IDH2) lead to a gain-of-function activity, wherein the enzyme converts α-ketoglutarate into an oncometabolite called 2-hydroxyglutarate (2-HG).
• This oncometabolite, 2-HG, accumulates in cancer cells and disrupts cellular metabolism by inhibiting enzymes dependent on α-ketoglutarate, such as histone and DNA demethylases.
• The inhibition of these enzymes leads to widespread epigenetic changes, such as hypermethylation of DNA and histones, driving tumorigenesis by altering gene expression.
  • 2-hydroxyglutarate (2-HG): This is the oncometabolite produced as a result of IDH mutations. It is responsible for the pathological effects seen in gliomas with IDH mutations. The accumulation of 2-HG inhibits several α-ketoglutarate-dependent enzymes, disrupting normal cellular processes and promoting cancer development.
  • α-ketoglutarate: This is the natural substrate of IDH enzymes in normal cells. In mutated IDH, α-ketoglutarate is abnormally converted into 2-HG instead of being utilized in the Krebs cycle or other cellular pathways. α-ketoglutarate is also an essential cofactor for several enzymes involved in DNA and histone demethylation, which are inhibited by 2-HG.

The correct options are: 1, 3, 4

Explanation:

• Formation of membrane-bound apoptotic bodies:
  During apoptosis, the cell breaks down into smaller, membrane-bound vesicles called apoptotic bodies. These bodies contain cellular debris and are eventually engulfed by macrophages or neighboring cells, preventing inflammation.

• DNA condensation and fragmentation into small fragments:
  In apoptosis, the DNA undergoes condensation and fragmentation into smaller fragments. This is a key event in the process and can be observed as a distinct pattern of DNA cleavage, often referred to as "DNA laddering."

• Disruption of mitochondrial membrane potential, leading to cytochrome c release:
  The mitochondria play a crucial role in apoptosis. A loss of mitochondrial membrane potential allows cytochrome c to leak out of the mitochondria into the cytoplasm, where it activates caspases, leading to the execution phase of apoptosis.

• Rapid expansion of cell size followed by membrane rupture:
  This is not a feature of apoptosis. Instead, in apoptosis, the cell shrinks (pyknosis) rather than expands, and the membrane remains intact until the formation of apoptotic bodies. The rupture of the membrane is typically seen in necrosis, not apoptosis.

• Caspase activation is central to apoptosis. Caspases are a family of proteases that mediate the dismantling of the cell during apoptosis.
• Apoptosis is a programmed, controlled process that prevents inflammation and damage to surrounding tissues, unlike necrosis, which is a result of cell injury and often leads to inflammation.

The correct option is: 1

Explanation:

• Apoptosis is a controlled process of cell death involving cell shrinkage, chromatin condensation, membrane blebbing, and disassembly into apoptotic bodies, which are then phagocytosed without causing inflammation.
• Apoptosis plays a critical role in removing damaged, infected, or excess cells, contributing to processes like tissue development, immune response, and cancer prevention.
• Necrosis is an uncontrolled form of cell death, typically caused by external factors such as trauma or lack of oxygen. It leads to cell swelling, rupture of the plasma membrane, and release of intracellular contents, which often causes inflammation and damage to surrounding tissue.
• Necrosis is often pathological, resulting from severe stressors like infection, chemical damage, or physical trauma, and can lead to tissue injury and a strong immune response due to the inflammatory response.

The correct answer is Development of red blood cells from hematopoietic stem cells.

Concept:

• Programmed Cell Death: This is a regulated process by which cells undergo an orderly death to serve a beneficial role in the organism, such as apoptosis during development and immune responses.

Explanation:

• Formation of the neural tube during embryonic development: This involves programmed cell death to remove certain cells and shape the developing neural tube.
• Apoptosis of webbed fingers in developing hands: This is a classic example of programmed cell death (apoptosis) that removes the webbing between fingers in the developing embryo.
• Development of red blood cells from hematopoietic stem cells: This is incorrect as an example of programmed cell death. Red blood cell development (erythropoiesis) is a process of cell differentiation and maturation, not cell death. It involves the production of new cells rather than the elimination of old ones via programmed cell death.
• Elimination of infected or damaged cells by immune cells: This often involves inducing apoptosis in the infected or damaged cells to prevent the spread of infection and remove dysfunctional cells.

Additional Information:

• Apoptosis: A form of programmed cell death that is crucial for development and homeostasis in multicellular organisms. It involves cell shrinkage, DNA fragmentation, and membrane blebbing, leading to the orderly elimination of cells without causing inflammation.
• Erythropoiesis: The process in the bone marrow where hematopoietic stem cells differentiate into red blood cells, characterized by cell division and maturation instead of cell death.