Cancer biology
52 flashcards covering Cancer biology for the MCAT Biology & Biochemistry section.
Cancer biology explores how normal cells transform into malignant ones, leading to uncontrolled growth and potential spread throughout the body. It involves key processes like DNA mutations, disruptions in cell cycle regulation, and the role of oncogenes and tumor suppressor genes. This topic is essential in biology because it explains one of the most common diseases affecting humans, helping us understand risk factors, prevention, and treatment strategies that save lives.
On the MCAT, cancer biology appears in Biology & Biochemistry questions that test concepts like cell signaling pathways, genetic alterations, and tumor progression through multiple-choice formats. Common traps include mistaking benign growths for cancerous ones or overlooking environmental influences on mutation rates. Focus on integrating knowledge of apoptosis, angiogenesis, and metastasis, as questions often require applying these to scenarios or experiments. For better preparation, practice linking these ideas to clinical examples.
Terms (52)
- 01
Cancer
Cancer is a disease characterized by uncontrolled cell growth and the potential to invade other tissues, often due to genetic mutations that disrupt normal cell regulation.
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Tumor
A tumor is a mass of cells that results from abnormal cell proliferation, and it can be either benign, meaning it stays in one place, or malignant, meaning it can spread.
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Benign tumor
A benign tumor is a non-cancerous growth that does not invade surrounding tissues or spread to other parts of the body, though it may still cause problems by compressing nearby structures.
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Malignant tumor
A malignant tumor is a cancerous growth that can invade nearby tissues and metastasize to distant sites in the body, leading to serious health risks.
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Metastasis
Metastasis is the process by which cancer cells spread from the primary tumor to other parts of the body through the bloodstream or lymphatic system, establishing new tumors.
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Oncogene
An oncogene is a mutated form of a normal gene that promotes cell division and can contribute to cancer development when activated, often by promoting uncontrolled growth.
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Proto-oncogene
A proto-oncogene is a normal gene that regulates cell growth and division, but when mutated or overexpressed, it can become an oncogene that drives cancer progression.
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Tumor suppressor gene
A tumor suppressor gene is a normal gene that inhibits cell division or promotes cell death, and its loss or inactivation can allow cancer cells to proliferate unchecked.
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p53 gene
The p53 gene is a tumor suppressor that halts the cell cycle in response to DNA damage, allowing for repair or triggering apoptosis if the damage is irreparable, and its mutation is common in cancers.
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Rb gene
The Rb gene, or retinoblastoma gene, is a tumor suppressor that prevents the cell cycle from progressing from G1 to S phase by binding to transcription factors, and its inactivation can lead to uncontrolled division.
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Apoptosis
Apoptosis is a programmed cell death process that eliminates damaged or unnecessary cells, and cancer often involves mechanisms to evade this process, allowing cells to survive inappropriately.
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Cell cycle
The cell cycle is the series of events that a cell undergoes as it grows and divides, consisting of phases like G1, S, G2, and M, and its dysregulation is a hallmark of cancer.
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G1 phase
The G1 phase is the first gap phase in the cell cycle where the cell grows and prepares for DNA replication, and abnormalities here can contribute to uncontrolled cancer growth.
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S phase
The S phase is when DNA replication occurs in the cell cycle, ensuring each daughter cell gets a complete set of chromosomes, and errors in this phase can lead to genetic mutations in cancer.
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G2 phase
The G2 phase is the second gap phase where the cell checks for DNA damage after replication and prepares for mitosis, with checkpoints that, if faulty, can promote cancer.
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M phase
The M phase is when mitosis occurs, dividing the cell's nucleus and cytoplasm to produce two daughter cells, and disruptions here can result in abnormal cell division seen in tumors.
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G1 checkpoint
The G1 checkpoint ensures the cell is ready to replicate DNA by checking for growth factors and DNA integrity, and its failure can allow damaged cells to proceed, contributing to cancer.
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G2 checkpoint
The G2 checkpoint verifies that DNA replication is complete and accurate before mitosis, and defects in this checkpoint can lead to the propagation of mutations in cancer cells.
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Cyclins
Cyclins are proteins that regulate the cell cycle by activating cyclin-dependent kinases at specific phases, and their overexpression can drive the uncontrolled proliferation seen in cancer.
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Cyclin-dependent kinases
Cyclin-dependent kinases are enzymes that, when bound to cyclins, phosphorylate proteins to advance the cell cycle, and their dysregulation is implicated in many cancers.
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Mutation
A mutation is a change in the DNA sequence that can alter gene function, and in cancer, somatic mutations often accumulate, leading to uncontrolled cell growth.
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Carcinogen
A carcinogen is any substance or agent that can cause cancer by damaging DNA or promoting mutations, such as tobacco smoke or UV radiation.
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Angiogenesis
Angiogenesis is the formation of new blood vessels, which tumors promote to supply themselves with nutrients and oxygen, enabling growth and metastasis.
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Hypoxia
Hypoxia is a low-oxygen condition in tissues that can occur in tumors, triggering signaling pathways that promote angiogenesis and further cancer progression.
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Telomeres
Telomeres are protective caps at the ends of chromosomes that shorten with each cell division, and in cancer cells, telomerase often maintains them to allow unlimited replication.
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Telomerase
Telomerase is an enzyme that adds nucleotides to telomeres, preventing their shortening, and its activation in cancer cells contributes to their immortality.
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DNA repair mechanisms
DNA repair mechanisms are cellular processes that fix DNA damage to maintain genomic integrity, and defects in these can lead to the accumulation of mutations that cause cancer.
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Mismatch repair
Mismatch repair is a DNA repair pathway that corrects errors made during DNA replication, and mutations in its genes, like those in Lynch syndrome, increase cancer risk.
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Base excision repair
Base excision repair is a process that removes and replaces damaged bases in DNA, and its failure can result in mutations that contribute to cancer development.
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Nucleotide excision repair
Nucleotide excision repair removes bulky DNA lesions caused by UV light or chemicals, and deficiencies in this pathway are linked to skin cancers.
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BRCA1 and BRCA2 genes
BRCA1 and BRCA2 are tumor suppressor genes involved in DNA repair, particularly homologous recombination, and their mutations significantly raise the risk of breast and ovarian cancers.
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Ras gene
The Ras gene is a proto-oncogene that encodes a protein in signal transduction pathways for cell growth, and its mutations can lead to constant activation, promoting cancer.
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Signal transduction pathways
Signal transduction pathways relay external signals to the cell's interior to regulate processes like growth, and their dysregulation, such as in the MAPK pathway, is common in cancer.
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Growth factors
Growth factors are proteins that stimulate cell division and are often overexpressed in cancer, leading to autocrine signaling that drives tumor growth.
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EGFR
EGFR, or epidermal growth factor receptor, is a cell surface receptor that, when mutated or overexpressed, can promote uncontrolled cell proliferation in various cancers.
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Epigenetic changes
Epigenetic changes are modifications to DNA or histones that affect gene expression without altering the sequence, and they can silence tumor suppressor genes in cancer.
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Cancer stem cells
Cancer stem cells are a subset of tumor cells that can self-renew and differentiate, contributing to tumor initiation, growth, and resistance to therapy.
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Immune evasion
Immune evasion is the ability of cancer cells to avoid detection and destruction by the immune system, often through downregulating antigens or creating an immunosuppressive environment.
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Tumor microenvironment
The tumor microenvironment is the surrounding tissue that includes blood vessels, immune cells, and stroma, which can support cancer growth and influence treatment responses.
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Hallmarks of cancer
The hallmarks of cancer are key characteristics that define malignant cells, such as sustained proliferative signaling, evasion of growth suppressors, and potential for metastasis.
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Aneuploidy
Aneuploidy is an abnormal number of chromosomes in cells, which is common in cancer and can result from errors in cell division, leading to genomic instability.
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Genomic instability
Genomic instability is a state where a cell's genome is prone to mutations and chromosomal rearrangements, accelerating cancer development by providing more genetic variations.
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Loss of heterozygosity
Loss of heterozygosity occurs when one allele of a gene is lost, and if it's a tumor suppressor, this can lead to complete inactivation, promoting cancer.
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Knudson's two-hit hypothesis
Knudson's two-hit hypothesis states that both alleles of a tumor suppressor gene must be inactivated for cancer to develop, as seen in retinoblastoma.
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Viral oncogenes
Viral oncogenes are genes from viruses like HPV that can integrate into host DNA and promote cancer by interfering with cell cycle regulation.
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Hyperplasia vs. neoplasia
Hyperplasia is an increase in cell number without abnormal growth, while neoplasia is uncontrolled, abnormal proliferation that can lead to cancer, a common point of confusion.
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Carcinoma
A carcinoma is a cancer that arises from epithelial cells, which line organs and surfaces, and it is one of the most common types encountered in clinical settings.
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Sarcoma
A sarcoma is a cancer that originates in connective tissues like bone or muscle, differing from carcinomas in its tissue of origin and behavior.
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Autophagy in cancer
Autophagy is a cellular process that degrades and recycles components, and in cancer, it can either suppress tumor formation or promote survival under stress conditions.
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Invasion and migration
Invasion and migration refer to the ability of cancer cells to move through tissues and enter the bloodstream, key steps in metastasis.
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Tumor heterogeneity
Tumor heterogeneity is the presence of diverse cell populations within a tumor, which can affect treatment responses and lead to resistance.
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Oncogenic viruses
Oncogenic viruses, such as Epstein-Barr virus, can cause cancer by integrating their genetic material into host cells and disrupting normal regulation.