In Burkitt's lymphoma, the Myc proto-oncogene is often converted into an oncogene. What is the most common mechanism for its overproduction in this cancer?
Explanation
This question focuses on a specific example of oncogene activation, illustrating how a chromosomal translocation can lead to cancer by deregulating the expression of a key gene like Myc.
Other questions
What are the two defining heritable properties of cancer cells?
Cancers that arise from epithelial cells are known as carcinomas. Approximately what percentage of human cancers do these account for?
The Philadelphia chromosome, a specific chromosomal abnormality that provides evidence for the clonal origin of cancer, is characteristically found in chronic myelogenous leukemia (CML). This abnormality is created by a translocation between which two chromosomes?
According to tumor genome sequencing data, approximately how many proteins with an altered amino acid sequence does a typical cancer cell contain, with the majority being passenger mutations?
The p53 gene is a critical tumor suppressor that is frequently altered in cancer. In what approximate percentage of all human cancers is the p53 gene found to be mutated?
What is the Warburg effect, a metabolic characteristic of many tumor cells?
How do oncogenes and tumor suppressor genes differ in their genetic effect on a cell?
The first human oncogene was identified by transfecting DNA from human tumor cells into cultured mouse cells. This led to the discovery of a mutated version of which gene?
The discovery of the first tumor suppressor gene, Rb, came from studying which rare type of human cancer?
Based on current estimates from large-scale genomic sequencing projects, what is the approximate total number of human genes that are strongly suspected to be cancer-critical for at least one type of tumor?
Infections with viruses, bacteria, or parasites are related to a significant minority of human cancers. What percentage of cancers worldwide are accounted for by such infections?
Certain strains of human papillomavirus (HPV) can cause cancer of the uterine cervix. The viral oncogenes E6 and E7 are primarily responsible. What are the two key host-cell tumor suppressor proteins that the E6 and E7 proteins target and inactivate?
The cancer therapy strategy known as synthetic lethality exploits a cancer cell's existing genetic weaknesses. PARP inhibitors are effective in killing cancer cells that have defects in which two specific DNA repair genes?
The drug imatinib (Gleevec) was a landmark in targeted cancer therapy. It was designed to specifically inhibit which oncogenic protein, characteristic of chronic myelogenous leukemia (CML)?
What is the primary reason that cancer incidence generally rises steeply with age?
What is the biological process that allows invasive cancer cells to break loose, enter blood or lymphatic vessels, and form secondary tumors at other sites in the body?
Most cancers are thought to derive from a single abnormal cell. What is the phenomenon called whereby an initial mild disorder of cell behavior evolves gradually into a full-blown cancer through successive rounds of mutation and selection?
In addition to genetic mutations, what other type of persistent, heritable change in gene expression, resulting from modifications of chromatin structure, is a fundamental feature of cancer development?
Many human cancer cells avoid replicative cell senescence, a built-in limit to cell proliferation, by reactivating which enzyme that maintains the ends of chromosomes?
What is the primary function of the tumor suppressor protein Rb?
According to the text, what is the most common mechanism for eliminating the second, good copy of a tumor suppressor gene like Rb in a cell that has already lost the first copy?
In the analysis of glioblastoma genomes, mutations were found to cluster into three key functional pathways. Which of the following is NOT one of those three core pathways?
The tumor suppressor PTEN is a phosphatase that is commonly mutated in cancer. What is the primary function of PTEN?
Which condition is NOT listed as a form of cellular stress that can activate the p53 pathway?
In the progression of most colorectal cancers, what is typically the first or earliest genetic alteration observed, detected at high frequency even in small benign polyps?
The APC protein is a tumor suppressor central to colorectal cancer development. Its loss leads to the excessive activity of which signaling pathway?
Hereditary nonpolyposis colorectal cancer (HNPCC), or Lynch syndrome, predisposes individuals to colorectal cancer. Mutations in which class of genes are responsible for this syndrome?
What is the estimated percentage of cancer deaths that can be attributed to modifiable risk factors like smoking, diet, and physical inactivity, suggesting they are potentially avoidable?
The chemical carcinogen aflatoxin B1 is produced by fungi that contaminate foods like peanuts and is a major cause of liver cancer in some regions. How does it become damaging to DNA?
Trastuzumab (Herceptin) is an antibody-based therapy used to treat about 25% of breast cancers. What is the specific target of this antibody?
The immune checkpoint inhibitor therapy targeting PD-1 or its ligand PD-L1 works by overcoming an immunosuppressive mechanism used by tumors. What is the primary function of the PD-1/PD-L1 interaction?
Some cancers evolve resistance to multiple cytotoxic drugs simultaneously, a phenomenon known as multidrug resistance. This often correlates with the amplification of a gene that encodes what type of protein?
What is the term for the supporting connective tissue, immune cells, and vascular cells associated with a carcinoma?
What is the typical diameter of a human tumor when it first becomes palpable, containing roughly 1 billion cells?
What is a benign tumor, such as an adenoma, distinguished from a malignant tumor, like an adenocarcinoma?
The phenomenon of chromothripsis, which can promote rapid steps in cancer evolution, refers to what type of genomic event?
Cancer stem cells are thought to be responsible for the growth of some tumors. What is the key difference between a cancer stem cell and a transit amplifying cell within a tumor?
What is the term for the dependence of most normal cells on attachment to a substratum for growth, proliferation, and survival, a control that is often lost in cancer cells?
What is the fate of most circulating tumor cells (CTCs) that enter the bloodstream or lymphatics?
How can a gain-of-function mutation in the gene for isocitrate dehydrogenase (IDH) contribute to tumorigenesis?
What is the key difference between a 'driver' mutation and a 'passenger' mutation in a cancer cell?
Which bacterium is cited as a major cause of stomach cancer due to its ability to cause chronic inflammation?
Cancers with defects in DNA mismatch repair, such as HNPCC, exhibit a specific type of genetic instability. What is the most notable characteristic of this instability?
The Ras proto-oncogene is mutated in about 30% of all human cancers. What is the biochemical consequence of these mutations?
What is a key reason that a single oncogene is generally not enough to turn a normal cell into a cancer cell, as shown by experiments in transgenic mice expressing Myc or Ras?
In the process of tumor metastasis, what is generally considered the most difficult and rate-limiting step for a cancer cell?
Which class of cancer-critical genes is typically identified by experiments that add DNA to tester cells to see if it causes cancerous transformation?
What is the typical cell-death mechanism that occurs on a massive scale in the interior of large solid tumors due to difficult living conditions like a lack of oxygen and nutrients?
The development of a tumor relies on a two-way communication between cancer cells and the supporting tumor stroma. What is the process by which tumors stimulate the formation of new blood vessels to support their growth?