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What are carcinogens quizlet

What are carcinogens quizlet

Термины в модуле (33)

1) Activation of oncogenes
2) Inactivation of TSGs, progress inhibitor receptors, apoptosis proteins, and so on.
3) Inactivation of DNA restore
4) Inactivation of antioxidant response

-Could also be epigenetic – change in gene expression however no DNA harm
-induce cell proliferation however not mutagenic

Observe: Initiated cells reply otherwise to promotor than regular cells

2) Promotion
a) Outcomes from publicity to a selling agent
b) Induces cell proliferation which is reversible, however doesn’t alter DNA
c) Will increase the probability of a second genetic mutation

Oblique-acting Compounds:
-Require metabolic conversion to generate the last word carcinogen (most cigarette carcinogens, for instance, should be transformed to carcinogenic kind and are thus INDIRECT-acting compounds)

Busulfan, cyclophosphamide, chlorambucil, and melphalan are direct performing alkylating brokers that switch alkyl teams (e.g. CH3-, C2H5-) to DNA’s guanine residues

Metabolized by P450-dependent blended perform oxidase product of the CYP1A1 gene to kind electrophilic epoxides that react with proteins, RNA and DNA.
->Polymorphisms on this gene play a major position in the truth that solely roughly 15% of people who smoke get lung most cancers.

Metabolized by way of cytochrome P450
-Give rise to a extremely reactive carbonium ion
-people who metabolize these quicker are at a better threat for most cancers than those that do not metabolize it in any respect (individuals who do not metabolize it do NOT accumulate the metabolites and do not get cell harm)

Present in cigarette smoke

Metabolized by way of cytochrome P450 into carcinogenic kind

Related to the rubber trade
->working for rubber trade = elevated incidence of urothelial carcinomas

Metabolized by way of cytochrome P450 within the liver into epoxides (very similar to polycyclic hydrocarbons in smoke)
->Epoxides bind to guanine of p53 gene = mutation -> no DNA restore
->Thus, it could possibly induce hepatocellular carcinoma

Naturally produced by the fungus Aspergillus flavus rising on improperly saved grain and peanuts

within the context of the immune protection results in elimination of remodeled cells -> very true within the case of acute inflammatory the place cytotoxic immune cells kill most cancers cells

Overexpressed in most cancers cells in addition to the mobile elements of the stroma (e.g. fibroblasts, endothelial cells, inflammatory cells, and osteoclast) that assist the tumor development

UVB radiation (290 – 320 nm) results in DNA photoadducts
->CC to TT transitions is the molecular signature of daylight publicity

-Inflammatory cells produce ROS, up regulate inflammatory genes (COX-2) ensuing within the manufacturing of prostaglandins (PGs)
->Promotors for cell division

-Predisposes the contaminated B cell to rearrange immunoglobulin genes, purchase the t(8;14) translocation that causes the lymphoma
->LMP-1 upregs bcl-2 intrinsic apoptosis suppressor and prompts c-myc growth-promoting pathways
-The lymphomas are characterised by quite a few macrophages surrounded by a transparent zone giving a “starry sky” look. All the opposite cells are malignant B cells.

-Widespread in HIV contaminated sufferers
-Neoplastic, spindle formed endothelial cells lining blood-filled vascular channels -> appear to be bulbous bloody balloons

What are carcinogens quizlet

Термины в модуле (59)

2) effectivity and constancy of DNA restore (how good you physique is at repairing broken DNA, particularly the reapair course of that ought to right the kind of mutation that the chemical has induced)

mutagens are extra electrophilic than the DNA construction so that they are in a position to displace a few of the atoms or electrons within the DNA as a result of mutagens have the next affinity for electrons

-nucleophilicity of accessible bases (the mutagen desires to bind to DNA that’s much less nucleophillic so that’s might be succesfull in outcompeting the DNA for the electron)

-chemical construction of the compound (does the construction enable it to combine and get near the molecule that’s desires to change)

-enzyme effectivity (how environment friendly are the enzymes that are in you physique that may restore the harm the mutagen causes)

a promoter will broaden the mutation that has already occured since by rising how typically a cell replicates, the extra seemingly it’s to have some form of error that may result in a mutaiton

inside molecular epidemiology we will have a look at:
-molecular dosimetery
-inherited most cancers predisposition
-human most cancers threat evaluation

molecular epidemiology (molecular dosimetry appears at inside publicity, inherited most cancers predisposition lookds at host susceptibility assesment, human most cancers threat evaluation)

you must think about the route of how you’ll be uncovered, whether it is one thing you’ll ingest or one thing that will are available contact along with your pores and skin, you must check the potential carcinogen in the identical approach

What are carcinogens quizlet

Термины в модуле (33)

1. p21 induces ______________.

2. GADD induces ___________.

3. BAX induces ____________.

___________% of cancers are environmentally induced, which embrace CHEMICAL, PHYSICAL, and MICROBIAL.

Direct performing carcinogens _____________ (do/do not) require metabolic activation.

1. direct-acting carcinogens are _____________ and bind to nucleophilic DNA to kind carcinogen-DNA adducts.

2. indirect-acting carcinogens want ___________________ into electrophilic species.

2. metabolic activation

_____________ and _________________ are an instance of a nitrogen mustard that will increase threat of leukemia. It’s a _______________ agent.

1. INITIATION: Carcinogen is already, or turns into metabolically activated to kind _________________. These bind to DNA forming ____________________. If DNA restore mechanisms do not work and the cell lives, you will have an initiated cell.

2. PROMOTION: ___________________ of initiated cell, forming a _________________ clone.

2. clonal enlargement, preneoplastic

Corn and peanuts coated by small mildew growths, which produces _________________, a carcinogen when metabolized.

various spectrum of p53 genes

1. decrease vitality kind however can harm collagen, deeper in pores and skin

2. most associated to most cancers. T-T dimers.

Japan: elevated threat of leukemia, strong tumors

1. HPV E6 inhibits ________, which usually prompts _________ to induce apoptosis

1. HPV E6 inhibits p53. BAX.

Promotion: initiated cells grow to be tumor or pre-neoplastic. Promoters are non-carcinogenic or weak carcinogens.

Hepatitis B Virus

Hepatitis C Virus

HPV: over-expression E6 (inhibit p53) and E7 (inhibit Rb), cervical most cancers (squamous cell carcinoma)

EBV: epithelium of oropharynx and B-lymphocytes (Burkitt’s lymphoma. c-myc oncogene attributable to translocation)

HepB: bind p53, hepatocellular carcinoma (HCC)

HepC: ssRNA, power liver illness, cirrhosis, HCC

Two of the primary kinds of genes that play a job in most cancers are oncogenes and tumor suppressor genes.


Proto-oncogenes are genes that usually assist cells develop. When a proto-oncogene mutates (modifications) or there are too many copies of it, it turns into a “unhealthy” gene that may grow to be completely turned on or activated when it’s not imagined to be. When this occurs, the cell grows uncontrolled, which might result in most cancers. This unhealthy gene is known as an oncogene.

It could be useful to think about a cell as a automobile. For it to work correctly, there have to be methods to regulate how briskly it goes. A proto-oncogene usually capabilities in a approach that’s very similar to a fuel pedal. It helps the cell develop and divide. An oncogene could possibly be in contrast with a fuel pedal that’s caught down, which causes the cell to divide uncontrolled.

Just a few most cancers syndromes are attributable to inherited mutations of proto-oncogenes that trigger the oncogene to be turned on (activated). However most cancer-causing mutations involving oncogenes are acquired, not inherited. They typically activate oncogenes by:

  • Chromosome rearrangements: Adjustments in chromosomes that put one gene subsequent to a different, which permits one gene to activate the opposite
  • Gene duplication: Having further copies of a gene, which might result in it making an excessive amount of of a sure protein

Tumor suppressor genes

Tumor suppressor genes are regular genes that decelerate cell division, restore DNA errors, or inform cells when to die (a course of generally known as apoptosis or programmed cell demise). When tumor suppressor genes do not work correctly, cells can develop uncontrolled, which might result in most cancers.

A tumor suppressor gene is just like the brake pedal on a automobile. It usually retains the cell from dividing too shortly, simply as a brake retains a automobile from going too quick. When one thing goes mistaken with the gene, reminiscent of a mutation, cell division can get uncontrolled.

An necessary distinction between oncogenes and tumor suppressor genes is that oncogenes consequence from the activation (turning on) of proto-oncogenes, however tumor suppressor genes trigger most cancers once they are inactivated (turned off).

Inherited abnormalities of tumor suppressor genes have been present in some household most cancers syndromes. They trigger sure kinds of most cancers to run in households. However most tumor suppressor gene mutations are acquired, not inherited.

For instance, abnormalities of the TP53 gene (which codes for the p53 protein) have been discovered in additional than half of human cancers. Acquired mutations of this gene seem in a variety of cancers.