Unit 3.1

Cancer-risk factors

-carcinogens -tobacco -obesity (eating processed foods, red meat, alcohol) -viruses and bacteria (vaccination can prevent) -harmful environments (pollutants, radiation exposure, wear sunscreen)

Somatic mutation (nonhereditary) vs. germline

Typically germinal mutations are not expressed in the individual containing the mutation (germ cells give rise to gametes, some gamete s will carry the mutation and it will be passed on to the next generation) Cancer is a somatic mutation! Somatic mutations do not occur in cells that give rise to gametes, the mutation is not passed along to the next generation by sexual means.

immunotherapy

a cancer therapy that uses the immune system to recognize and destroy cancer cells. some cancers evade the immune system bc they produce a molecule on their surface that signals immune cells to leave the cancer cell alone. immunotherapy uses antibodies to block these cancer molecules so the cell can be recognized and killed by the immune system. proven effective for melanoma, lung, and kidney cancer.

targeted therapy

a cancer therapy this is specific for cancer cells and not harmful to normal cells. often by combatting a specific defect in a cancer cell (ex: mutated protein made from an oncogene or tumor suppressor)

malignant tumor

a cancerous tumor whose cells can spread throughout the body. have the capacity to metastasize (invade other tissues and spread) after several more mutations, a malignant tumor may result.

Cell cycle checkpoint

a cellular mechanism that ensures that each stage of the cell cycle is completed accurately. at one checkpoint, proteins scan dna for damage or incorrect base pairing. If problems are detected, one of 2 things happens: either the cell ramps up DNA repair mechanisms (giving itself time to fix DNA mistakes) or if the damage is sever/irreparable, the checkpoints direct a cell to commit suicide (apoptosis)

Mutation

a change in the nucleotide sequence of DNA. it may have been inherited, it may have occurred randomly during DNA replication, or it may have been the result of an environmental insult.

contact inhibition

a characteristic of normal cells that prevents them from dividing once they have filled a space and are in contact with their neighbors. as genetic mutations accumulate, cancerous cells usually lose this property, so cells grow on top of each other.

cancer

a disease of unregulated cell division. vast majority of cancers are caused by mutations that occur during a person's lifetime (acquired mutations). a small minority of cancers run in families, due to inheritance of mutations in cancer-associated genes. cancer kills by crowding out normal cells and invading organs, causing them to fail. cancer cells secrete a variety of chemicals that wreak havoc on the body's biochemistry.

tumor

a mass of cells resulting from uncontrolled cell division.

benign tumor

a noncancerous tumor whose cells will not spread throughout the body. cells divide more frequently than cells in normal tissues, but do not spread to other areas, so much less dangerous. After one or two "hits" (mutations), a benign tumor may form.

centromeres

a specialized region of a chromosome where the sister chromatids are joined; it is critical for proper alignment and separation of sister chromatids during mitosis.

mutagen

any chemical or physical agent that can damage DNA by changing its nucleotide sequence. aka agents that cause mutations in DNA. not all mutagens originate outside the body (some of the reactions that occur int he mitochondria during cellular respiration produce DNA-damaging molecules called free radicals)

radiation therapy

beams of ionizing (high-energy) radiation are focused on a tumor damages DNA in dividing cells. cancer cells are less able to repair this DNA damage (compared to normal cells) so the cells die.

as people age

cancer affects people more as they age: as cells accumulate mutations over time through exposure to carcinogens and repeated rounds of cell division, the chances increase that a cell will accumulate enough mutations to become cancerous.

chromosomes in humans

complete set of 46

multi-hit model of cancer

each "hit" is a mutation, and multiple hits are needed the cause the disease. in most cases, hereditary cancer occurs only when additional, non-hereditary mutations in a cell accumulate. the accumulation of harmful acquired mutations in a cell can lead to cancer, even in someone with no genetic predisposition.

stem cells

immature cells that can divide and differentiate into specialized cell types

mutagens

many components of the environment, our food, and even our cells can cause mutations. - radiation - chemicals - infectious agents (hepatitis C) - cellular reactions (produce mutagenic free radicals)

BRCA1

mutated gene in a particular region of chromosome 17. unusually common in families where breast cancer is common.

how cancer is formed in cells

mutations occasionally slip thru the cell cycle and divide. (especially likely if the mutations affect genes that code for proteins that function as checkpoints! as additional mistakes accumulate in these cells) when cells accumulate enough dna damage to interfere w/multiple checkpoints, the result is cancer

genes mutated

mutations that cause cancer typically occur in two types of genes that influence the cell cycle: proto-oncogene and tumor suppressor genes.

Proto-oncogene

normal proto-oncogenes activate cell division, but only in response to appropriate signals. when mutated, the can become permanently turned on, stimulating cells to divide all the time. in this state they are called "oncogenes" (translation: "genes that cause cancer") oncogenes = proto-oncogenes that have mutated to become permanently activated, drive cells to divide continually. (it's like the accelerator is stuck down and cell division keeps going)

Tumor suppressor gene

normal tumor suppressor genes make proteins that normally pause cell division, repair damaged DNA, or initiate apoptosis (suicide) mutations can inactivate this gene, causing cancer. (it's like the breaks are broken and the cell division can't be stopped) the BRCA proteins are tumor suppressors.

mutations from DNA replication error

on average, 1 mutation occurs for every 10 billion base pairs that are replicated.

Apoptosis

programmed cell death, often referred to as cellular suicide. when the cell checkpoint cycle detects damage which is sever and irreparable. this cellular suicide prevents cells from producing more damaged daughter cells.

Metastasis

spread of cancer from original site to other parts of the body

types of mutations

study: page 221 table 10.1

carcinogen

substances that are known to cause cancer, or increase its risk of forming. most carcinogens are mutagens.

treating cancer

surgery is generally effective for solid tumors that are diagnosed early, but not for cancers that have spread or cancers that don't produce tumors (like leukemia) in these cases, the best option is usually chemotherapy. treat tumor with radiation therapy radiation and chemo cause severe side effects bc they damage all dividing cells, including healthy cells.

angiogensis

the growth of new blood vessels. cancer cells promote the growth of new blood vessels (angiogenesis) to acquire oxygen and nutrients for growth.

anchorage dependence

the need for normal cells to be in physical contact with another layer of cells or a surface. cancer cells usually lose this constraint, so are enabled to detach and spread.

Cell cycle

the ordered sequence of stages through which a cell progresses in order to divide. preparatory phases and division phases.

cytokinsesis

the physical division of a cell into two daughter cells.

cell differentiation

the process by which a cell becomes specialized to carry out a specific role by turning specific genes on and off and making different suites of proteins.

BRCA1 and BRCA2

the proteins help to repair dna damage, specifically a type of damage called a double-strand break. when mutated, no longer can repair this damage so additional mutations (genetic mistakes) accumulate eventually leading to cancer. BRCA1 is in chromosome 17, BRCA2 is in chromosome 13.

hereditary (inherited) cancer

the risk of getting cancer is inherited, cancer itself is not inherited. cancer can't be passed from parent to child, it means that they have inherited a genetic mutation (from one or both parents. this makes the development of cancer much more likely. inherited mutations account for about 5-10% of all cancers. the other 90-95% of cancers are caused by non-inherited (acquired) mutations.

mitosis

the segregation and separation of replicated chromosomes during cell division.

metastasis

the spread of cancer cells from one location in the body to another. malignant tumors have the capacity to metastasize.

interphase

the stage of the cell cycle in which dividing cells spend most of their time, preparing for cell division. there are three distinct subphases: G1, S, G2.

mitotic spindle

the structure that separates sister chromatids during mitosis. the chromosomes are pushed and pulled into position by protein fibers of the mitotic spindle.

Sister chromatids

the two identical dna molecules that result from the replication of a chromosome during S phase.

chemotherapy

using toxic chemicals to kill the cancer cells in the body. work by interfering with one or more steps of the cell cycle in dividing cells. interfere with cell division.

BRCA mutation and breast cancer

women with mutated BRCA genes who have not yet developed cancer, ovary removal cuts risk of breast cancer by 50% and risk of ovarian cancer by 90%. Double mastectomy cuts risk of breast cancer by 95%.

mammogram

x-ray of the breast. best primary screening method for breast tumors.