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Carcinomas

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90% of all cancers; arise from epithelial cells which cover internal and external body surfaces (lung, breast and colon)

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Sarcomas

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develop from supporting tissues- bone, cartilage, fat and muscle

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Lymphomas and Leukemias

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arise from cells of blood and lymphatic origin

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Lymphoma

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tumors grow as solid masses of tissue

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Leukemia

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cancer cells proliferate mainly in the bloodstream

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2 Lethal Properties of Cancer

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1) ability to proliferate uncontrollably 2) ability to spread throughout the body

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Tumor

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mass of growing tissue resulting from cancer

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Cancer

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abnormal type of tissue growth; some cells divide and accumulate in uncontrolled and autonomous fashion leading to a progressive increase in the number of dividing cells -Malignant tumor

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Do tumors always divide more rapidly than normal tissue?

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no- the issue is the balance between cell division and cell differentiation or cell death

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Cell differentiation

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cells acquire specialized properties to distinguish different types of cells; as they acquire they traits, they usually lose ability to divide; ex. basal skin cell divides: one stays in basal layer and maintains ability to divide, other cell moves toward surface, differentiates, makes keratin and flattens, and loses ability to divide

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cell differentiation results

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no increase in number of cells, new cells are made to replace the dying ones and one retains the ability to divide

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Tumor differentiation

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cell division is uncoupled from differentiation and cell death, and so greater numbers of cells are produced than needed; growth of tumor regardless of speed of division

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Benign Tumor

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grow in confined local area and are rarely dangerous

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Malignant Tumor

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invade surrounding tissue, enter bloodstream, and spread to distant parts of the body

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Anchorage-independent growth

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cancer cells grow well when anchored to a surface and when freely suspended in liquid or semi-solid medium (normal cells need anchor)

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Anchorage safe guards

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when normal cells cannot anchor to something like an integrin, apoptosis occurs so they do not float away and start a new life somewhere else, cancer cells are not destroyed in this way

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Density dependent inhibition of growth

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cells will divide until surface of the culture is covered w/ single layer of cells; cancer cells have reduced sensitivity to this, they will begin to pile up

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Cancer and telomeres

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most cells are restricted by their telomere length for how many times they can divide, but cancer cells replenish some of the telomere and overcome this problem by keeping telomere length above threshold

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Mechanisms for telomere lengthening

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1) producing telomerase 2) enzymes that exchange DNA sequence info between chromosomes

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How do cancer cells proliferate uncontrollably

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1) defects in signaling pathways- they alterate signaling pathways, like those involving growth hormones 2) Cell cycle control issues- arent arrested at G1 even in bad conditions or if DNA is damaged 3) Apoptosis- they have means to block apoptosis, which should normally kill them

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Angiogenesis

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growth of blood vessels; tumors release signals for surrounding tissue so that they can grow beyond a tiny localized clump

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first experiments involving tumors and blood vessels

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tumors could not grow on isolated thyroid, but regained the ability when injected into animals tumors could not grow large when on outside of eye, but when placed near iris, it took over the blood vessels and could grow large

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angiogenesis exp involving chambers

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cancer cells placed in chambers with pores and inserted into animals: new capillaries proliferate normal cells: no stimulation of vessel growth conclusion: cancer cells make molecules that activate angiogenesis in surrounding tissue

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VEGF/FGF

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vascular endothelial growth factor and fibroblast growth factor; when these proteins are released by tumors, they bind to receptor proteins on endothelial cells activating a pathway making the endo cells divide and secrete MMPs which breakdown extracell matrix so that the endo cells can migrate to the surrounding tissue - the proliferating endo cells become organized into hollow tubes

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Angiogenesis inhibitors

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many exist and the angiogenesis activators must overcome them to work

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Invasion

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direct migration of cancer cells into neighboring tissues

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Metastasis

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cancer cells enter bloodstream and travel and form tumors (metastases) that are not connected to the primary tumor

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3 Steps of Metastasis

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1) cancer cells invade surrounding tissue and penetrate into the bloodstream 2) transport via circulatory system 3) leave blood stream and enter organs where they establish new metastic tumors

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3 means of invading surrounding tissue and vessels

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1) decreased cell-cell adhesion 2) increased motility 3) Protease Production

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Decreased adhesin

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cells lack or have defective surface proteins; cancer cells have less E-cadherin; cells can more readily disassociate from tumor

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increased motility

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stimulated by surrounding tissue or cancer cells themselves, some serve as chemoattractants for migrating cancer cells

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Production of Proteases

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degrade protein containing structures that would normally inhibit cancer cell movement; they degrade basil lamina (once to get into underlying tissue and again to get into vessels)

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Basal lamina

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protein layer between epithelial and underlying tissues, cancer cells secrete proteases to break through

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Plasmin

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cancer cells secrete a plasmigen activator to form plasmin from plasminogen; it can: -degrade components of basal lamina and extracell matrix -cleaves inactive precursor of MMPs so they are active and degrade bl and em

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Life in the bloodstream

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some cells go through lymphatic vessels and into lymph nodes, but will move on from there into blood; blood is inhospitable and only 1/1000 cells can survive

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differential metastasizing ability

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cells that are repeated isolated and reinjected from metastases are selected for in terms of how well they metastasize; clones of original tumor cells show varying abilities to metastasize

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Determinants of Sites of Metastasis

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1) blood flow patterns- after most tumors enter bloodstream, they go to lungs, where they get stuck in caps and enter lungs; cancers of stomach and colon enter bloodstream and are first brought to liver 2) interactions between cancer cells and environment of particular tissues they are delivered to- bone cells have growth factors that stimulate prostate cancer growth

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Immune system surveillance theory

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immune destruction of cancer cells is common; cancer reflects the occasional failure of an adequate response to these cells

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How does cancer overcome the immune response

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1) immune system more successful in protecting from virus-induced cancer while more common types are not affected 2) tumors express different antigens; tumor cells eliciting smaller immune response are selected for 3) produce molecules that kill T lymphocytes 4) surround themselves w/ dense tissue 5) rapidly divide so immune system can't keep up

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Tumor Microenvironment

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includes: normal cells, extracell molecules, and components of extracell matrix; can allow or assist cancer cells in growing and metastasizing, or can inhibit their growth

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Epidemiology

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investigation of frequency and distribution of diseases in human populations; helps identify particular agents as carcinogens; once identified as correlations, experiments must be done to determine causal link

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Environment/Lifestyle vs heredity

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studies indicate that environment and lifestyle are more important; Japanese who move to US have cancer rates similar to US rates as opposed to Japan's

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Precarcinogens

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a chemical capable of causing cancer, but only after it has been metabolically activated ( like 2-naphthylamine, which causes bladder cancer, but only after it has been activated in the liver)

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Ames Test

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measures mutagenic activity; bacteria lacking the ability to produce histidine are placed on a culture with the chemical to be tested which has been previously incubated with liver enzymes (in case they are precarcinogens); total number of colonies is a measure of mutagentic effect; -correlation between mutagentic effect and ability to cause cancer

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Types of DNA damage caused by carcinogens

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-binding to DNA and disrupting base-pairing -generating cross-links between two strands of double helix -creating chemical links btwn adjacent bases -hydroxylating or removing bases -breaking one or more DNA strands - can even target specific genes

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3 Stages of Cancer Development

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Initiation Promotion Tumor Progression

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Initiation

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normal cells converted to precancerous state; they cause DNA mutation that puts cells in this state

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Promotion

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stimulates altered cells to divide and form tumors; more gradual process- prolonged or repeated exposure to promoting agent -they stimulate proliferation

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Tumor Progression

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tumor cell propterties change and acquire more aberrant traits and become increasingly aggressive -driving force= tumor cells w/advantages(increased growth rate, invasiveness, ability to survive bloodstream and immune attack etc) are selected for

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how do cancer cell properties change in the tumor progression stage

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-new mutations -changes in gene expression (epigenetic changes)

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X-ray

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create DNA mutations -cause cancer in direct proportion of dose administered

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Ionizing Radiation

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radiation emitted by radioactive elements -remove electrons from molecules which makes highly reactive ions which cause DNA damage (ie. single and double stranded breaks)

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UV Radiation

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sunlight damages DNA and causes cancer -it triggers pyrimidine dimer formation (CC-TT)

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How do we know skin cancer is caused by sunlight

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it induces dimer formation, and this affects the p53 gene; it preferentially involves base changes that alter amino acids (1 and 2 bases in a codon) opposed to changing the third base which would not affect the amino acid sequence

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Oncogenic virus

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virus that causes cancer; discovered by rous when he ground up tumor tissue and passed it through a filter that not even bacteria could pass through, and put it into a healthy chicken who developed sarcoma; the sarcoma was transmitted via agent smaller than bacteria

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Burkitt Lymphoma

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lymphocytic cancer of neck and jaw that occured in periodic epidemics localized to specific regions (he proposed it was an infectious agent)

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EBV

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Epstein-Barr virus, responsible for Burkitt Lymphoma 1)EBV DNA and proteins found in tumor cells but not in normal cells of same individual 2) Adding EBV to normal cells in culture causes them to acquire some cancer cell properties 3) injection of EBV(monkies) causes lymphomas to arise

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Infectious agents that can cause cancer

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viruses, bacteria, and parasites - identifying them opens door to treatment, like HPV vaccines

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mechanism of infectious agents causing cancer

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1) cause tissue destruction and inflammation; immune system tries to destroy them, and in the process produces mutagenics (oxygen free radicals) 2) certain viruses stimulate the proliferation of infected cells (either through viral genes or host cell genes) -affects viral cancers and cancers caused by chems or radiation

Molecular Bio CH 24.1 – Flashcards

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