Chapter 23. Cancer Development Flashcards

1
Q

Aneuploid

A

Abnormal karyotype with more or fewer than 23 pairs of chromosomes

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2
Q

Benign

A

Altered cell growth that is harmless and does not require intervention.

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3
Q

Blood-borne metastasis

A

Release of tumor cells into the blood. Most common cause of cancer spread

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4
Q

Carcinogenesis

A

Cancer development

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5
Q

Carcinogen

A

Any substance that changes the activity of genes into a cell so that the cell becomes a cancer cell

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6
Q

Commitment

A

Occurrence in which early embryonic cells start changing into differentiated cells

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7
Q

Doubling time

A

Amount of time it takes for a tumor to double in size

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8
Q

Euploid

A

Having the correct number of chromosome pairs for the species

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9
Q

Metastasize

A

To spread cancer from the main tumor site to many other body sites
˜Metastasis occurs when cancer cells move from the primary location by breaking off from the original group and establishing remote colonies.
˜Even though the tumor is now in another organ, it is still a cancer from the original altered tissue. For example, when breast cancer spreads (primary tumor) to the lung and the bone, it is still breast cancer in the lung and bone-not lung cancer and not bone cancer
˜Metastasis occurs through:
ØExtension into surrounding tissues by secreting enzymes that open up areas of surrounding tissue, or pressure created as the tumor increases in size, forces tumor cells to invade new territory
ØBlood vessel penetration can spread to distant organs and tissues
ØRelease of tumor cells is bloodborne metastasis as enzymes secreted by the tumor cells also make large pores in the blood vessels, allowing tumor cells to enter the blood and circulate throughout the body.
ØInvasion is when conditions in the remote site can support tumor cell growth, the cells stop circulating (arrest) and invade the surrounding tissues, creating secondary tumors
ØLocal seeding is when tumor cells circulate through the blood and enter tissue at remote sites
ØLymphatic spread is related to the number, structure, and location of lymph nodes and vessels. Primary sites that are rich in lymphatics have more early metastatic spread than areas with few lymphatics

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10
Q

Mitosis

A

Cell division

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11
Q

Mitotic index

A

The percentage of actively dividing cells within a tumor

Mitotic index less than 10% is slow growing; index of 85% is fast growing.

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12
Q

Neoplasia

A

A new or continued cell growth not needed for normal development or replacement of dead and damaged tissues. Always abnormal. Has a parent cell that was normal. May not always cause harm.

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13
Q

Oncogene

A

Proto-oncogene that has been turned on and can cause cells to change from normal cells to cancer cells. They are early embryonic genes that have been turned off.

Oncogene activation is the main mechanism of carcinogenesis regardless of the specific cause
About 70 different oncogenes have been identifies. These oncogenes are not abnormal genes but are part of every cell’s normal makeup. Oncogenes become a problem only if they are overexpressed as a result of exposure to carcinogenic agents or events. Both external and personal factors can activate oncogenes

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14
Q

Oncogenesis

A

Cancer development

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15
Q

Ploidy

A

The number and appearance of chromosomes used to describe cancer cells

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16
Q

Pluripotency

A

The unlimited potential of early embryonic cells to mature into any body cell; also called multi potency or totipotency

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17
Q

Primary prevention

A

Strategies used to avoid or delay the actual occurrence of a specific disease. Avoidance of carcinogens, Modifying associated factors, Removal of at risk tissues such as moles, polyps, breasts, Chemoprevention which are drugs that’ll reduce risk, Vaccination
˜Avoidance of known or potential carcinogens (e.g., wear sun screen, do not smoke, avoid asbestos)
˜Modification of associated factors such as alcohol intake, diet high in fat and low in fiber, obesity, multiple sex partners
˜Removal of “at-risk” tissues include removing moles to prevent conversion to skin cancer, polyps from colon, breast

˜Chemoprevention uses drugs, chemicals, natural nutrients, to disrupt one or more steps in cancer development (e.g., aspirin and Celebrex to reduce risk of colon cancer, the use of vitamin D and tamoxifen to reduce the risk for breast cancer, and lycopene to reduce the risk for prostate cancer)
˜Vaccination such as Gardasil to prevent several forms of the human papilloma virus (HPV)

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18
Q

Promoters

A

A substance that promotes or enhances growth of the initiated cancer cell; maybe a hormone, drug, or chemical, viruses

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19
Q

Secondary prevention

A

Early detection of a disease or condition, sometimes before signs and symptoms are evident, to prevent or limit permanent disability or death
Yearly mammogram and physical exam over 40
Colonoscopy at 50 and every 10 years
Yearly fecal occult blood for adults
Yearly prostate specific antigen and digital rectal exam for men over 50
Altering damage genes
Genetic screening

˜Regular screening
˜Altering damaged genes
˜Genetic screening

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20
Q

Staging

A

System of classifying clinical aspects of a cancer tumor

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21
Q

Suppressed Gene

A

A particular gene that has been turned off

22
Q

Expressed

A

When a particular gene has been turned on

23
Q

Generation time

A

The time it takes one cell to divide into two cells

24
Q

Grading

A

System of classifying cellular aspects of a cancer tumor

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Hyperplasia
Growth that causes tissue to increase in size by increasing the number of cells; abnormal overgrowth of tissue
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Hypertrophy
Enlargement or overgrowth of an organ; tissue increases in size by the enlargement of each cell
27
Malignant cell growth
Altered cell growth that is serious and, without intervention, leads to death: cancer. Abnormal, serve no useful function, harmful to normal body tissues.
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Malignant transformation
The process of changing a normal cell into a cancer cell
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Metastasis
The growth and spread of cancer
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Apoptosis
Programmed cell death. Normal cells have a finite lifespan.
31
Anaplasia
Feature of cancer cells. The cell loses the specific appearance/shape of their parents cell. Many types of cancer cells look alike. As a cancer cell becomes more malignant, it becomes smaller and rounded. This appearance change can make diagnosis of cancer type difficult, because many different types of cancer cells look alike
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Initiation
The first step in cancer development. Anything that can penetrate a cell, get into the nucleus, damage DNA can mutate or change genes. This can activate genes that should remain suppressed and can turn off normal genes.
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Latency period
The time between a cells initiation in the development of an overt tumor. Can range from months to years.
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Cancer development
Malignant transformation occurs thru: Initiation: ØInitiation is the first step in carcinogenesis. Normal cells can become cancer cells if their genes promoting cell division, oncogenes, are turned on excessively (overexpressed) ØInitiation is an irreversible event that can lead to cancer development ØA cancer cell is not a health threat unless it can divide. If it cannot divide, it cannot form a tumor ØIf growth conditions are right, however, widespread metastatic disease can develop from just one cancer cell Promotion which enhances growth: ØIs the enhancement of growth of an initiated cell. Promoters are substances that promote or enhance growth of the initiated cancer cell. ØOnce a normal cell has been initiated by a carcinogen and is a cancer cell, it can become a tumor if its growth is enhanced (e.g., normal hormones and body proteins like insulin and estrogen can act as promoters and make altered cells divide more frequently) Progression, continued change making it more malignant, includes tumor angiogenesis factor Metastasis (blood borne most common) ØA detectable tumor is formed (a 1-cm tumor has at least 1 billion cells in it), must develop its own blood supply, and makes substances that trigger nearby capillaries to grow new branches into the tumor
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Tumor angiogenesis factor
Triggers capillaries and blood vessels to grow new branches into the tumor. This gives tumor its own blood supply. This occurs when the tumor is about 1 cm
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Two categories of cancers
Solid tumors develop from specific tissues such as breast, lung. Hematologic cancers arise from blood cells forming tissues such as leukemias and lymphomas
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Grading cancer
Classifies the cellular aspect of cancer. Such as the aggressiveness insensitivity to treatment. Some are more malignant than others. We compare nation wide.
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Staging of cancer
Determines the exact location of the cancer and its degree of metastasis. TNM, tumor, node, metastastis. Tx cant be assessed. T0 no evidence, T1,2,3 Clinical staging uses the manifestations and clinical signs for tumor size and possible spread Surgical staging gifts tumor size, number, site, and spread by evaluating during surgery. Pathological staging is the best type, determining size, number, sites, and spread by pathological examination of tissues from surgery
39
TNM/tumor, node, metastasis
Not useful for leukemia or lymphomas. This helps guide treatment and is useful for prognosis and comparison.
40
Three factors that influence cancer development
Exposure to carcinogens, genetic predisposition, and immune function
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Carcinogens effect on cancer
External factors, including environmental exposure is responsible for 80% of cancer in North America. 30% of cancers are related to tobacco use. It is the single most important source of preventable carcinogenesis
42
Cancers associated with tobacco
Lung, oral cavity, Pharyngeal, laryngeal, esophagus, pancreatic, cervical, kidney, bladder, liver, stomach, myeloid leukemia
43
Cancer-causing radiation
Ionizing and ultraviolet. Ionizing is found naturally in elements such as radon, uranium, and radium. Most rocks and soil containing this. Other types of ionizing are x-rays, cosmic radiation. UV radiation is solar radiation, Tanning beds, and germicidal lights. This is usually skin cancer
44
Oncoviruses
Viruses that cause cancer. Viral carcinogenesis. Viruses that can cause cancer are Epstein-Barr, hepatitis B and C, HPV, human lymphotrophic virus type I and II
45
Dietary factors related to cancer
Diet is suspected to alter cancer risk. Suspected dietary factors include low fiber, hi redmeat, high animal fat intake. Preservatives, contaminants, preparation methods, and additives also promote cancer.
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Personal factors that can cause cancer
Immunosuppression. Natural killers and helper T cells help get rid of cancer. Advancing age is the single most important risk factor for cancer Genetics Ethnicity
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Seven warning signs of cancer | CAUTION
``` Changes in bowel or bladder habits A sore that doesn't heal Unusual bleeding or discharge Thickening or lump Indigestion or difficulty swallowing Obvious change in a wart or mole Nagging cough or hoarseness ```
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Features of malignant cancer cells.
˜Cancer (malignant) cells are abnormal, serve no useful function and are harmful to normal body tissues ˜Rapid or continuous cell division ˜Anaplasia ØIs the cancer cells’ loss of the specific appearance of their parent cells. As a cancer cell becomes more malignant, it becomes smaller and rounded. This appearance change can make diagnosis of cancer type difficult, because many different types of cancer cells look alike ˜Large nuclear-to-cytoplasmic ratio ØOccurs in cancer cells with the cancer cell nucleus being larger than that of a normal cell and the cancer cell being small. The nucleuns occupies much of the space within the cancer cell, creating a large nuclear-to-cytoplasmic ratio ˜Specific functions lost ØAre lost partially or completely in cancer cells. Cancer cells serve no useful purpose ˜Loose adherence ØIs typical for cancer cells because they do not make fibronectin. As a result, cancer cells easily break off from the main tumor ˜Migration ØOccurs because cancer cells do not bind tightly together and have many enzymes on their cell surfaces which allow the cells to slip through blood vessel walls and between tissues, spreading from the main tumor site to many other body sites. This ability to spread (metastasize) is unique to cancer cells and a major cause of death ˜No contact inhibition ØDoes not occur in cancer cells, even when all sides of these cells are in continuous contact with the surfaces of other cells. This persistence of cell division makes the disease difficult to control ˜Rapid or continuous ØOccurs in many types of cancer cells because they re-enter the cell cycle for mitosis continuously. They do not respond to signals for apoptosis and can have an unlimited lifespan ˜Abnormal chromosomes ØAre common in cancer cells as they become more malignant. Chromosomes are lost, gained, or broken; thus cancer cells can have more than 23 pairs or fewer than 23 pairs. Cancer cells may have broken and rearranged chromosomes
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Cancer etiology and genetic risk
˜Chemical carcinogenesis can occur from exposures to many known chemicals, drugs, and other products used in everyday life. Occupations with exposure to asbestos can cause lung cancer, and hairdressers are at risk for bladder cancer. Tobacco is the single most important source of preventable carcinogenesis and can cause small cell lung cancer and bladder ˜Physical carcinogenesis from physical agents or events causes cancer by the same mechanism as for chemical carcinogenesis. Two physical agents that are known to cause cancer are radiation and chronic irritation. Protect from sun exposure. ˜Viral carcinogenesis occurs when viruses infect body cells and break the DNA strands (e.g., Hepatitis B and C, human papiloma, Epstein-Barr ) ˜Dietary factors related to cancer development are poorly understood although dietary practices are suspected to alter cancer risk. Suspect dietary factors include low fiber diet, high intake of red meat, and high animal fat intake, preservatives, preparation methods, and additives ˜Personal factors ØImmune function immunosuppressed, adults over 60 less-than-optimal levels of function, organ transplant, AIDS ØAge that is advanced is the single most important risk factor ØGenetic risk occurs in a small percent of the population, genetic testing is available to confirm or rule out a person’s genetic risk for a few specific cancers. These tests do not diagnose the presence of cancer; they only provide risk information. ØWhen a patient tests positive for a cancer-causing gene mutation, his or her risk for cancer development is greatly increased; however, the cancer still may never develop
50
Benign tumor cells
˜Continuous or inappropriate cell growth ØBenign tumors are normal cells growing in the wrong place or at the wrong time (e.g., moles, uterine fibroid tumors, skin tags, endometrosis, and nasal polyps) ˜Specific morphology ØOccurs with benign tumors. They look like the tissues they come from, retaining the specific morphology of parent cells ˜Small nuclear-to-cytoplasmic ratio ØIs a feature of benign tumors just like completely normal cells ˜Specific differentiated functions ØContinue to be performed by benign tumors (e.g., endometriosis, a type of benign tumor, the normal lining of the uterus (endometrium) grows in an abnormal place such as an ovary, on the peritoneum, or in the chest cavity) ØThis displaced endometrium acts just like normal endometrium by changing each month under the influence of estrogen. When the hormone level drops and the normal endometrium shed from the uterus, the displaced endometrium, wherever it is, also sheds ˜Tight adherence ØOf benign tumors cells to each other occurs because they continue to make fibronectin, In addition, many benign tumors are “encapsulated” helping to hold the benign tissue together ˜No migration Ø or wandering of benign tissues occurs because they remain tightly bound and do not invade other body tissues ˜Orderly growth ØWith normal growth patterns occurs in benign tumor cells even though their growth is not needed. Growth may continue beyond an appropriate time or occur in the wrong place, but the rate of growth is normal. The benign tumor grows by hyperplastic expansion, it does not invade. ØEven though benign tumors do not invade, they can compromise or even destroy surrounding normal tissue. This particularly a problem when a benign tumor arises in a location that does not expand to accommodate growth, such as in the skull ˜Normal chromosomes ØAre usually found in benign tumor cells, although there are exceptions. Most of these cells have 23 pairs of chromosomes, the correct number for humans
51
Features of cancer cells
˜Cancer (malignant) cells are abnormal, serve no useful function and are harmful to normal body tissues ˜Rapid or continuous cell division ˜Anaplasia ØIs the cancer cells’ loss of the specific appearance of their parent cells. As a cancer cell becomes more malignant, it becomes smaller and rounded. This appearance change can make diagnosis of cancer type difficult, because many different types of cancer cells look alike ˜Large nuclear-to-cytoplasmic ratio ØOccurs in cancer cells with the cancer cell nucleus being larger than that of a normal cell and the cancer cell being small. The nucleuns occupies much of the space within the cancer cell, creating a large nuclear-to-cytoplasmic ratio ˜Specific functions lost ØAre lost partially or completely in cancer cells. Cancer cells serve no useful purpose ˜Loose adherence ØIs typical for cancer cells because they do not make fibronectin. As a result, cancer cells easily break off from the main tumor ˜Migration ØOccurs because cancer cells do not bind tightly together and have many enzymes on their cell surfaces which allow the cells to slip through blood vessel walls and between tissues, spreading from the main tumor site to many other body sites. This ability to spread (metastasize) is unique to cancer cells and a major cause of death ˜No contact inhibition ØDoes not occur in cancer cells, even when all sides of these cells are in continuous contact with the surfaces of other cells. This persistence of cell division makes the disease difficult to control ˜Rapid or continuous ØOccurs in many types of cancer cells because they re-enter the cell cycle for mitosis continuously. They do not respond to signals for apoptosis and can have an unlimited lifespan ˜Abnormal chromosomes ØAre common in cancer cells as they become more malignant. Chromosomes are lost, gained, or broken; thus cancer cells can have more than 23 pairs or fewer than 23 pairs. Cancer cells may have broken and rearranged chromosomes