unit 4 Cancer Chptr 23 Flashcards
(41 cards)
Apoptosis
Programmed cell death
This ensure that organs have cells at their functional peak.
Every time mitosis happens the DNA strand gets a little shorter till it’s gone and then a signal triggers apoptosis (death)
Contact inhibition
Only when a cell is in contact with all sides, does it stop dividing (mitosis)
Normal chromosomes aka–>
Euploidy
23 pairs
Benign cells
Normal cells growing at the wrong place or at the wrong time
Ex) moles, fibroid tutors, skin tags, endometriosis, nasal polyps
Features of a benign tumor (7)
1) Specific morphology–look like their parent cell
2) Small nuclear-to-cytoplasmic ratio
3) Specific differentiated function- no matter where it is it acts like all the other ex) endometrium grows in a abnormal place estrogen release still makes it shed not matter where it’s at
4) tight adherence
5) no migration
6) orderly growth-May not be in correct place but it is at correct rate and continue beyond normal space
7) normal chromosomes (23pairs)
Features of a cancer (malignant) cell (8)
1) anaplasia– as they become malignant they loose they normal shape– they become smaller and rounded, this can make diagnosis of “types” of cancers hard because many look alike
2) a large nuclear to cytoplasmic ratio
3) specific functions are lost
4) loose adherence- because they do not make fibronectin, as a result they can easily break off from main tumor
5) migration- cancer cells do not bind tightly together and have a lot of enzymes on their surface sand this makes it easy for them to slip through blood vessel walls and between tissues (metastasize)
6) contact inhibition– does NOT occur, even when all side are in contact they still divide
7) rapid or continuous cell division–re-enter mitosis almost continuously. And some have as short generation time (2-3 hours). But most have that of their parent cell. Theses cells also do no respond to apoptosis signals. Most have a lot of enzymes (telomerase) which maintain telemedicine DNA. Do not respond to apoptosis signal and have unlimited life span (IMMORTAL)
8) abnormal chromosomes aka (Aneuploidy)- common the more malignant they become, chromosomes are lost, gained, broken; as a result some have more than 23 or less broken or rearranged
Benign tumors grow by expansion
Malignant tumors grow by invasion
X
Carcinogenesis and oncogenesis are? AKA
Other names for cancer for cancer development
Malignant transformation occurs through 4 steps
1) Initiation- is the 1st step in carcinogens. Normal cells can become cancer cells if their genes promoting cell division “oncogenes”, are turned on excessively (over expressed) is an irreversible event that can lead to cancer development.
* *a cancer cell is not a threat unless it can divide, if it can’t it cannot form a tumor. Pg399
2) Promotion- promote or enhance the growth of an initiated cancer cell— many normal hormones like estrogen, insulin and body proteins can act as promoters and make altered cells divide more frequently. (Latency period) is time between cell’ initiation and development of of an overt tumor
3) Progression– starts to get its own blood supply (1cm tumor has at least 1 billion cells)
4) Metastasis- ex) when breast cancer spreads to lungs or bone it is still breast cancer not lung or bone cancer
(Blood born metastasis) tumor released into the blood is the most common cause of cancer spread
Another way spread–> Lymphatic
Primary and secondary prevention
Primary prevention- avoiding exposure to cancer causing agents
Secondary– screening for early detection
Carcinogens
Substances that change the activity of a cells genes so that the cell becomes a cancer cell– May be chemical physical agents or viruses.
There are more than 50 substances known to cause but over 200 suspected
Solid tumor
Hematologist tumors. Arise from what
Solid from specific tissues ( breast cancer and lung cancer)
Hematologic cancer arises from blood cell forming tissue ( leukemia and lymphomas)
Ploidy
Classifies tumor chromosomes as normal or abnormal.
Staging
Classifies clinical aspects of the cancer
The higher the rating the less they resemble their parent cell.
Gx–cannot be determined
G1–tumor cell closely (well defined) resemble parent cell
Low grade of malignant
Are malignant but are relatively slow growing
G2–moderately defined ( differentiated) they still retain some characteristics of normal cells but Laos have more malignant char. than G1
G3–poorly differentiated, but the tissue of origin can usually be established. Have few normal cell char.
G4–poorly diff. and retain NO normal cell char.
determination of origin is difficult
Euploidy
Normal diploid number. 46 chromosomes (23 pairs)
Aneuploidy
Some cancer cells gain or lose whole chromosomes and may have structural abnormalities of the remaining chromosomes.
Further Staging
Determines the exact location cancer and it’s degree of metastasis.
Primary Tumor (T) Tx-- Primary tumor cannot be assessed To--No evidence of Primary tumor Tis--carcinoma in situ T1, T2, T3, T4,-- Increasing size and/ or local extent of the primary
Regional Lymph Nodes (N) Nx-- Regional lymph nodes cannot be assessed No-- No regional lymph node metastasis N1, N2, N3-- Increasing involvement of regional lymph nodes
Distance Metastasis (M) Mx-- Presence of distance metastasis cannot be assessed Mo-- No distance metastasis M1-- Distance metastasis
Staging is not useful for what cancers.
Leukemia and lymphomas
Doubling time
Mitotic index
Tumor growth is assessed in terms of doubling time, the time it takes to dbl in size
And mitotic index the % of actively dividing cells within a tumor
The smallest detectable tumor is 1 cm and has a billion cells, it dbls about 30 times to get to this size
A tumor with a mitotic index of less than 10% is a slow-growing tumor.
A tumor with a index of 85% is a fast growing
3 factors that influence cancer development
1) exposure to carcinogens
2) genetic predisposition
3) immune function
Oncogene
Are a normal part of every cells normal makeup. ( they r turned on under controlled conditions when cells need to divide for normal growth or to replace dead cells) They become a problem only if they are overexpressed as a result of exposure to carcinogenic agents or events
Cancer etiology and genetic risks(6)
1) Oncogene activation
2) Chemical carcinogenesis
3) physical carcinogenesis
4) viral carcinogenesis
5) Dietary factors
6) Personal factors
Immune function
Age
Genetic risks
Chemical agents
Smoking and alcohol but many more
Physical agents
Radiation (ionizing and ultraviolet (uv) and chronic irritation
