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90 Cards in this Set
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whats the most common cause of cancer death in women (top 4)
what are the top 4 cancers that will kill a woman What about men |
Women Top 4:
Breast, Lung, Colon/Rectal Men Top 4: Prostate, Lung, Colon/Rectal Deaths in women: lung, breast colon/rectal Deaths in Men Lung, prostate, colon/rectal |
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at what age do we see most cancers
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50-85
female 40-79 male 60-79 |
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where do kids get cancers (what tissues) whats the most common
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in things that are growing, bone, organs, bone (not so much in epithelium)
Acute leukemia and CNS tomor is most common |
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what factors influence cancer
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environment and genetics
there is a whole wide array of what causes, some are totally genetic like FAP and some are pure environment like UV radiation induced |
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where is burkitt lymphoma common
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subsahara africa
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what are the 3 main categoreis of carcinogens
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1. Chemical: endogenous as well as exogenous
2. Infectious: usually a transforming virus (HPV) 3. radiation: |
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what cancers are associated with EtOH abuse
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Oropharynx
Larynx Esophagous Hepatocellular 2 to cirrhosis rectal carconoma with beer, increased breast |
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what cancers are assocaited with Tobacco
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1. Lip, mouth, oropharynx
2. Larynk, lung 3. Esophagous 4. Pancreas 5. Urinary tract 6. cervix |
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what cancers are associated with UV radiation
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Squamous cell carcinoma
Basal Cell Carcinoma Malignant melanoma PPl at risk are those with are pale and get lots of sunburns Both UvA and UVB rays are bad |
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whats the effect of EtOH and TObacco use with cacner
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SYNERGISTIC
if you do both the risks shoot WAY up |
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renal cell carcinoma, transitional cell carcinoma of the kidney/ureter/baldder are assicaoted with that environmental factors? what are some other cancers associated with this
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Tobacco
*also mouth, larynx, lung, pancreas, esophagous, cervix |
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if you are exposed to ______ at work what cacner are you at increased risk for
1. Arsenic 2. Asbestos 3. Benzene 4. Beryllium 5. Ethylene Oxide 6. Naphthylamines 7. Radon 8. Vinyl Choloride |
1. Lung, skin, angiosarcoma
2. Lung, mesothelioma 3. Leukemia, lymphome 4. lung 5. leukemia 6. bladder 7. lung 8. angiosarcoma |
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if someone works with... they cancer they may get is...
1. in semiconductors, fungicides in apple orchards (Arsenic) 2. really strong association with lung cancer but another buzzword one (Asbestos) 3. gas pump (benzene) 4. space workers (beryllium) 5. makes fruit ripen (ethylene oxide) 6. Rubber (naphthylamines) 7. Radon 8. Makes plastics (vinyl chloride) |
1. lung, skin, angiosarcoma
2. lung, mesothelioma 3. Leukemia, lymphoma 4. Lung 5. Leukemia 6. bladder cacner 7. lung 8. angiosarcoma |
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what does chronic inflammation have to do with cancer?
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increased risk of cacner
- the cytokines that stim inflammation will also stim GF --> increased stem cells, also inflammation makes ROS |
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what are some things that you can acquire that predisposes you for cancer
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1. inflammation: GF, ROS, stem cells
2. anything that prolongs/increases regeneration/proliforation: repair from burns, estrogen --> hyperplasia, 3. Liver Cirrhosis: includes regeneration AND inflammation 4. Hyperplasia --> Metaplasia --> Dysplasia. ex of smoking Surprisingly NOT benign tumors |
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ROS, GF and stem cells are a breeding grouonds for... these elements are seen together when,,,
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seen in inflammation, increased risk for cancer
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why might a burn lead to cancer? what are some other examples
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burns lead to lots of regeneration, this increases risk of malfunction :/
anything that increases proliforation/regeneration- estrogen leads to endometrium proliforation, inflammation/infection Cirrhosis of liver hyperplasia --> metaplasia --> dysplasia NOT benign tumors |
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will a benign neoplasm increase liklihood of getting a malignant one
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not really
EXCEPT when: 1. adenoma type colon polyps- these are precancerous by definition 2. large/longstanding benign neoplasm |
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adenoma type (adenomatous) colon polyps are benign or malignant
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well they are precancerous by definition they will turn malignant
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ok so cancer is either familial or sporadic. what things are affecred in familial
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1. enzyme fx
2. receptor polymorphysm 3. defective DNA repair not many cancers are related to a cancer gene but familial and sporadic both will have the same genes affected |
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what are some characteristics of familial cancers
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1. clusters in the family
2. happen in younger ppl 3. multiple or BL cancers 4. AD or multifactoral inheritence bc of low penetrance alleles |
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what types of genes are most associated with familial cancers. what are some common familial cacners
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Inheritance is AD or multifactorial, low penetrance
Gense are: 1. Tumor suppressors, no associated phenotye 2. Breast, colon, ovary, brain, malig melanoma, endocrine |
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1. what percent of breast cancer is due to inherited cancer gene
2. what gene/gene category 3. what inheritance pattern 4. Function of the gen |
1. 10%
2. BRCA 1/2- tumor suppressor 3. when one mutated copy is inherited you are miuch more likely to have additional mutation that leads to cancer |
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if you have a BRCA1/2 mutation what does this mean? what type of gene is it
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increased risk for breast cancer
-younger -BL -multiple cancer, increased risk of ovarian BRCA is a tumor suppressor gene and is also involved in DNA repair maternal and paternal both count |
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what familial cancers are inherited in an AD fashion and display a characteristic phenotype
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1. FAP (adenomatous polyposis)
2. Neurofibromatosis 3. MEN 2B |
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ok so we know tumor supressors are common in cancers, like BRCA1/2 what is the inheritance pattern
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Autosomal Dominant
germ line mutation, one copy is mutated and so our other copy is at increased risk for mutation. when the 2 one is mutated its called loss of heterozygosity |
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whats Retinoblastoma, what gene is defectiev
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Rb, its a malignant tumor of the eye seen in infants
ALL cases have defective Rb gene, can be a sporadic mutation or inherited |
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talk to me about knudsons 2 hit hypothesis
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need 2 "hits" to develop cancer.
Hit 1: inherit mutated Rb (germ line mutation) ALL cells have one mutated copy and a normal copy Hit 2: somatic mutation, this is the malignant transformation, now there has been a LOH |
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how would one get a sporadic retinoblastoma?
what are the 2nd complications assocated with familial retinoblastoma |
1. 2 independent somatic mutaitons
2. i germ line mutation in ALL cells and then an independent somatic mutation that occurs later. -increased likelihood for cacner -increased chance to get a 2 cancer -BL cancer - cancer at young age 13q deletion |
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ok so if you had the BRCA 1/2 mutation it was something like 10% you would get cancer, if you have FAP mutaiton whats the liklihood you will get cacner
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100%!!!!
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what cancer is assocaited with
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MEN 2B
marfanoid habitus (long tall and skinny) with ganglioneuromas of tongue RET gene, its a familial cacner with marker phenotype |
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whats Neurofibromatous disease?
hwo do you get it |
inherited tumor suppressor gene
NF1 gene mutation gives several benign neurofibromas that can transform into a neurofibrosarcoma manifest: -lisch nodules (in eye, hamratomas- jumbled tissue normal for the eye but in the wrong site- so pretty) -cafe au lait spots |
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whats a hamartoma of the eye? what disease is it seen
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its a lisch nodule in the eye, what happens is a normal eye component is all mixed up and jumbeld in such a way that it is no longer normal
**its clumps of melanocytes, rather than nice straight lines |
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what are the 4 AR syndromes of defective DNA repair
clinical features, gene type/action, cancer risks |
1. XERODERMA PIGMENTOSA- NER gene, UVB rays form DNA dimers increase skin cancer risks
2. ATAXIA TELANGIECTASIA- ATM is mutated and makes DNA fragile. It binds to and Pi TP53 and increases sensitivity to radiation --> risk for leukemia/lymphoma. clinical with cerebellar dysfx and dilate BV in eyes 3. bloom syndrome: BLM mutation. similar to AT bc of sensitivity to UV radiation. immune defecit, skin manifestations 4. fanconias anemia; ALL blooc cess are decreased, chromosomes are fragile and increased risk for leukemia, squamous cell carcinoma and heptoma |
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defective DNA repair is seen in what syndromes, whats the inheritance
clinical features, gene type/action, cancer risks |
1. Xermoderma Pigmentosa- defective nucleotide excision repair genes due to AR inheritence. UVB dimers cant be removed and we get increased chance for skin carcinoma
2. Ataxia Telangiectasia- its when ATM binds to damaged DNA and phosphorylates TP53 which makes you sensitive to ionizaing radiation- this makes you more likely to get lymphoma or leukemia when given an x ray. clinical manifestations are related to the name: ataxia- abnormal movemnt bc of cerebellar dysfx and telangiectasia- tortous BV in the eye often |
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xeroderma pigmentosum adn ataxia telangiectasia are what
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defective DNA repair due to autosomal recessive inheritance
1. Xermoderma pigmentosum- increased risk for skin carcinoma bc NER repair is defective. cant take out the dimers that form with UVB exposure 2. Ataxia Telangiestasia- ATM is mutated and makes DNA fragile, it binds to and Pi TP53 and increases sensitivity to radiation, increased risk for leukemia/lymphome. Clinical with cerebellar dysfx and dilated BV in the eye |
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talk to me about xeroderma pigmentosa
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its an inherited (AR) defect in DNA repair
the NER (nucleotide excision repair) gene is wrong and so UVB can form dimers that when not repaired leads to carcinoma of the skin **becuase its autosomal recessive we know its rare and we also know that we need 2 mutated copies *seen in white ppl with fair skin |
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talk to me about ataxia telandiectasia
what is it, what are the manifestations, whats the gene |
its an AR inherited defect in DNA repair
Clinical: abnormal cerebellar movement, dilated tortuous dilated BV in the eye. IgA defeciet so increased infections/recurrent *ATM is the gene (ataxia telangiectasia MUtated) and makes the chromosome fragile, ATM binds to damaged DNA and phosphorylates TP53 *this makes ppl sensitive to ioizing radiation and can develop leukemia/lymphoma when exposed Bloom Syndrome is simliar but has more cutaneous manifestations along with an immunodefecit- BUT also sensitive to UV and can cause leukemia/lymphoma |
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what are the 2 AR syndromes that make defective DNA repair and make you sensitive to radiation, what cancers are at increased risk for development
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1. AT- ATM gene
2. Bloom- BLM gene **leukemia/lymphoma |
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run down of carcinogens
2 main things that cause 3 classes, how they interact |
genetics and envoronment
Environment: 1. Chemical 2. Radiation 3. Microbes **are SYNERGISTIC, more than one thing will super increase the risk |
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who got lots of scrotal carcinoma, what did it imply
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chimny sweeps the ENVIRONMENTAL influence of cancer
**this is a chemical that caused it |
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whats an initiator
whats a promoter |
Initiation: fast, permanent "signature" DNA damage. wont elicit cacner alonw
Promoter: reversible damage that will induce a tumor in cells that are initiated. helps cells grow- more divions increase liklihood of DNA damge. lots of dif things are promoters |
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ok so what will cause permanent damage but cant cause cancer alone
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Initiator! needs a promoter to make a tumor
THe initiation happens first and is permamnet, then there needs to be promotion in an initiated cell for tumor development BOTH MUST BE PRESENT FOR TUMOR DEVELOPMENT, the initiator needs to come first interesting if you have an initiator and then give the body some time to heal b4 the promotor does its thing you can prevent cancer sometimes *the DNA damage is unique, has a "signature" |
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initiators can act in what 2 ways
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1. Direct: dont need to be metabolized, attach to DNA directly. ex cyclophosphamide
2. Indirect: the metabolised form forms Adducts on DNA. More potent. ex Nitrosamines, polycyclic, aromatic, hydrocarbons, amides, plants and microbes **recall the initiator happens first and is PERMANENT DNA damage. alone wont cause cancer. in either case the DNA damage has a signatur ethat is unique |
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ok so a cell that has a PERMANENT DNA damage is what? what is cool about the DNA damag
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initiated,
*its unique, will give a "signature" mutation based on the chemical ex p53 damage with tobacco |
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whats the deal with promoters, what kinds of things can be promoters
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well its just something that makes cells divide more (hormones, bole acids, cytokines etc)
the problem is when we have an INIITATED cell (permanent signature DNA damage) that gets the promoter signal. this means with MORE replication we INCREASED RISK OF another muitation. when BOTH initiation adn promotion have occured we can get cacner |
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what are some direct and indirect chemical carcinogens. are they weak or strong
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1. DIRECT: ex. cyclophosphamide adn metals. dont need metabolic conversion. initiator. less common
2. Indirect: need to be metabolized before they cause damage. POTENT ex nitrosamines, polycyclic amines, aromatic hydrocarbons/amines/amides. plants, microbes |
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talk to me about polycyclic aromatic hydrocarbons
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its a type if INDIRECT initiator, potent, common
1. Benzopyrene- in tob smoke. related to lung cacner 2. Vinylchloride- angiosarcoma of the liver |
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Cyclophosphamide
2. Polycyclic Aromatic Hydrocarbons (2) 3. Nitrosamines 4. Natural Occuring |
1. cyclophosphamide: direct acting initiator (chemical carcinogen)
2. Polycyclic Aromatic Hydrocarbond, indirect initiators. ex benzopyrene in tobacco linked to lung cacner, Vinyl chloride- plastic, relate to angiosarcoma of liver 3. INDIRECT, it the nitrates in lunch meats. potent carcinogen in lab tests. GI malignancy, UG in smokers, Esophageal cancers 4. Natural- indirect. Aflatoxin B1 from peanuts. p53 mutation assocated with hepatocellular carcinoma. potent |
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whats assocated with a p53 mutation and hepatocellular carcinome
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Aflatocin B1
its a naturally occurions carconiogen,. its an indirect acting potent initiator |
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why is smoking SOOO bad? and why even more so with EtOH
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its an initiator (first, permanent) AND a promoter
Initiator: benzopyrere, nitrosamine Promoter: lots of irritatns (start growth for another mutation) EtOH is a PROMOTER |
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does smoking just increase risk of cacner bc its an initiator and promoter all on its own
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ya but it also is a co carcinogen with asbestos and radon gas etc
SYNERGISTIC risk |
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what type of virus is HTVL1, what disease is associated with it, what gene
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1. RNA retrovirus
2. Causes T cell leukemia/lymphoma (leukemia and lymphoma were also increased with AT and Bloom) 3. TAX gene which promotes genetic instability and lets polyclonal expansion of infected T cells. we know that when things are replicating increased risk of cancer can be latent for a long time, transmitted sex, IV, mom to kid |
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besides HTVL1 causing T cell leukemia and lymphoma what other virus can cause cacner
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1. HPV- squamous cell carcinoma (E2 --> increased E6/7)
2. EBV 3. Hep B 4. HH8 (human herpes virus 8, kaposi sarcoma) |
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what neoplasms are related to HPV infection
what are the features of "high risk" HPV |
*Squamous Epithelial cells, squamous cell CARCINOMA (epithelium)
-vulva -cervix -penis -perianal *E2 viral repressor is lost *E6/7 overexpression. -E6 inactivates p53, degrades BAX, activates telomerase -E7binds RB, cell cycle no longer inhibited, promote cell cycle progression |
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what is the course of HPV infection
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1. HPN virion invades squamous epithlium
2. Viral DNA incorporated into the cell 3. Infected cells multiply and can form warts 4. viral shedding |
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what 3 things is HPV infection associated wiht
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BENIGN
1. Verruca vulgaris, warts 2. condyloma accuminatum, venereal warts 3. Squamous papilloma in mouth, eye, respiratory tract Cancerous 3. Dysplasia, carcinoma in situ (squamous cell carcinoma) |
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chondyloma accuminatum is what
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venereal warts associated with HPV- benign
Verruca Vulgaris, warts on hands/feet Squamous Papillomas- in mouth, eye, respiratory tract ALL of these are benign HPV leisions. can also cause squamous cell carcinoma |
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what are the viral oncogenes associated with HPV
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E2 repressor is lost! so we get E6, E7 overexpression
E6: inactivates p53, degrades BAX (makes cells die), activatestelomerase E7: binds to RB. When RB is bound the cell cycle is promoted RB is a cell cycle inhibitor **in this case the viral genome is incorporated into the host **increased risk for cancer when we have smoking or other sTI |
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what is the role of E2, E6 and E7 in ____ (type of cancer)
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HPV- squamous cell carcinoma
E2- viral repressor is lost so we get over expression of E6/7 E6: inactivates p53, decreased BAX (bax makes cells die) , activates telomerase increased risk of cancer with environmental things- smoke, other STI E7: Binds to RB, RB likes to inhibit the cell cycle, can not do this when bound so we proliforate like mad **viral genome is integreated into host DNA |
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EVB is associated with what cancers
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1. Burket Lymphoma
2. B cell lymphoma- in ppl who are immunosuppressed via CD21 3. Hodgkin disease/hodgkin lymphoma 4. Nasopharyngeal Carcinoma |
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when might you see Burkitts lymphoma, what would you see if the person has AIDS. what are some other things they may have
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EBV causes burkitts lymphoma
If AIDS- B cell lymphoma Can also cause 1. Hodgkins disease/hodgkins lymphoma 2. Nasopharyngeal carcinoma |
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what are the oncogenes assocated with EBV
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B cells infected via CD21
can infect epithelium in mouth/larnyx LMP1 EBNA2 vIL10- prevents T activation |
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LMP1
EBNA2 vIL10 thse are ongogenic things associated with... |
EBV
recall EBV can lead to 1. Burkits lympnome 2. B cell lymphoma (AIDS) 3. Hodgkins disease/Hidgekins lymphoma 4. Nasopharyngeal carcinoma |
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OMG!! my patient is sero+ for EBV, lets talk burkitts...
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ehh not really. most ppl are sero+ but got rid of the EBV bc their T cell recognized the LMP1
**when you dont have T cells (AIDS) you cen get B cell lymphoma CD21 |
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tell me a bit about Burkitts
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EBV causes infection with B cells via CD21 and makes them proliforate.
then another thing (maleria often) will cause another mutation and we can get chromosomal translocation |
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what virus is associated with hepatocellular carcinoma. how does the virus lead to cancer
where is it common |
Hep B- DNA virus
Hep C- RNA virus **the virus leads to hepatocyte deat, cytokines are released and can increase proliforation and regeneration of the dead cells, we can then have genetic accidents in replication aflotoxin will increase carcinogenic effects recall aflotoxin is a potent indirect initiator that is naturally occuring, p53 signature mutation Common in asia and africa (prbly something to do with nuts) |
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what is caused by peanuts and a virus, what virus
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Hepatitis and hepatocellular carconoma
common in asia and africa bc hepatitis is common |
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what two viruses work together to cause kaposi sarcoma, how do they do it
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1. HH8 human herpesvirus 8
2. HIV *neoplasm of vessel forming mesenchyme *before HIV association KS was rare and occured in medeterrenean/african MEN, was in the legs and didnt really metastasize *now that its associated with HIV it is much more aggressive and much more common. AIDS defining illness- can occurs in viscera **so the KS mesenchyme is stim to grow by the CD45 T cells infected with HIB that make TAT and cytokines |
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whats the pathogenesis of KS
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its when HIV and HHV8 work together to make vessel forming mesenchyme neoplasm
**mesenchyme is infected with KS virus, then the T cells (CD45) that are infected with HIV make TAT and other cytokines that cause the KS infected mesenchyme to proliforate |
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what malignancies are associated with H pylori
what else does H pylori cause |
1 Gastric Cancer
2. Adenocarcinoma in mouth- CagA toxin producers 3. GALT (gastric assocated lymphoid tissue) the H pylori infection leads to chronic gastritis and ulceration which means the cells are irritated adn will replicate more can also cause duodenal ulcer |
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how might you get an adenocarcinoma in the mouth
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H pylori infection that has the CagA toxin
- this toxin mimics GF initiating signaling we get polyclonal then monoclonal B cells proliforation- regresses with AB tx |
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lets say you get H pylori as a kid, what happens
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well it hangs out adn causes chronic gastritis, then it can lead to a duadonal ulcer whn you are older
then as a old geezer the H pylori adn cause MALT lymphoma, Gastric carcinoma or gastric ulcer |
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what effect does a tumor have on a host
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1. cachexia
2. Local impingemnet 3. Metastasus 4. hromone synthesis 5. paraneoplastic syndromes |
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compare/contrast the local effects of a tumor and the metastasis with paraneoplastic syndrome
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LOCAL
- impingement on nearby structures (BV, lymph) - erosion of BV - endocrine/BM dysfx bc of tissue replacement - necrosis, infection |
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what are the clinical features and mech of cachexia
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lean mm mass and fat are lossed.
weakness (>10% body weight, disproportional to anorexia) anorexia, anemia common! often IT is the cause of death, not the cancer **the tumor secreted things like PIF and LMF and the host releases pro inflammatory things this leads to Ubiquitin-proteosome path and myosin degradation. sl mm is broken and there is a loss of dystrophin |
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ok so my pt told me they were loosing weight (like >10% of their body weight) and food tastes weird, what am I htinking . how does it happne
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Cachexia assocaited with cancer
**the cancer secretes PIF and LMF and the host makes proinflammatory cytokines, together these activate the ubiquitin- proteosome path to destroy myosin. mm wasting! |
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what superior vena cava syndrome
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when lung cancer impeded flow into the SVC you can have congestion build up in the neck and UE
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what are paraneoplastic tumora, what arent
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paraneoplastic- when non endocrine tissue that is a tumor spits out hormines
NOT paraneoplastic when an endocrine tumor spits out the normal hormones that it always secretes |
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what is a paraneoplastic syndrome? what are 2 types
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its when non endocrine tumors secrete hormones
1. Endocrinopathies: elaboration of hormone like substance -hypercalcemia due to parathormone related protein in tumor -polycythemia due to EPO from renal tubular carcinoma -cushings due to ACTH from lungs cancer 2. AB - peripheral neuropathy/CNS degeneration - myasthmatic syndrome: mm weakness bc of AB to mm associated with cancer **paraneoplastic can be used for early dx, or can mimic metastasis or can be lethal |
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ok so in renal tubule carcinoma what substance can be secreted, what does it cause. what is this an example of, what are some other examples
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its an endocrinopathy type of paraneoplastic syndrome
the renal cells secrete EPO to cause polycistemia Others: Hypercalcemia due to tumor production of a parathromone related protein chusing syndrome due to ACTH from lung cancer |
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AB mediated paraneoplastic syndromes are...
Endocrine associated paraneoplastic syndromes are... |
Peripheral/CNS neuropathis
Myasthenic Syndrome- mm weakness bc of AB mediated damage. associated with lung cancer Endocrine 1. Coushings: lung cancer secreted ACTH 2. Renal Tubular Carcinoma: secreted EPO and makes polycysthemia 3. others |
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Acanthosis Nugricans is what?
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a paraneoplastic syndrome, when hormones are secreted from non endocrine cancers
black pigment is found in folds of skin, commonin gastric carcinoma and breask.lung cancer |
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what are some serum tumor markers
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CEA: colon cancer
a-fetoproteinL liver, testicular b-HCG: choriocarcinoma (placenta or germ cell derived cacner) PSA: prostate specific AG VMA: HVA: NSE- neuroblastoma CA15-3 breast cancer CA 125 ovarian cancer |
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if we get a great correlation btwn a caner can its serum marker can we dx cacner
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Nope, they dont make the dx, they help aid and screen
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what tumor is assocated with this serum marker
1. CEA 2. a Fetoptotein 3. bHCG 4. PSA 5. VMA, HVA, NSE 6. CA 125 7. CA 15-3 |
1. Colon
2. Liver/testicular 3. choriocarcinoma (placents/germ cell) 4. PSA 5. VMA, HVA, NSE 6. Ovarian 7. Breast |
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elevated bHCG in the blood means what
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well it can mean you are preggo but it is also increased in choriocarcinoma (placental or germ cancer)
*tumor markers aret 100% for dx |
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what does elevated VMA, HVA, NSE mean
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neuroblastoma
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what does increased CA125, CA15-3 mean
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CA125- ovarian
CA 15-3 breast |
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liver and testicular cancer is assocated with what tumor marker
colon |
a fetoprotein
CEA |
