Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

100 Cards in this Set

  • Front
  • Back
a very general term that encomppasses neoplasms as well as non-neoplasm lesions
an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of normal tissues and persists in the same excessive manner after cessation of the stimuli which evoked the change
adaptive change from one fully differentiated cell type to another fully differentiated cell type in adult tissue
varying size and shape
forming finger like growths with a central stalk and epithelial surface

papillomas are benign epithelial neplasm which produces finger like projectsions from epithelial surface
some degree of loss of normal differentiation of cells and tissues,
a lesion which is histologically malignant but has not yet invaded
carcinoma in situ
a benign neoplasm with components representing all three germ layers
a benign but disorderly mass of tissues normally present at the site usually not considered neoplasm

totally benign - sometimes considered a neoplasm
the vascular connective tissue supporting the parenchyma of an organ, or supporting the proliferating cells of a neoplasm
malignant tumor of striated muscle cells
tumors of smooth muscle cells
Leiomyoma, leiomyosarcoma
fibroma, fibrosarcoma
tumors of fibroblasts
normal cells in an abnormal location
two ways to define malignancy
1. ability of neoplasm to metastasize
2. ability of neoplasm to invade normal tissue
a synonym for "malignant neoplasm"
the movement of malignant neoplastic cells from the primary tumor to another site formaing a new mass
how might neoplastic cells transfer to to a new location
may break off and float there where they attach and proliferate
or, might invade through basement membran to gain access to lymphatic or blood vessel
they have cell surface molecules which allow them to "home" / attach to endothelium in the "new tissue"
an epithelial malignancy
a mesenchymal malignancy
a benign neoplasm of a gland
a malignant neoplasm of the gland
a benign neoplasm of squamous epithelim

malignant = squamous cell carcinoma
a benign neoplasm of neuroendocrine cells - all are potentially malignant - likelihood of metastasize varies with location
malignant neoplasm of melanocyte

this is weird - should technically be called melanocarcinoma but historically is referred to as melanoma
benign neoplasm of blood vessel

malignant: angiosarcoma
immunopersoxidase marker for malignant epithelium (carcinoma)
keratin intermediate filament
immunopersoxidase marker for malignant mesenchyme (sarcoma)
vimentin intermediate filament
immunopersoxidase marker for hematolymphoid (lekemia/lymphoma)
cell surface markers (LCA
immunopersoxidase marker for melanocytes (melanoms)
S100 protein
A Immunoperoxidase marker for "neuroglial cells" (astrocytoma)
GFAP, neurofilament
can high grade dysplasia regress to a lower grade dysplasia?
The degree to which neoplastic cells resemble normal cells (both morphologically and functionally)
differentiation (high differentiation would be more normal)
in a purely epithelial neoplasm the non-stromal component or epithelial component
"reactive" non-neoplastic mesenchymal tissue associated with an epithelial neoplasm
stroma (although sometimes the stroma can be neoplastic - "mixed tumor"
what promotes angio-genesis w/ metastasis
growth factors produced by tumor cells
formation of adhesion or fibrosis in vascular stroma of a neoplasm
autonomous growth in vivo involves the uncontrolled growth of a clone of cells to bome a "mass", "tumor", or "spot" what are three additiona growth charcteristics that define malignant phenotype
1. invasion
2. metastasis
3. transplantability (one human to mouse)
Autonomous growth in vitro happens do to what three mechanisms
1. loss of contact inhibition
2. ability to grow w/o attachment
3. immortality (ability to grow indefinately in cell culture)
three ways you get altered differentiation
1. loss of normal products
2. new products (metaplasia)
3. expression of fetal genes
indirect mutagens requires
metabolic activation (indirect mutagens are metabolized to electrophilic species that are able to react with cellular DNA)
genetic accidents leading to mutation happen during DNA replication, albeit at a very low rate
stochastic events
ability of cell to divide and produce all the differentiated cells in an organism
can give rise to several other cell types, but those types are limited in number.
disorganized mature specialized cells that normally occur in the affected part
two components to neoplasm
parenchyma and stroma
component of neoplasm that consists of one cell type (clonal)
parenchyma (sometimes you get mixed neoplasm)
epithelial and melanocytic tumor where the epithelial cells are the only neoplastic component
basal cell carcinoma
teratoma is derived from
totipotent cells (gonadal cells) - differentiation along cell line
lymphatic spread is usually carcinoma or sarcoma
carcinoma - sometimes sarcoma
sarcomas (and sometimes carcinoma) usually spread via
hematogenous spread
hematogenous spread is via venous or arterial system and goes where?
venous - to liver and lungs
arterial spread is less likely due to thick wall but access might be gained through
grade is an attempt to predict? and depends on what two factors?
the behavior or aggressiveness and relates to degree of differentiation and mitotic activity
an attempt to stratify the extent of spread
cancer stage
what are the three parameters fo cancer stage
1. size of primary
2. nodal involvement
3. hematogenous disemination
(parameters are different for diff tumor types)
What are the two staging systems in current use
TNM staging (Union Internationle Contre Cancer)
American Joint Committe on Cancer staging
TNM stagig - what does T and N and M stand for
levels of each
T = tumor (0-4 w/ increasing size)
N = nodes (1-3 w/ increasing number of nodes)
M = metastases (0-2) w/ more distant metastases
predicts aggressiveness of tumor
4 ways that chemical carcinogens cause DNA damage
1. alkylation
2. damage leading to depurination/depyrimidation
3. bulky DNA adducts
4. double strand breaks
do direct acting mutagenic chemicals require metabolic activation to be reactive w/ DNA
Hereditary nonpolyposis colocn cancer (HNPCC) is associated with a defect in
DNA mismatch repair linked ot hMSH2 and related genes
Bloom's syndrome is a rare human recessive disease characterized by
chromosomal instability with predisposition to develop leukemia, lymphoma, and carcinoma
Indirect acting carcinogens are usually activated by what enzymes
three things in the diet that are protective
Antioxidants, Vit A (cell differentiation), and low caloric intake
intial exposreu to carcinogen is called
after initiation the subsequent events that accelaerate the development of the neoplasm is called
promotion (now refered to epigenetic events that favor tumor development
genetc events that are required to confer malignant phenotype
the time between initiation and clinical detection of tumor
latent period
the lesion after promotion and before progression
preneoplasmic lesion
the somatic mmutation hypothesis of cancer states that
cell growth, differentiation, and survival are under genetic control, and that malignant transformation comes about through accumulation of mutations in specific classes of genes that regulate these properties
the dysregulation of cell proliferation by constinuative activation of growth-stimulatory pathways or independence from physiologic proliferation signal involve what kind of genes
insensitiviety to growth inhibitory signals or loss of cell cycle inhibitors involve what kind of genes
tumor suppressor genes
Evasion of apoptosis invovolve what kind of genes
Pro and Anti- apoptotic proteins
Limitless replicative potential "immortalization" involve what kind of genes
Angiogenesis as a phenotype of cancer involve what kind of genes
multiple complex pathways
invasion and matastasis of cancer involve what type of genes
proteins involved in cell-cell and cell-matrix adhesion and matrix degradation
genetic instability involves what kind of genes
DNA repair genes "caretaker genes"
a gene that encodes a protein that stimulates or mediates cell prliferation the normal counterpart of an oncogene
activated proto-oncogne (oncogene) may be activated via either mutation or
aberrant expression (over-expression or ectopic expression)
lack of differentiation
anaplasia vs. dysplasia
anaplasia is lack of differentiation and dysplasia is disorderly growth. note: dysplasia usually happens in epithelia
this staining uses markers of differentiation to help determine the cell type of the neoplasm when the degree of differentiation or morphology alone does not allow exact classification
a grade of one is more or less differentiated than a grade 3 neoplasm
grade one is well differentiated and grade 3 is poorly differentiated.
The highest grade denotes an anaplastic neoplasm
tumor which display desmoplasia are called what
scirrhous ("stony hard")hard due to the collagenous stroma
lack of differentiation or anaplasia lead to the following morphological changes (5)
1. pleomporhic: cells and nuclei
2. nuclear morphology (hyperchromatic, large, variable shape)
3. mitosis increased
4. loss of polarity
5. sometimes giant cells
in naming neoplasms the prefix usually describes the
phenotype of nepolasm
in naming neoplasms the suffix describes
the benign or malignant state
precancertous or premalignant might involve what two types of lesions
1. carcinoma in situ, CIS

2. some benighn neoplasms (adenomas and colon)
barrett's esophgus might lead to what type of cancer

hyperpasia - metaplasia - dysplasia - adenocarcinoma
which has the higer risk of becoming malignant - tubular or villous adenoma?
villous adenoma
dysplasia-carcinomal sequence
premalignant epithelial lesions are recognized because of dysplasia

e.g cervix and esophagus
adenoma-carcinoma sequence

some adenomas progress to malignancy

e.g colon
one of the most important species involved in metabolism of polycyclic aromatic hydrocarbons such as benzopyrene in cigarette smoke
CYP1A1 - plymorphisms increase risk of lung cancer in smokers
Potts studied what population in his effort to understand carcinogenesis
chimney sweeks - developing cancer
XP is heterogenous w/ at least how many variants
7 - each variant represents abnormality in different gene whose product is involved in nucleotide excitsion repair -
what happens in promotion
clonal expansion of initiated cells

recognized on the histologic level as dysplasia or "pre-malignant"

these dividing cells are more sensitive to carcinogenic mutations
why are dividing cells (say in the promotion phase) more prone to carcinogens than inactive genes
DNA repair takes time. resting cells have time to repair DNA. actively dividing cell have less time for DNA repair. DNA replication before repair may lead to mutation
what is the difference between initiation and promotion
initiator is mutagenic, initiation is irreversible. Promotor is not mutagenic, promotion is reversible
how does RNA virsu such as Rous Sarcoma bring about a inheritable genetic change
Reverse transcriptase allows viral RNA code to be transcribed into DNA