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

127 Cards in this Set

  • Front
  • Back
what is the difference between a neoplasm and a tumor?
neoplasm: uncontrolled tissue growth
tumor: space occupying neoplasm
what are the two basic components in all neoplasms that are both benign and malignant?
1. Parenchyma (neoplastic cell population)
2. Stroma (supporting connective tissue - NOT NEOPLASTIC)
1. a desmoplastic tumor means...
2. a scirrhous tumor means...
1. neoplasm stimulates formation of collagen in stroma (generally agressive)
2. neoplasm is hard (and slow growing)
1. a neoplasm that does not penetrate or invade surrounding tissues is known as?
2. a tumor that has the ability to invade surrounding tissues and metastasize is known as?
1. benign
2. malignant
do benign tumors ever metastasize?
1. nomenclature (suffix) for a benign neoplasm?
2. nomenclature (suffix) for a malignant neoplasm derived from any one of the three germ layers?
3. nomenclature for a malignant neoplasm derived from mesenchymal origins?
1. -oma
2. -carcinoma
3. -sarcoma
1. adeno-
2. squamous-
3. transitional, urothelial
1. an epithelial neoplasm often forming glandular structures
2. an epithelial neoplasm resembling squamous epithelium
3. neoplasm arising from urothelium
what does the prefix "terato" mean?
a neoplasm made up of parenchymal cells derived from more than one germ cell layer. (most often all three)
1. lipo-
2. rhabdomyo-
3. leiomy-
1. a mesenchymal neoplasm arising from adipocytes
2. a mesenchymal neoplasm arising from skeletal muscle cells
3. a mesenchymal neoplasm derived from smooth muscle cells
1. angio-
2. fibro-
1. a mesenchymal neoplasm derived from endothelial or vascular cells
2. a mesenchymal neoplasm derived from fibroblasts
a "papillo-" or "papillary" neoplasm would mean?
a neoplasm with the (gross or microscopic) appearance of warty projections
what would you expect to see in a "cysto-" or "cystic" neoplasm?
a neoplasm with the (gross or microscopic) pattern of cystic spaces
oat cell neoplasms are now termed?
small cell neoplasms
a benign neoplasm that contained mature cells indigenous to that site would be called?
a benign mass of histologically normal tissue found in an abnormal location would be called?
1. adenocarcinoma
2. liposarcoma
3. squamous cell carcinoma
1. malignant neoplasm of a gland producing tissue
2. malignant neoplasm arising from adipose tissue
3. malignant neoplasm arising from squamous cells
1. melanoma
2. lymphoma
3. astrocytoma
1. MALIGNANT neoplasm arising from melanocytes (exception to rules)
2. MALIGNANT neoplasm arising from lymphocytes (exception to rules)
3. MALIGNANT neoplasm arising from astrocytes of the brain (another exception)
what is anaplasia
a neoplasm with no differentiating features (can't determine cells of origin)

Most often associated with a malignancy
which type of tumor is more biologically active: a well differentiated one or an anaplastic one?
a well differentiated one
1. which type of neoplasm is slow growing?
2. which type of neoplasm is known for rapid and erratic growth?
1. benign
2. malignant
1. what is grading
2. what is staging
1. measure of histological differentiation
2. measure of clinical extent and progression
how many "grades" for neoplasms are there?
what are they?
four grades
grade I - well differentiated
grade II - moderately differentiated
grade III - poorly differentiated
grade IV - anaplastic
how could tumor markers be useful?
1. diagnosis (cell of origin)
2. treatment (certain receptors or genetic alterations)
3. early detection in serum
(monitor therapy response or recurrence)
what does TNM in TNM staging mean?
T - tumor (how big, how far spread)
N - nodes (spread?, distant?)
M - metastatic (where, how many)
what are four effects the tumor can have on the host?
1. local effects (compression, infarction, ulceration, hemorrhage)
2. hormonal/paraneoplastic effects
3. cachexia/metabolic effects
4. systemic effects
what are para-neoplastic effects?
secretion of hormone-like substances from the tumor
what are the three cancers that most commonly cause para - neoplastic syndromes.
Bronchiogenic carcinoma
Renal cell carcinoma
pancreatic carcinoma
why do most cancer patients have hypercalcemia?
metastatic lesions in the bone
what para-neoplastic factors would be released in carcinoid syndrome? (3)
what would cause polycythemia?
increased erythropoietin (or erythropoietin like substance)
which hematologic change is commonly seen with chemotherapy?
What is Trousseau's sign?
A DVT is the presenting symptom in a number of cancers (mainly pancreatic cancer)
what is Acanthosis nigrans?
* half of patients that develop this have underlying cancer*
which 2 inflammatory cells are involved with the inflammatory response to a tumor?
mostly a cell mediated mechanism
recently; which cancer has increased?
which 2 cancers have decreased?
increased - lung
decreased - stomach, cervical
what are some factors that cause variation in cancers?
currently, what are the 5 most common cancers in men?
currently, what are the 5 most common cancers in women?
what is an index cancer?
cancer that occurs with the same frequency in all ethnic, racial and geopgraphic populations.
(prototype = Wilm's tumor)
genetic damage lies at the heart of carcinogenesis. what are the two categories of ways this damage can occur?
1. inherited in the germ line
2. aquired later in life by somatic cell mutation
what do we mean when we say tumors are monoclonal?
tumor came from a clonal expansion of ONE progenitor cell that had aquired a mutation (and sustained the genetic damage)
if tumors are monoclonal - why do we see that tumors are heterogenous?
all cells came from the same progenetor cell
they aquired additional individual mutations during the growth of the tumor making them heterogenous
there are two classes of regulatory genes that are the primary targets of genetic damage leading to oncogenesis. what are they?
1. oncogenes (growth promoting)
2. tumor suppressor genes (growth inhibiting)
describe the genetics of growth promoting oncogenes
growth promoting oncogenes are known as "dominant oncogenes"
* mutant alleles considered dominant*
describe the genetics of tumor suppressor genes
tumor suppressor genes are sometimes referred to as "repressive oncogenes"
* both allelles must be mutatant for transmission of effect*
what can maybe account for the fact that a tumor progresses over time?
mutations accumulate (cell becomes more anaplastic and heterogenous)
where in the gene would the transcription and other factors bind to control the level of gene expression?
regulatory region (non-coding region)
what are some possible ways to alter gene expression?
1. Change transcription factor levels
2. Mutate regulatory region that controls interaction with transcription factors or RNA polymerase
3. Translocation ("borrowed", new more powerful promoter)
4. mutation within coding area of the gene
how does contact inhibition differ between normal and malignant cells
normal - still have, grow as a single layer of cells
malignant - lost it, grow as a multilayer of cells
would immortal cells in culture show normal or malignant characteristics?
can show both (or either)
oncogenes are derived from ?

*proto-oncogenes (normal) mutate into oncogenes*
how were oncogenes first discovered?
"hitchhiking" on retroviruses

(a result of recombination with the human genome)
are human neoplasms normally caused by retroviruses?
(the retroviruses just assisted us in discovering the causative oncogenes)
oncogenes cause alterations in what controls of cell growth and division? (4)
1. growth factors
2. growth factor receptors
3. signal transduction (2nd messenger system)
4. transcription factors
what is an autocrine loop?
cell stimulates its own growth

-growth factor is normally overproduced
- excess growth factor binds to the same cells growth factor receptors resulting in further stimulation of growth factor production
can increased growth factor alone cause neoplasia?

- increases risk of spontaneous or induced mutations
- favors progression
what happens when there is a mutation in the growth factor receptor?
persistent tyrosine kinase activity occurs (even when there is no growth receptor bound)

- result is continuous signal for cell division -
what are the two most common types of mutations in the tyrosine kinase receptor that lead to neoplasia?
1. point mutations
2. truncation
besides mutation of the growth factor receptor, what is a common mechanism of growth receptor alteration resulting in neoplasia?
overexpression of normal growth factor receptors
what is the connection between expression of growth factor receptors and prognosis?
the more the growth factor receptors are overexpressed -the worse the prognosis
several oncoproteins mimic the function of the normal signal transducing proteins. which class of proteins is the "most important" in regards to oncogenesis?
GTP-binding proteins
(Ras is one of them)
describe the MOA of the unmutated Ras
* cycles back and forth between active and inactive forms
* Inactive – bound to GDP
* Active – exchanges GDP for GTP
(ras is only activated for a short period: an intrinsic GTPase constantly returns ras to its inactive state)
* GAPs (GTPase activating proteins). “brakes” that prevent uncontrolled ras activity, they catalyze the inactivation of ras
describe what happens when ras becomes an oncogene
the mutated ras protein binds to GAP, but for some reason their intrinsic GTPases are not enhanced

* ras is trapped in the active state: results in unregulated signal transduction
mutations affecting genes that encode nuclear regulatory proteins are associated with malignancy. what is the most common transcription factor that is mutated?
myc gene is the most commonly involved in human tumors
(others include jun, fos)
describe the MOA of the unmutated myc
* c-myc moves to nucleus and forms a heterodimer with max
* c-myc/max heterodimer binds to DNA sequences in growth-related genes and activates transcription
* myc is tightly regulated and only expressed during parts of cell cycle
what are the two major mechanisms that mediate conversion of a pro-oncogene into an oncogene?
1. Change in Structure (ie. point mutation)
2. Change in Regulation (ie. translocation, gene aplification)
1. describe a point mutation.
2. what is the best studied example?
1. one base change in DNA sequence alters entire protein
describe a chromosomal translocation
gene moves to a different chromosome (results in different regulation)
2 types of chromosomal translocations that result in oncoprotein formation?
1. translocation with overexpression (Burkitt's lymphoma)
2. translocation with genetic damage to gene (results in a newly formed gene)
what is the result of amplification of gene expression?
overexpression of protein products
(often an amplification of a transcription factor)
retinoblastoma is caused by a mutation in what type of gene?
caused by a mutation in the tumor suppressor gene
inheritance pattern of Retinoblastoma?
autosomal dominant
however; both normal alleles of Rb must be mutated for the development of retinoblastoma
describe the two-hit hypothesis
two mutations are required to cause cancer
- either one inherited and one somatic
- two somatic aquired mutations
What is loss of heterozygosity?
conversion of a genetic locus to homozygous: many tumors are associated with homozygosity
give an example of two genes that, when they undergo loss of heterozygosity, mediate many human cancers?
p53, Rb
describe the regulation domains of the Rb gene
regulation of cell growth

protein products are involved in
- cell cycle control
- regulation of apoptosis
describe the mutation that occurs in the Rb gene

loss of heterozygosity causes a defect in Rb protein function
describe the MOA of the Rb gene
active state - underphosphorylated form
inactive state - hyperphosphorylated form

* Rb is normally active: it stops cells from entering the S phase of the cell cycle. (does this by sequestering transcription factors)

* when cells are stimulated to divide the Rb protein is inactivated and the cell divides (transcription factors are no longer sequestered)
* Rb is activated again by dephosphorylation
where do mutations of the Rb gene normally occur
mutations involve the transcription binding domain of the Rb gene (transcription factors themselves can't be regulated)
describe the concept of genetic instability and tumor growth
constant, random mutations of cells that are already cancerous promotes malignancy
most tumor supressor genes encode products that have what function?
nuclear transcription factors
is p53 a major player in the regulation of cell growth?
if the cell is unmutated, p53 is not present
if both alleles of p53 are mutated what is the result?
formation of mutations without a proofreading/repair function

* allows mutations to accumulate

* allows genetic instability to be fixed in the abnormal population
why is p53 elevated when it is mutated in cells?
mutation keeps p53 from degrading properly.
(tells us there is a mutation)
what would happen if you had a p53 mutation in a cell that doesn't grow
cell must be growing for mutation to have an effect
it is not rapid growth that defines cancer, instead it is?
progression of malignant cells that are
* genetically unstable
* do not undergo apoptosis
what is the MOA of almost all chemotherapeutic agents?
induction of apoptosis

(chemo resistance is usually because the cell will not undergo apoptosis)
what is multistep carcinogenesis?
cancer is not a result of one mutation in one gene.

*There must a mutation of several oncogenes and at least 2 tumor supressor genes*
what is the growth fraction?
the proportion of cells within a tumor that are in a proliferative pool
describe the size of the proliferative pool as tumor size progresses
early - most cells are within proliferative pool

late - most cells are not in proliferatiave pool
how does the growth fraction help us clinically?
a tumor with a larger growth fraction responds better to chemotherapy

(vs. lower growth fraction cancers - breast, colon - refractory to chemo)
what do tumors do to obtain a blood supply
they release ANGIOGENESIS FACTORS - factors that stimulate host blood vessel growth
what else secretes angiogenic factors?
inflammatory cells secrete them because they sense a necrotic area
what are the three distinct steps in tumor invasion and metastasis?
1. Invasion of the ECM
2. Vascular dissemination
3. Tumor cell growth in new location
how exactly do tumor cells degrade the ECM?
they secrete proteases (or induce host cell to secrete proteases)
* serine proteases
* cysteine proteases
* metalloproteases
describe penetration of the basement membrane
1. Loss of Cell Attachment
2. must attach to matrix
3. must degrade ECM
4. locomotion (migration through BM)
what do tumor cells do when they are in circulation?
they like to clump together
can all tumor cells metastasize?
only a small percentage of cells can metastasize
prostate cancer prefers to metastasize to?
breast cancer prefers to metastasize to?
ovarian cancer prefers to metastasize to?
what are the two stages of chemical carcinogenesis?
1. initiation
2. promotion
*neither are sufficient for tumor formation when they are alone*
does initiation cause temporary or permanent damage?
in relation to chemical carcinogenesis:
what is the difference between a direct acting compound and an indirect acting compound?
direct - requires no chemical transformation for carcinogenicity
indirect - require metabolic conversion
in regards to chemical carcinogenesis:
what effect do promoters have on the 2nd messenger pathway?
they speed the pathway up

*speeds up cell division*
what effect do electrophiles have on DNA?
electrophiles damage DNA

(they are attracted to DNA and proteins)
what are two examples of radiation carcinogens?
1. UV rays
2. Ionizing radation (X-rays, gamma rays)
three wavelength ranges of UV rays?
UVC - most carcinogenic: ozone layer keeps it out
what is the only human retrovirus that is implicated in human cancer?
(Human T-cell Leukemia Virus type I -> luekemia/lymphoma)
1. HTVL-1 binds to?
2. is transmitted by?
1. CD4+ T cells
2. body fluids (semen/blood/breast milk)
what are the three DNA viruses that show a strong correlation with human cancer?
1. HPV
2. EBV
3. HepB
what is an episome?
a piece of DNA that is not integrated into the DNA.
which DNA virus "lives" in an episome?

(also, certain forms of HPV)
EBV is associated with what type of cancer?
Burkitt's lymphoma

(prone to develop in Africa: reason for this unknown)
HBV is associated with what type of cancer?
hepatocellular carcinomas
what is the theory behind hepatocellular carcinoma caused by HBV?
HBV damages hepatocytes
Liver regenerates
regeneration keeps going resulting in a tumor
HPV is associated with what type of CA?
Cervical cancer
(HPV DNA seen in 90-100% of cases)
there are subtypes of HPV. which two are:
1. linked to warts?
2. indicated to cancer?
1. HPV 6 and 11
2. HPV 16 and 18 (20% chance of developing CA)
Describe the HPV lifecycle
1. HPV infection requires a mucosal epithelial cell that is still able to proliferate
2. virus lies dormant in epithelial cells as they migrate and mature
3. close to the surface - virus replicates and infects cells
what cells does HPV target?
HPV targets the cells in the basal layer of the cervical epithelium
HPV produces E6 - what does this protein do?
E6 inactivates p53
HPV produces E7 - what does this protein do?
E7 inactivates Rb protein (sits in active site)

*results in uncontrolled cell division
What about E2?
CONTROLS expression of E5, 6, 7

(high risk HPV has a nonfunctional E2 = loss of control of expression)
How is the HPV genome related to low and high risk of infection?
low risk: HPV DNA is an episome, does not integrate into host cell
high risk: HPV DNA is integrated into the host chromosome (the integration cleaves E2 gene)
what happens when the E2 gene is damaged?
E6 and 7 are able to be active: they shut down p53 and Rb
besides HPV, what are two other co-factors in generation of Cervical Tumors?
anatomically, where does the HPV infect cervical cells?
in the transition zone