Neoplasms I

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a very general term that encomppasses neoplasms as well as non-neoplasm lesions

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tumor

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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

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neoplasm

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adaptive change from one fully differentiated cell type to another fully differentiated cell type in adult tissue

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metaplasia

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varying size and shape

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pleomorphism

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forming finger like growths with a central stalk and epithelial surface

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papillary

papillomas are benign epithelial neplasm which produces finger like projectsions from epithelial surface

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some degree of loss of normal differentiation of cells and tissues,

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dysplasia

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a lesion which is histologically malignant but has not yet invaded

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carcinoma in situ

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a benign neoplasm with components representing all three germ layers

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teratoma

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a benign but disorderly mass of tissues normally present at the site usually not considered neoplasm

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hamartoma

totally benign - sometimes considered a neoplasm

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the vascular connective tissue supporting the parenchyma of an organ, or supporting the proliferating cells of a neoplasm

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stroma

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malignant tumor of striated muscle cells

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rhabdomyosarcoma

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tumors of smooth muscle cells

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Leiomyoma, leiomyosarcoma

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fibroma, fibrosarcoma

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tumors of fibroblasts

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normal cells in an abnormal location

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choristoma

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two ways to define malignancy

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1. ability of neoplasm to metastasize
2. ability of neoplasm to invade normal tissue

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a synonym for "malignant neoplasm"

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cancer

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the movement of malignant neoplastic cells from the primary tumor to another site formaing a new mass

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metastasis.

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how might neoplastic cells transfer to to a new location

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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"

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an epithelial malignancy

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carcinoma

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a mesenchymal malignancy

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sarcoma

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a benign neoplasm of a gland

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adenoma

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a malignant neoplasm of the gland

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adenocarcinoma

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a benign neoplasm of squamous epithelim

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keratoma

malignant = squamous cell carcinoma

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carcinoid

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a benign neoplasm of neuroendocrine cells - all are potentially malignant - likelihood of metastasize varies with location

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malignant neoplasm of melanocyte

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melanoma

this is weird - should technically be called melanocarcinoma but historically is referred to as melanoma

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hemangioma

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benign neoplasm of blood vessel

malignant: angiosarcoma

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immunopersoxidase marker for malignant epithelium (carcinoma)

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keratin intermediate filament

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immunopersoxidase marker for malignant mesenchyme (sarcoma)

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vimentin intermediate filament

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immunopersoxidase marker for hematolymphoid (lekemia/lymphoma)

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cell surface markers (LCA

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immunopersoxidase marker for melanocytes (melanoms)

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S100 protein

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A Immunoperoxidase marker for "neuroglial cells" (astrocytoma)

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GFAP, neurofilament

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can high grade dysplasia regress to a lower grade dysplasia?

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yes

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The degree to which neoplastic cells resemble normal cells (both morphologically and functionally)

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differentiation (high differentiation would be more normal)

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in a purely epithelial neoplasm the non-stromal component or epithelial component

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parenchyma

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"reactive" non-neoplastic mesenchymal tissue associated with an epithelial neoplasm

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stroma (although sometimes the stroma can be neoplastic - "mixed tumor"

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what promotes angio-genesis w/ metastasis

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growth factors produced by tumor cells

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formation of adhesion or fibrosis in vascular stroma of a neoplasm

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desmoplasia

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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

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1. invasion
2. metastasis
3. transplantability (one human to mouse)

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Autonomous growth in vitro happens do to what three mechanisms

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1. loss of contact inhibition
2. ability to grow w/o attachment
3. immortality (ability to grow indefinately in cell culture)

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three ways you get altered differentiation

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1. loss of normal products
2. new products (metaplasia)
3. expression of fetal genes

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indirect mutagens requires

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metabolic activation (indirect mutagens are metabolized to electrophilic species that are able to react with cellular DNA)

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genetic accidents leading to mutation happen during DNA replication, albeit at a very low rate

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stochastic events

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ability of cell to divide and produce all the differentiated cells in an organism

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totipotency

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can give rise to several other cell types, but those types are limited in number.

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multipotent

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disorganized mature specialized cells that normally occur in the affected part

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hamartoma

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two components to neoplasm

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parenchyma and stroma

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component of neoplasm that consists of one cell type (clonal)

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parenchyma (sometimes you get mixed neoplasm)

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epithelial and melanocytic tumor where the epithelial cells are the only neoplastic component

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basal cell carcinoma

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teratoma is derived from

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totipotent cells (gonadal cells) - differentiation along cell line

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lymphatic spread is usually carcinoma or sarcoma

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carcinoma - sometimes sarcoma

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sarcomas (and sometimes carcinoma) usually spread via

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hematogenous spread

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hematogenous spread is via venous or arterial system and goes where?

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venous - to liver and lungs

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arterial spread is less likely due to thick wall but access might be gained through

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capillaries

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grade is an attempt to predict? and depends on what two factors?

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the behavior or aggressiveness and relates to degree of differentiation and mitotic activity

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an attempt to stratify the extent of spread

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cancer stage

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what are the three parameters fo cancer stage

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1. size of primary
2. nodal involvement
3. hematogenous disemination
(parameters are different for diff tumor types)

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What are the two staging systems in current use

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TNM staging (Union Internationle Contre Cancer)
American Joint Committe on Cancer staging

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TNM stagig - what does T and N and M stand for
levels of each

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T = tumor (0-4 w/ increasing size)
N = nodes (1-3 w/ increasing number of nodes)
M = metastases (0-2) w/ more distant metastases

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predicts aggressiveness of tumor

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grade

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4 ways that chemical carcinogens cause DNA damage

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1. alkylation
2. damage leading to depurination/depyrimidation
3. bulky DNA adducts
4. double strand breaks

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do direct acting mutagenic chemicals require metabolic activation to be reactive w/ DNA

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no

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Hereditary nonpolyposis colocn cancer (HNPCC) is associated with a defect in

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DNA mismatch repair linked ot hMSH2 and related genes

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Bloom's syndrome is a rare human recessive disease characterized by

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chromosomal instability with predisposition to develop leukemia, lymphoma, and carcinoma

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Indirect acting carcinogens are usually activated by what enzymes

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CYP

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three things in the diet that are protective

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Antioxidants, Vit A (cell differentiation), and low caloric intake

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intial exposreu to carcinogen is called

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initiation

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after initiation the subsequent events that accelaerate the development of the neoplasm is called

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promotion (now refered to epigenetic events that favor tumor development

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genetc events that are required to confer malignant phenotype

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progression

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the time between initiation and clinical detection of tumor

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latent period

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the lesion after promotion and before progression

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preneoplasmic lesion

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the somatic mmutation hypothesis of cancer states that

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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

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the dysregulation of cell proliferation by constinuative activation of growth-stimulatory pathways or independence from physiologic proliferation signal involve what kind of genes

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proto-oncogens

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insensitiviety to growth inhibitory signals or loss of cell cycle inhibitors involve what kind of genes

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tumor suppressor genes

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Evasion of apoptosis invovolve what kind of genes

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Pro and Anti- apoptotic proteins

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Limitless replicative potential "immortalization" involve what kind of genes

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telomeres

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Angiogenesis as a phenotype of cancer involve what kind of genes

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multiple complex pathways

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invasion and matastasis of cancer involve what type of genes

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proteins involved in cell-cell and cell-matrix adhesion and matrix degradation

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genetic instability involves what kind of genes

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DNA repair genes "caretaker genes"

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a gene that encodes a protein that stimulates or mediates cell prliferation the normal counterpart of an oncogene

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prote-oncogene

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activated proto-oncogne (oncogene) may be activated via either mutation or

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aberrant expression (over-expression or ectopic expression)

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lack of differentiation

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anaplasia

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anaplasia vs. dysplasia

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anaplasia is lack of differentiation and dysplasia is disorderly growth. note: dysplasia usually happens in epithelia

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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

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Immunoperoxidase

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a grade of one is more or less differentiated than a grade 3 neoplasm

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grade one is well differentiated and grade 3 is poorly differentiated.
The highest grade denotes an anaplastic neoplasm

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tumor which display desmoplasia are called what

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scirrhous ("stony hard")hard due to the collagenous stroma

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lack of differentiation or anaplasia lead to the following morphological changes (5)

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1. pleomporhic: cells and nuclei
2. nuclear morphology (hyperchromatic, large, variable shape)
3. mitosis increased
4. loss of polarity
5. sometimes giant cells

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in naming neoplasms the prefix usually describes the

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phenotype of nepolasm

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in naming neoplasms the suffix describes

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the benign or malignant state

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precancertous or premalignant might involve what two types of lesions

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1. carcinoma in situ, CIS

2. some benighn neoplasms (adenomas and colon)

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barrett's esophgus might lead to what type of cancer

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adenocarcinoma

hyperpasia - metaplasia - dysplasia - adenocarcinoma

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which has the higer risk of becoming malignant - tubular or villous adenoma?

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villous adenoma

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dysplasia-carcinomal sequence

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premalignant epithelial lesions are recognized because of dysplasia

e.g cervix and esophagus

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adenoma-carcinoma sequence

e.g?

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some adenomas progress to malignancy

e.g colon

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one of the most important species involved in metabolism of polycyclic aromatic hydrocarbons such as benzopyrene in cigarette smoke

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CYP1A1 - plymorphisms increase risk of lung cancer in smokers

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Potts studied what population in his effort to understand carcinogenesis

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chimney sweeks - developing cancer

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XP is heterogenous w/ at least how many variants

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7 - each variant represents abnormality in different gene whose product is involved in nucleotide excitsion repair -

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what happens in promotion

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clonal expansion of initiated cells

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

these dividing cells are more sensitive to carcinogenic mutations

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why are dividing cells (say in the promotion phase) more prone to carcinogens than inactive genes

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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

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what is the difference between initiation and promotion

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initiator is mutagenic, initiation is irreversible. Promotor is not mutagenic, promotion is reversible

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how does RNA virsu such as Rous Sarcoma bring about a inheritable genetic change

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Reverse transcriptase allows viral RNA code to be transcribed into DNA