Neoplasia Flashcards
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NEOPLASIA DEFINITION
A
abnormal mass of tissue that’s growth exceeds the surrounding normal tissue and grows without stimuli
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Benign Neoplasm Definition
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neoplasm which lacks the ability to invade, destroy tissue and metastasize
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Malignant Neoplasm Definition
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A neoplasm that possesses the ability to invade, destroy tissue and metastasize
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Cancer definition
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referring to all types of malignant neoplasms.
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Urothelium
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Transitional epithelium, lining majority of GU tract
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Squamous stratified epithelium
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multilayered flattened epithelial cells arranged on a basement membrane (mitosis occurs near BM)
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Polyp
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mass arising from a mucous membrane protruding into the lumen of a hollow viscus
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Poly origin
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epithelial cell origin
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Sessile polyps
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flat, arising directly from the mucosal epithelial layer
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Pedunculated polyps
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extending from the mucosa through a fibrovascular elongated stalk + surrounding epithelium
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Cyst
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outer capsule + inner surface lined with epithelium, hollow-cavity filled with mucin
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Pseudocyst
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lacks inner epithelial lining
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Adeno-
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glandular epithelial origin
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Squamo-
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flat, scale-like epithelial origin
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Papillary
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epithelial growth that extend outward as small nipple-like structure or protuberance
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Papillo-
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referring to a epithelial polyp
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Myxo-
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mucin producing mesenchymal origin
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Rhabdomyo-
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skeletal muscle mesenchymal origin
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Leiomyo-
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smooth muscle mesenchymal origin
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Hemangio-
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blood vessel mesenchymal origin
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Lymphangio-
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lymph vessel mesenchymal origin
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Lympho-
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lymphoid organ origin
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Myelo-
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myeloid origin: part of marrow- eosinophil, basophil, neutrophil, and monocyte
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-oma
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Benign neoplasm suffix
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Carcinoma
malignant epithelial-derived cancer cells
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Sarcoma
malignant mesenchymal-derived cells
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Lymphoma
ALL are malignant lymphoid-derived cells
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Myeloma
ALL are malignant marrow-derived cells
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Leukemia
ALL are malignant hematologic-derived cells
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Melanoma
Malignant neoplasm of melanocytic origin
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Nevi
small benign melanocytic neoplasia
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Myelodysplastic syndromes
hematologic dysplastic neoplasm
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Plasmacytomas
discrete, solitary mass of plasma cells extramedullary or in bone
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plasma cell dyscrasias
expansion of the number of monoclonal bone marrow plasma cells
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Heterotopia
NOT NEOPLASTIC; congenital growth of microscopically normal cells or tissues in an abnormal location
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Choristoma
NOT NEOPLASTIC; congenital growth of microscopically normal cells or tissues in an abnormal location
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Hamartoma
NEOPLASTIC; excessive, focal overgrowth of cells and tissues native to the organ in which it occurs
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Differentiation
degree to which the cellular constituents of a neoplasm resemble mature elements of the cell type
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Differentiation of benign tumors
Highly differentiated
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Differentiation of malignant tumors
tend to be less differentiated
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Poorly differentiated tumors correlates with
advanced malignancy
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Maturation
Directly related to differentiation; advancement of differentiation
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Maturation of benign tumors
Very mature
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Maturation of malignant tumors
tend to be less mature
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Poorly maturated tumors correlate with
advanced malignancy
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Dysplasia
Atypical nuclear and cytoplasmic changes which are considered PREmalignant
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High grade dysplasia =
a lot of cellular atypia
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Anaplasia
Atypical and aberrant changes within a cell or group of cells reflective of a MALIGNANT neoplastic changes
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The greater the anaplasia
the more aggressive the tumor and the greater likelihood that the malignant cells become metastatic
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Neoplastic rate of growth
When cellular replication and survival exceeds cellular loss
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The greater the differentiation of a tumor, the _________ the growth
SLOWER; greater differentiation correlates with a slow growing tumor
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In-situ carcinoma growth
Carcinomas begin to grow in the epithelium, but are confined by the basement membrane.
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Why can't you have in situ sarcomas?
Sarcomas derived from mesenchymal cells are not confined because there is no BM
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What's the difference between a high-grade dysplasia and in situ carcinoma?
Nothing, virtually impossible to tell
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Encapsulated
Benign neoplasms: limited cohesive expansion
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Unencapsulated
Malignant neoplasms: have the capacity for local infiltration and invasion leading to extensive tissue destruction
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If an in situ carcinoma cell undergoes genetic alterations that allow it to invade the BM, it is now
a microinvasive carcinoma that has the ability to enter vessels if it comes into contact
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Metastasis
tumor cells ability to leave their primary site or origin (primary neoplasm) and spread to a distant area of the body (separated in space) where they implant and replicate
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Metastasis can occur via
direct seeding, lymphatic spread or hematogenous spread
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Metastasis: lymphatic spread
tumor embolus is carried by lymph until it reaches a point where it lodges and begins to grow (generally at regional lymph nodes)
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Lymphatic spread from breast cancer generally occurs at
axillary lymph nodes
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Metastasis: Hematogenous spread
tumor embolus is carried by blood vessels, there are no gate keepers - wide-spread
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Secondary Brain tumor indicates
Hematogenous spread, there is no lymph to brain
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Metastasis: Direct seeding
the cancer is exposed to a cavity and cancer cells are carried in the fluid within the cavity and carried to another surface
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Benign Neoplasm Characteristics
Encapsulated, well-differentiated, limited growth due to contact inhibition, freely moveable upon palpation due to capsule, no local invasion
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Malignant Neoplasm Characteristics
Well-differentiated to undifferentiated, loss of maturity, loss of tissue and cellular organization, nuclear atypia, increased levels of mitoses, large nucleus, tumor giant cells, non-encapsulated, fixed position, often necrotic of hemorrhaging, local invasion, capacity to metastasize
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Malignant tumor cell features
Large nucleus, abnormal increased mitoses, large, multi-nucleated cells, mitotic figures
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Grading
Related to degree of differentiation of malignant neoplasm - phenotypic property
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grade 1 neoplasms
well differentiated
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Grade 4 neoplasms
poorly differentiated
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High grade tumors have more
atypical cells and atypical mitotic figures, higher capacity to metastasize
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Low anaplastic potential
low-grade tumor
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Staging
classification of a tumor based on the extent of spread throughout the human body as determined by the UICC and AJC
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Staging considers
tumor size, the degree of regional lymph node involvement and the presence or absence of metastasis
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AJCC Staging
TNM (tumor size, number of nodes, metastasis)
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pT2N2 versus T2N2
'p' indicates pathologists staging based on the tissue biopsy; other indicates clinical staging based on diagnostics
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Incidence of cancer types is due to
environmental (geographical) and genetic determinants
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Cancer incidence in males
14% lung, 33% prostate, 11% colorectal
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Cancer incidence in females
33% breast, 12% lung, 11% colorectal
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Mortality from cancer in males
31% lung, 10% colorectal, 10% prostate
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Mortality from cancer in females
25% lung, breast 15%, 11% colorectal
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Autosomal dominant inherited cancer syndromes
means the person is born with a mutation in one gene and only needs to acquire 1 mutation in the other gene throughout life for cancer to develop (1 mutation = increased risk of cancer)
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Sporadic cancer
requires 2 mutations to occur throughout life, 1 in each chromosome, which is less likely to occur than if born with a mutation
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Familial Retinoblastoma
pt is heterozygous for Rb gene - when a mutation is acquired sporadically in the normal Rb gene chromosome (usually UV light), the patient becomes homozygous for mutant Rb gene, and retinoblastoma occurs
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Examples of Autosomal dominant inherited cancer syndromes
Retinoblastoma, MEN syndrome, Familial Adenomatous polyposis, hereditary nonpolyposis colon cancer, Li-Fraumeni Syndrome
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Li Fraumeni Syndrome
autosomal dominant p53 mutation, predisposes a person to a variety of cancer developments
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Autosomal Recessive Syndromes of Defective DNA Repair
pt is homozygous for the defective gene, inherits 2 copies of the mutated gene which puts them at increased risk for cancer
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Examples of Autosomal Recessive Syndromes
Xeroderma pigmentosum, Ataxia-telangiectasia, Fanconi anemia, HNPCC, Bloom Syndrome
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Familial Clustering
No clear defined transmission pattern, but som egene specificity; early age of onset, tumors in 2+ relatives
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Acquired Preneoplastic Disorders Include
Preceding inflammatory conditions, viral infection, chemical carcinogenesis, pre-existing benign neoplasm
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Growth-promoting proto-oncogenes
normal functional gene that regulates growth and differentiation, that when mutated is likely to lead to cancer due to its regulatory functions in a normal cell. Proto-oncogene -\> mutation -\> oncogene
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Oncogenes may alter
GFs, GFRs, signal transduction proteins, nuclear regulatory proteins, cell cycle regulators
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sis gene
oncogene that increases GF production
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erb-B2 gene
oncogene that increases GF receptors
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ras gene
oncogene that encodes for a mutated signal transducer protein (constitutively active)
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myc gene
oncogene coding for mutant TF (nuclear regulatory proteins); active w/o signal transduction
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Mutation examples
point mutation, chromosomal rearrangement, gene amplification
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Burkitt's Lymphoma - c-myc mutation type
chromosomal rearrangement of 8 and 14
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n-myc mutation type
gene amplification
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anti-oncogenes
regulate nuclear transcription, cell cycle, signal transduction, stimulate cell surface suppressor molecules; normally act as BRAKES to cell cycle
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Growth inhibiting cancer suppressor genes (anti-oncogenes)
Normally suppress growth, but when mutated can no longer suppress growth
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Genes which regulate apoptosis
prevent or promote programmed cell death
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Multi-step carcinogenesis
requires a mutation that activates an oncogene AND suppresses an anti-oncogene, followed by clonal expansion and neoplasm formation
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Point mutation example
retinoblastoma
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Examples of anti-oncogenes
Rb, p53, BRCA1-2
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Clonal expansion characteristic
polyclonal cell population
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malignant cells have a high number of cells in G1-M phase
G1-M phase
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Malignant neoplasms have the ability to recruit
angiogenesis
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Angiogenesis - Proto-oncogenic regulation
Stimulate blood vessel growth.
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Angiogenesis - Tumor suppressor gene regulation
Normally inhibit blood vessel growth, unless mutated
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an invasive tumor that has gained the ability to breach basement membrane has likely undergone genetic alteration and now has the ability to bind
laminin of basement membrane
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monoclonal expansion --\>
heterogeneity of the cell population overtime due to mutations in various daughter cells leading to sub-types of cells with various capabilities
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In situ transformation to invasive carcinoma
Cell must lose adhesion molecules to adjacent cells, obtain an active collagenase to break down ECM, tumor cells then bind to laminin receptors of BM
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Intravasation
attach and invade the BM of the vessel and migrate through the tight junctions of the endothelial cells
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Satellite nodules
earliest example of metastasis (intra-organ metastasis)
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Secondary tumor
arises in a distant location from primary
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Chemical initiator
causes a change in the cell which makes it susceptible to the development of a neoplasm. Initiation alone is insufficient for neoplasia to occur
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2 types of initiators
Direct acting agent and Indirect acting agents
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Indirect acting agents
Require in-vivo metabolic conversion into an active definitive carcinogen (metabolite or free radicals)
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v-onc
proto-oncogene mutation due to viral transduction
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c-onc
proto-oncogene mutation due to influences that alter their function in situ
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p53 is an example of
tumor suppressor (anti-oncogene)
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Rb is an example of
tumor suppressor (anti-oncogene)
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BRCA-1/2 is an example of
tumor suppressor (anti-oncogene)
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Direct acting initiator
Require no chemical transformation to induce their carcinogenic potential
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chemical initiators are
mutagenic at the molecular level inducing mutations in oncogenes
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Promoters
themselves are not mutagenic. Rather they stimulate activation and production of enzymes capable of inducing cell growth and proliferation.
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Examples of direct-acting initiators
alkylating agents, cyclophosphamide, chlorambucil, busulfan, melphalan, immunosuppressants
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direct-acting initiators are
weak carcinogens
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Examples of indirect-acting initiators
Polycyclic aromatic hydrocarbons, Aromatic amines/azo dyes, Aflatoxin B1 – Produced by Aspergillus flavus, Nitrosamines and amides
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Polycyclic aromatic hydrocarbons
indirect-acting initiator, potent carcinogen, can cause skin, colon, lung, bladder cancer, sarcoma
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Aromatic amines/azo dyes
indirect-acting initiator, activated by the cytochrome P-450 oxygenase activator systems, associated with HCC
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β-naphthylamine
indirect-acting initiator, present in aniline-dyes, associated with bladder cancer
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Aflatoxin B1
indirect-acting initiator, Produced by Aspergillus flavus, when Hep B infected person is exposed = increased risk of HCC
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Nitrosamines and amides
indirect-acting initiator, common food preservatives activated by gut bacteria, gastrointestinal carcinomas
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Exogenous promoters
Saccharin and cyclamates, Diethylstilbestrol (DES), Exogenous hormones
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Endogenous Promoters
Hormones, Bile salts/Dietary Fat
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UV exposure
causes pyrimidine dimers in DNA that overrides the body's inherent Nucleotide Excision Repair (NER) mechanisms
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UV exposure primarily causes
cutaneous malignancies
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UV, electromagnetic, particulate, radon
Many can act directly by inducing DNA breaks or indirectly by generating free radicals
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Cytotoxic viruses
inject their DNA/RNA into a cell, this becomes incorporated into cells DNA and causes mutations/altered genes
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HPV
DNA oncogenic virus
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HPV Types 16 and 18 are associated with
invasive squamous cell carcinoma
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HPV Types 1, 2, 4, 7 are associated with
Benign squamous papillomas
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HPV Types 6 and 11 are associated with
Genital lesions with low malignant potential
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Epstein Barr virus (EBV)
DNA oncogenic virus
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EBV is associated with
Burkitt's Lymphoma, B-cell lymphoma
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HBV virus
DNA oncogenic virus
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HBV is associated with
HCC esp in combo with Aflatoxin B1
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Kaposi virus
DNA oncogenic virus
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Kaposi virus KSHV is associated with
development of AIDS related Kaposi sarcoma
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Human T cell leukemia virus (HTLV-1)
RNA oncogenic virus
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Human T cell leukemia virus (HTLV-1) is associated with
T cell leukemia/lymphoma
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Hep C virus
RNA oncogenic virus
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Hep C virus is associated with
HCC
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Helicobacter pylori
gastric bacteria associated oncogenesis (gastric carcinoma, MALT lymphoma)
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MALT lymphoma caused by h/ pylori can be treated with
abx
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Local effects from tumor on host
Effects caused at site due to tumor growth
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Hormonal effects from tumor on host
tumors may possess the ability to secrete hormones or hormone-like factors
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Small cell cancer of the lung often secretes
ACTH causing Cushing's Syndrome
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Cachexia
systemic effect due to tumor, causing increased TNF-alpha and cytokine release, resulting in increased basal metabolic rate, in addition to tumor cells increased need for nutrients
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Paraneoplastic syndrome
Constellation of physical findings that are in association to products of the tumor
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migratory thrombophlebitis
Malignancies associated with hypercoagulability
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Tumor lysis syndrome
group of metabolic complications that can occur after treatment of cancer: hyperkalemia, hyperphosphatemia, hyperuricemia and hyperuricosuria, hypocalcemia, and consequent acute uric acid nephropathy and acute renal failure
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Anti-tumor defenses include
CTL, NK, Macrophages, immunosurveillance, immunotherapy against tumor antigens
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Histology
staining and viewing tissue morphology and cells in relation to another
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Cytology
Cellular staining to look for characteristics of individual cells
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DNA probe
look for specific DNA sequences characteristic of cancer type
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Carcinoembryonic Antigen (CEA):
colon cancer
170
Alpha-Fetoprotein (AFP):
HCC
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Beta Subunit Human Chorionic Gondotropin (β-HCG):
choriocarcinoma
172
CA-125
ovarian cancer
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Flow cytometry
use to quantify B and T cells
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exfoliative cytology
scrape away epithelium and stain
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Fine needle aspiration
insertion of a needle into the neoplasm to collect fluid and cells
