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Path - Chapter 7
Path
| Question | Answer |
|---|---|
| What are the two basic components of tumors? | clonal neoplastic cells (parenchyma); Reactive stroma (CT, blood vessels, macros and lymphos__important for growth) |
| What is a desmoplasia? | abundant collagenous stroma stimulated by parenchymal cells (in breast cancers it can be hard or Scirrhous) |
| These are benign epithelial neoplasms producing microscopically and macroscopically visible finger-like or warty projections? | papillomas |
| Define adenoma, papilloma, cytadenoma, papillary cytadenoma, polyp? | glandular; warty projections from epithelial surfaces; large cystic masses; papillary protrusions into cystic space; projection above a mucosal surface |
| malignant tumors arising in mesenchymal tissue are called what? | sarcomas |
| What are malignant neoplasms of epithelial cell origin (any germ layer)? | carcinoma |
| A patient has an enlarged right cheek, and a biopsy reveals proliferation of ducts as well as myxoid stroma that resembles cartilage, what is the process that resulted in this tumor? | divergent differentiation of a single neoplastic clone along two lineages (MIXED TUMORor pleomorphic adenoma) |
| what is the difference between mixed tumors and teratomas? | mixed tumor (single germ layer); teratoma (multiple germ layers) |
| What differentiates a benign vs malignant teratoma? | benign |
| Which dermal layer does the ovarian cystic teratoma principally differentiates through? | Ectodermal (dermoid cyst contains skin, hair, teeth, glands) |
| A heterotopic rest of cells, such as a well-developed nodule of organized pancreatic tissue found in the submucosa of stomach is termed what? Is it a serious complication? | choristoma; Very trivial |
| What five categories can differentiation be made between malignant and benign tumors? | differentiation; anaplasia; rate of growth; local invasion; metastasis |
| In general, benign tumors are (less differentiated or more differentiated)? | More differentiated (malignancy can also be well differentiated) |
| What aspect of differentiation is a hallmark of MALIGNANCY? | anaplasia (lack of differentiation) |
| A biopsy of a malignant tumor reveals non-uniform looking cells, both the size and shape. What term best describes this? | Pleomorphism |
| What changes to the nuclear morphology will be seen in anaplastic tumors? | abundant chromatin (clumped and dark staining); 1:1 nuclear to cytoplasm; large nucleoli |
| Abnormal mitoses such as tripolar spindles (as well as quadripolar or multipolar) is a sign of what? | anaplastic tumor |
| A student looks at a ditigal slide and thinks he sees Langhans Giant cells, however these cells have on or two large abnormal apearing nuclei and are surrounded by similar cells of varying sizes and shapes, what is the student really seeing? | Tumor giant cells in an anaplastic tumor |
| A biopsy of skin is done and the entire epidermal surface apears disordered with mitoses occuring not only in the basal layers but throughout, the basement membrane is intact and dermis appears normal, what is going on? | Carcinoma in situ (dysplasia) |
| What are the three factors affecting the rate of growth of a tumor? | doubling time; fraction of replicating tumor cells; rate at which cells die |
| A tumor with a small growth fraction is (faster or slower) and (responds well or doesn't respond well) to chemotherapy? | Slower; Does not respond well to chemotherapy (less dividing cell pool) |
| How can you treat a tumor with a very low growth fraction (small dividing pool)? | debulking the tumor with surgery/radiation forces cells into the cell cycle, then use chemotherapy (combined-modality treatment) |
| Do most malignant tumors grow more rapidly than benign lesions (in general)? | YES (growth rate correlates with the differentiation) |
| Why are cancer stem cells difficult to kill? | low rate of cell division; expression of drugs such as MDR1 (multiple drug resistance-1) |
| What are tumor initiating cells (T-ICs)? | cells that allow a human tumor to grow and maintain itself when transplanted to mice |
| T/F All benign tumors grow as cohesive expansile masses and all develop a fibrous capsule? | False; All grow as cohesive expansile masses, but some don't develop capsules (hemangiomas) |
| A well-defined cleavage plane is more likely to be found in a (benign or malignant) tumor? | Benign |
| Next to the development of metastases, what is the most reliable feature that differentiates malignant from benign tumors? | Invasiveness |
| This aspect of tumors unequivocally marks a tumor as malignant ? | Metastasis |
| All malignant tumors can metastisize except for these? | gliomas (glial cells of CNS); basal cell carcinomas of the skin |
| What are three methods by which cancers spread? | direct seeding of body cavities; lymphatic spread; hematogenous spread |
| What are some "open fields" that penetration of by malignant neoplasms may result in metastasis? | peritoneal cavity, pleural, pericardial, subarachnoid, joint space |
| What is a pseudomyxoma peritonei? | Mucus secreting appendiceal (appendix metastisized outside into peritoneum and stayed put) carcinomas fill the eperitoneal cavity with a gelatinous neoplastic mass |
| What is the most common pathway for initial dissemination of carcinomas? | lymphatics |
| How does "skip-metastisis" occur (when a lymph node in a chain is bypassed)? | due to venous-lymphatic anatomoses or obliteration of lymphatic channels |
| Does enlargement of lymph node in close proximity to cancer indicate dissemination ? | NO; it could be spread/growth of cancer OR reactive hyperplasia (due to increase antigen) |
| What are more readily penetrated by cancers (arteries or veins)? | Veins |
| What two organs are frequently involved due to hematogenous spread due to their capillary beds? | lungs and liver |
| Where do thyroid and prostate cancers typically metastasize to? | vertebral metastasis due to embolis through the paravertebral plexus |
| In general sarcomas prefer which route of metastasis? | hematogenous (this is a generality) |
| A patient has a mass on her left breast. A biopsy reveals the following; well differentiated structures with very few normal mitotic figures, a well-demarcated fibrous capsule and no evidence of metastasis. Is this tumor benign or malignant? | Benign |
| What are the major cancers in men and women? | Men: lung, prostate, colorectum Women; breast, lung, and colorectum |
| What is the leading cause of cancer deaths in women? | Lung cancer (breast has highest incidence) |
| What is one cause of the substantial rise in primary liver cancer in the past 30 years? | Hepatitis C |
| What is the single most important environmental factor contributing to premature death in the US? | Cigarette Smoking |
| Carcinomas are rare among children T/F? | TRUE; |
| A mutant form of RB tumor suppresor gene will give a 10000 fold increase chance of developing what? | retinoblastoma |
| Mutation of the APC (adenomatous polyposis coli tumor suppressor gene) increases the chance for development of what? | Familial adenomatous polyposis/colon cancer |
| Li-Fraumeni syndrome results from germline mutations of what gene? | p53 |
| MEN-1 and MEN-2 (multiple endocrine neoplasia) result from what mutations respectively? | menin transcription factor (MEN-1 Pituitary, parathyroid, pancreas) and RET tyrosine kinase (MEN-2 Thyroid, parathyroid, adrenals) |
| HNPCC (hereditary nonpolyposis colon cancer) has a defect in what? | DNA mismatch repair gene (MSH2, MLH1, MSH6) |
| What are some common features that characterize autosomal dominant cancers? | arise in specific sites or tissues (exception is Li-Fraumeni); Associated with specific marker phenotype; incomplete penetrance; variable expressivity |
| What is the most common cancer predisposition syndrome, accounting for the increased sucseptibility of cancer of the colon, small intestine, endometrium, and ovary? | HNPCC (Auto-Dom) |
| What are some of the inherited autosomal recessive disorders of defective DNA repair which may increase predisposition of cancer? | xeroderma pigmentosa, ataxia-telangiectasia, bloom syndrome, fanconi anemia |
| What are some features that characterize familial cancers? | early age of onset, close relatives, multiple/bilateral tumors |
| In familial melanoma, a mutation in this gene only accounts for 20% of cases? | p16 |
| What are some reasons chronic inflammation is linked with cancer? | inflammation injures tissues> proliferation of cells to repair tissues is aided by growth factors ect > increased number of stem cells > genotoxic radical oxygen species |
| This enzyme is increased in chronic inflammation, colon cancer, and other cancers, and is responsible for the conversion of arachodonic acid into prostaglandins? | COX-2 |
| These are examples of precancerous conditions? | chronic atrophic gastritis of pernicious anemia; solar keratosis of the skin; chronic ulcerative colitis; leukoplakia of the oral cavity, vulva, penis |
| What are the four classes of normal regulatory genes that are targets of mutation leading to cancer? | growth-promoting proto-oncogenes; growth inhibiting tumor suppresor genes; death regulating genes (apoptosis); DNA repair genes |
| T/F Over a period of time, many tumors become more progressive and aquire greater malignant potential (tumor progression)? | True; |
| What are the seven fundamental changes in cell physiology that together determine malignant phenotype? | self-sufficiency in growth signals (oncogene activation); insensitivity to growth inhibitory signals; evasion of apoptosis; limitless replicative potential; sustained angiogenesis; ability to invade and metastasize; defects in DNA repair |
| genes that promote autonomous growth in cancer cells are called what? | oncogenes |
| How are oncogenic growth factor receptors different than their non-oncogenic relatives? | Activation without growth factor binding; Constitutive dimerization |
| This growth factor receptor is constituitavely activated by point mutation and can cause MEN 2a and MEN 2b? | RET (Extracellular |
| Greater than 90% of gastrointestinal stromal tumors have a constitutively activating mutation in this receptor, which can be amenable with Imatinib Mesylate "targeted therapy"? | c-Kit or PDGFR (receptor tyrosine kinase) |
| An example of overexpression of growth factor receptor is seen in this receptor, which is overexpressed in squamous cell carcinoma of the lung, glioblastomas, and head and neck tumors? | ERBB1 (EGF) |
| What is the single most common abnormality of proto-oncogenes in human tumors? | point mutation of the RAS family genes |
| What are the three RAS genes in humans, and which cancers bear mutations in these genes? | KRAS (colon pancreas carcinoma); HRAS (Bladder); NRAS (hematopoetic) |
| Neurofibromatosis type 1 exemplifies what process of altered RAS activity? | GTPase activating protein (GAP) is mutated and cannot increase the GTPase activity of RAS hence leaving it in its active form |
| In Chronic myelogenous leukemia, what is the genetic abnormality? | translocation moves the non-receptor tyrosine kinase (ABL) to fuse with the BCR and create a constitutively active oncogene |
| What cancer can evolve if a translocation moves the MYC oncogene from chromosome 8 to Chromosome 14 fusing it with the IG gene? | Burkitt Lymphoma |
| These transcription factors are over-amplified in neuroblastomas; they are expressed in virtually every eukaryotic cell and belong to immediate early response genes? | MYC (N-MYC specifically) |
| CDKS become activated by binding to what? | cyclins |
| What inhibit CDKS? | CDKI (CIP/KIP family p21,p37 or INK4/ARF family p16 , p14) |
| What are the two checkpoints in the cell cycle? | G1/S (prevents replication of cells that have defects in DNA); G2/M (wether cell can safely inititate mitosis and separate sister chromatids) |
| Which checkpoint is particularly important for cells exposed to ionizing radiation? | G2/M |
| This tumor suppressor gene is altered in many cancers, causes cell cycle arrest through p21 by activation of pro-apoptotic genes such as BAX; it is REQUIRED by the G1/S checkpoint, and involved in the G2/M checkpoint? | p53 |
| Which checkpoint invovles only p53 mediated cell cycle arrest? | G1/S |
| Patients with retinoblastoma are at increased risk of developing these other cancers? | osteosarcomas and soft-tissue sarcomas |
| phosphorylation of Rb by this CDk-cyclin complex allows the cell to proceed theough the G1/S restriction point? | CDK4-Cyclin D |
| What is the two-hit hypothesis of oncogenesis and how does it apply to retinoblastoma? | both alleles need mutations; one hit is germ line and the other hit is somatic |
| Loss of heterozygosity of the von Hippel-Lindau(VHL) gene leads to what? | familial clear cell renal carcinoma |
| How does Rb control the entrance of the cell cycle into S? | Rb is hypophosphorylated & bound to E2F, which is needed for trasncription of cyclin E. Cyclin E activates CDK2 and the complex allows progression from G1 to S. Phosphorylation of Rb by CDK4-cyclinD removes Rb from E2F allowing transcription of cyclin E |
| This is the region of the Rb protein where mutations in tumors are normally found? | "Rb pocket" binding pocket for E2F |
| What are two mechanisms that Rb control Cyclen E transcription? | Sequester E2F; recruit histone methyltransferase and histone deacetylase to bind to promoters of E2F-responsive genes like cyclin E |
| This inhibitor binds to D-CDK4 and promotes the inhibitory effect of Rb? | p16 |
| one of these 4 key regulators of the cell cycle is altered in a variety of cancers | Rb, p16 (INK4a), cycling D, CDK4) |
| Certain viruses like HPV alter cell cycle progression by what mechanism? | they can bind Rb in the "pocket" preventing it from sequestering E2F; They can also bind p53 promoting its degradation |
| This gene is located on chromosome 17p13.1 and is the most common target for genetic alteration in human tumors? | p53 |
| homozygous mutations of p53 are (somatic or germ-line)? | Somatic (germline is rare and is called Li-Fraumeni) |
| What is the syndrome called when you inherit one mutated p53 allele? | Li-Fraumeni (autosomal dominant, large number of varied tumors occur at younger age) |
| What are three interlocking mechanisms by which p53 prevents neoplastic transformation? | quiescence, senescence, apoptosis |
| p53 has a short half life because of what? | It is associated with MDM2, a protein that targets it for destruction. Upon DNA damage p53 is post-transcriptionaly modified and released from MDM2 which activates its effects |
| This micro-RNA is involved in p53 signaling and targets both pro-proliferative genes (cyclins) as well as anti-apoptotic genes (BCL2)? | miRNA 34 |
| ATM is mutated in patients with this disease? | Ataxia-telangiectasia (increased incidence in cancer because of inability to repair certain kinds of DNA damage) |
| What are the two DNA damage sensing proteins that phosphorylate p53 and DNA-repair proteins after being triggered? | ATM and ATR (Rad3 related) |
| Tumors that retain normal p53 activity such as testicular teratocarcinomas and childhood acute lymphoblastic leukemia are more or less resistant to chemotherapy and irradiation (which induce DNA damage and apoptosis)? | Less resistant to these modalities; cancers with lost p53 activity cannot induce apoptosis based on DNA damage |
| What contributes to the poor prognosis of the basal subset of breast cancers? | mutations of p53 along with dominant negative function of p63 which antagonizes p73 (musketeers are down) |
| p53 induces apoptosis through transcription of these two pro-apoptotic genes? | BAX and PUMA |
| Loss of one APC gene results in this familial disorder? | familial adenomatous polyposis |
| WNT signaling is needed to prevent APC - associated complex destruction of B-catenin (T/F)? | TRUE; This is leads to B-catenin entering the nucleus and promoting proliferation |
| Mutations of B-catenin, which prevent it from binding to APC-destruction complex can lead to what? | excessive proliferation and some colon tumors |
| B-catenin normally binds to this surface protein, and loss of this "contact inhibition" can lead to certain carcinomas? | E-cadherin |
| The INK4a/ARF tumor suppressor gene has these two activites? | block CDK2-D via p16 (this keeps Rb hypophosphorylated); Inhibits MDM2 by p14 (keeps p53 active) |
| T/F 100% of pancreatic cancers and 83% of colon cancers have at least one-component of TGF-B mutated? | TRUE; TGF-B > SMADR > SMAD4 > transcription and inhibition |
| This tumor suppressor is mutated in COWDEN syndrome (autosomal dominant)? | PTEN |
| This may be the most commonly mutated pathway in human cancer? | PI3K/ATK |
| What does PTEN do? | Stops PI3K/ATK pathway |
| Describe briefly PI3K/ATK pathway? | Ligand binding > PI3K > IP3 > PDK1 > ATK > (inhibits TSC1 and TSC2) > mTOR > Proliferation |
| TSC1 and TSC2 are normally mutated in this disease, characterized by developmental malformations, unusual benign neoplasms such as cardiac rhabdomyomas, renal angiomyolipomas, and giant cell astrocytes? | tuberous Sclerosis |
| What is the molecular basis for neurofibromatosis type 1? | NF1 normally creates neurofromin which has GTPase activity taking activated RAS to inactivated RAS |
| Nuerofibromatosis type 2 is a result of NF2 mutation which prevents what? | neurofibronin 2 is a membrane cytoskeleton protein which normally is involved with cell-cell signaling and without it cells are unable to get normal growth arrest signals |
| Lack of this gene prevents ubiquitination and degradation of HIF-alpha and results in increased levels of angiogenic growth factors? | VHL (with oxygen HIFa is normally degraded by VHL) |
| This gene is associated with the development of Wilms tumor, is invovled with renal and gonadal differentiation and mesenchymal-to-epithelial transformation in the kidney? | WT1 |
| WT2 gene mutation is seen in this syndrome? | Beckwith-Wiedemann Syndrome (macroglossia, large birth weight, midline defects, ear crease/pit, hypoglycemia) |
| Mutations in PTCH (patched/hedgehog pathway) are involved with this disease, which predisposes to basal cell carcinoma and results in unusual facial appearances? | Gorlin syndrome (nevoid basal cell carcinoma syndrome) |
| Describe the extrinsic pathway of apoptosis? | FAS-FASL > trimerization of death domains > FADD binding > Activation of caspase 8 > Caspase 3 |
| Describe the intrinsic pathway of apoptosis? | DNA damage > p53 > increase BAX > shift balance of pro-apoptosis > pore in mitochondria > release of cytochrome c > caspase 9 > caspase 3 |
| Caspases can be inhibited by this protein family, which is upregulated in certain cancers? | AIPs |
| Some tumors have high levels of this protein, which can bind to the death inducing signal complex and prevent activation of caspase 8? | FLIP |
| This anti-apoptotic protein is often upregulated in 85% of b-cell lymphomas with the t(14;18)(q32;q21) translocation? | BCL2 (recall burkitts lymphoma) |
| Cytochrome c released from the mitochondrial membrane binds what to activate caspase 9? | APAF-1 |
| How can tumors avoid mitotic catastrophe? | Upregulation of temolerase; or; alternative lengthening of telomeres (allows cells to escape the bridge-fusion breakage cycle that eventually leads to instability and mitotic catastrophe) |
| What is the dual effect of neovascularization for tumors? | provide oxygen/nutrients; New endothelial cells promote adjacent growth of tumors by growth factors (IGF and PDGF) |
| Solid tumors cannot enlarge beyond 1-2 mm unless they are what? | vascularized |
| what does p53 do in terms of angiogenesis? | represses expression of pro-angiogenic molecules such as VEGF; stimulates expression of anti-angiogenic molecules such as thrombospondin-1 |
| Many tumors begin the process of metastasis by dissociation of cells from one another mediated by down-regulation of this membrane protein? | E-Cadherin (or mutations in catenin can reduce E-cadherin as well) |
| What are the two mechanisms of tumor migration? | protease (MMP, cethepsin, urokinase plasminogen activator); Ameboid movement |
| How is migration of tumor cells directed through the ECM? | tumor-derived cytokines (autocrine motility factors); cleavage products of matrix components(collagen and laminin); growth factors; Paracrine effectors produced by stromal cells (hepatocyte growth factor-scatter factor) |
| What is anoikis? | apoptosis stimulated by loss of adhesion (some tumor cells die in the vasculature by this method) |
| Overexpression of what adhesion molecule found normally on T-cells favors metastatic spread of tumors? | CD44 |
| What are some reasons why we see organ tropism (tumors favoring certain organs instead of resting at the first capillary bed)? | organ specific adhesion molecules; chemokines; nonpermissive environment |
| What are the two candidates for metastasis oncogenes, whose function is to promote a process called epithelial-to-mesenchymal transition (EMT) | SNAIL and TWIST (downregulate E-Cadherin) |
| What is the underlying defect in HNPCC (hereditary nonpolyposis colon cancer syndrome)? | Defect in DNA mismatch repair genes MSH2 and MLH1; microsattelites become unstable causing new alleles to be formed |
| Patients with xeroderma pigmentosum are increased risk for developing cancers of the skin after UV exposure. What is underlying defect? | mutation in genes involving nucleotide excision repair |
| Bloom syndrome defect is a gene that encodes what? | a helicase involved in homologous recombination |
| BRCA1 and BRCA2 are DNA repair genes that are involved in 25% of what? | familial breast cancer (BRCA2 is also in Fanconi anemia) |
| What is the warburg effect? | High aerobic glycolysis (less efficient) in tumor cells |
| What are some reasons why tumor cells prefer a less efficient means of metabolism (glycolysis-Warburg)? | hypoxic environment; allows carbons to be shunted into the anabolic pathway (building blocks needed for DNA synthesis) |
| Peutz-Jegher syndrome, associated with benign and malignant epithelial proliferations of the GI tract is a result of mutations of this tumor suppressor gene? | LKB1 |
| What does LKB1 do? | (peutz-Jegher syndrome); activates AMPK which is a negative regulator of mTOR (PIK3/ATP) halting anabolic metabolism and slowing tumor growth |
| What are two kinds of chromosomal rearrangements that can activate proto-oncogenes? | translocations and inversions (translocations are more common) |
| What gene is overexpressed by juxtaposition to an IGH locus in Mantle Cell Lymphoma? | cyclin D1 gene |
| Deletions are more common in nonhematopoietic solid tumors (T/F)? | True; |
| Amplification of proto-oncogenes results in these two mutually exclusive patterns identified microscopically? | double minutes; homogenous staining regions |
| N-MYC and and ERBB2 seen in neuroblastomas and breast cancers respectively are examples of (chromosomal rearrangements; gene amplification; epigenetic changes)? | gene amplification (double minutes and homogenous staining regions) |
| Hypermethylation of tumor suppressor genes will or will not promote cancer? | Promote (silencing) |
| T/F miRNAs can act as both a tumor suppressor and an ocogene? | TRUE; oncogene if it silences tumor suppressor |
| T/F no single oncogen can transform non-immortalized cells in vitro? | TRUE; |
| Carcinogenic initiators are all nucleuphiles or electrophiles | electrophiles (react with nucleophilic sites in cells) |
| Some cancer chemotherapeutic drugs which treated cancer only to evoke a seconf form of cancer (usually AML) are what group of initiators of carcinogenesis (direct or indirect)? | Direct |
| Which carcinogens require metabolic conversion to an ultimate carcinogen (direct or indirect)? | Indirect |
| Polycyclic hydrocarbons are indirect carcinogens present in what? | fossil fuels, animal fats (broiling meat), smoked meat |
| What is the active product in hydrocarbons which is carcinogenic? | epoxides (form adducts with molecules in the cell , DNA, RNA, proteins) |
| Where is benzo[a]pyrene found in? | cigarette smoke |
| Carcinogenic potency of a chemical is determined by what factors? | electrophilic reactivity; balance between metabolic activation and metabolic inactivation (p450) |
| Individuals with a suceptible form of CYP1A1 (a p450 gene) and who smoke are at higher risk for what? | Lung cancer |
| What can aflatoxin B1 (Aspergillus) increase the incidence of, by mutations of the p53 gene? | hepatocellular carcinoma (Africa and far east) |
| What are promoters and what purpose to they serve in chemical carcinogenesis? | they promote the division of already mutated cells so as to fix the change in the DNA created by the initiator |
| What are the cancers that are increased by exposure to UV rays? | squamous cell carcinoma, basal cell carcinoma, melanoma of the skin |
| Nonmelanoma skin cancers are associated with (intense exposure or total cumulative exposure) while melanoma of the skin is associated with (intense exposure or total cumulative exposure)? | Nonmelanoma |
| Which UV rays are responsible for the induction of cutaneous cancers? | UVB (pyramidine dimers) |
| Which DNA repair system is employed and overworked with excessive sun exposure? | nucleotide excision repair (faulty in xeroderma pigmentosum) |
| What are the most frequent radiation (ionizing) induced cancers? | AML and CML (followed closely by thyroid cancer) |
| Infection of this virus occurs though sexual intercourse, blood products, breastfeeding, and has tropism for CD4+ cells. It causes a form of T-cell leukemia/lymphoma and is endemic in certain parts of japan and carribean? | HTLV-1 |
| Does HTLV-1 have an oncogene? | NO |
| What aspect of HTLV-1 promotes tumor formation? | tax |
| tax is a region in HTLV-1 that promotes leukemia of T-cells, how? | promotes transcription of T-cell growth factors; upregulates cyclin D and downregulates p16; upregulates NF-kB (proliferative); interferes with ATM-mediated DNA repair functions >>>> all leads to monoclonal cell population emerging |
| What are the four DNA oncogenic viruses implicated in causation of human cancers? | HPV, EBV, Hep B, KSHV |
| The two products of HPV viral genes that are responsible for the oncogenetic potential of HPV are what? | E6 and E7 |
| What does E6 and E7 viral proteins do to promote carcinogenesis? | E6 binds and degrade p53 and BAX; E7 displaces E2F from Rb and promotes cell cycle progression, inactivate p21 and p27, activates cyclins |
| Are there differences in the affinity of E6/E7 from high risk HPV to low-risk HPV? | Yes; low risk has lower affinity and less incidence of cancer |
| What cancers has EBV been implicated for? | African form of burkitt; B-cell lymphomas (immunocomprimised); Hodgkin lymphoma; nasopharyngeal and some gastric carcinomas; rare T-cell and NK-cell lymphoma |
| What genes in EBV virus alter B-cell signaling pathways and help promote B-cell growth? | LMP-1 (behaves like constitutively active CD40 receptor; Activates BCL2); EBNA-2 (constitutively active NOTCH receptor > increase cyclin D) |
| How do infected B cells (EBV) prevent macrophages and monocytes from activating T-cells? | viral cytokine vIL-10 |
| What is the receptor for EBV located on B cells? | CD21 (CR2 complement receptor) |
| Describe the relationship of EBV with Burkitt's Lymphoma? | EBV acts as a B-cell mitogen causing polyclonal exoansion of B-cells; Majority are killed in CTL response; surviving B-cells are more prone to c-MYC t(8;14) which then creates neoplastic clone |
| 100% of nasopharyngeal crcinomas contain what virus? | EBV |
| What are the dominant effects of HBV that appear to lead to hepatocellular carcinoma? | immunologically mediated chronic inflammation (compensatory proliferation of hepatocytes, O2 radicals are mutagenic and genotoxic >> NF-kB activation blocks apoptosis >> hepatocytes accumulate mutations |
| This bacteria is implicated in the development of both gastric adenocarcinomas and gastric lymphomas? | Helicobacter Pylori |
| In early stages of gastric lymphoma, why is eradication of H.Pylori effective and capable of "curing" the cancer? | The B-cell lymphoma is monoclonal and requires (anti-H.Pylori - Tcell stimulation). Without H.Pylori, the T-cells will not activate the B-cells and promote growth (by activating NF-kB) |
| What immune cells are the major defense mechanism against tumor antigens? | CTL (CD8) via MHC 1 pathways (if APC phagocytoses the dead tumor products than CD4 cells can also react) |
| Melanomas over-express this NON-MUTATED protein, which stimulates an immune response by acting as an antigen and does not induce self-tolerance because it is normally produced in VERY little amounts? | Tyrosinase |
| What are the different kinds of tumor antigens? | Mutated genes (mutates p53); Over-expressed/Abberrantly expressed (tyrosinase/MAGE); Oncogenic viral proteins (E6); Oncofetal antigens (aFetoprotein); Altered cell surface glycolipids(mucins, MUC-1); cell type-specific differentiation antigens |
| A mass in a patient is detected and Elisa with anti-human anti-CD20 antibodies comes back positive, what kind of cancer is it (what cells)? | B-cell lymphoma (CD20) |
| Tumors that fail to express MHC class 1 on their surface are targeted by these immune cells? | NK-cells |
| A boy is infected with EBV and shortly afterwards he dies. Autopsy reveals a large lymphoma comprised of B-cells, further testing reveals a mutated SAP (adapter protein) gene. What syndrome did the boy suffer from? | XLP (X-linked lymphoproliferative syndrome) |
| What are some methods of immune escape seen in tumor cells? | Selection (tumors that are immunogenic are destroyed); reduction of MHC; reduced expression of costimulators (B7); Immnuosuppresion (secretion of TGF-B/CTLA-4 response); Antigen masking (glycocalyx); expression of FAS |
| This happens to individuals with cancer and includes loss of body fat and lean body mass, as well as profound weakness, anorexia, and anemia? | Cachexia |
| T/F cachexia is caused by the nutritional demands of the tumor? | FALSE; |
| This cytokine, secreted in high amounts by macrophages responding to tumor-cells may be responsible for cachexia because it mobilizes body fat and suppresses apetite? | TNF |
| How does cachexia hamper effective chemotherapy? | reducing the dosage that can be given |
| This is the most common endocrinopathy and 50% of individuals haev small cell lung cancer. Caused by ACTH or ACTH-like substance? | Cushing syndrome |
| What are the two processes associated with cancer-associated hypercalcemia? | osteolysis of bone; production of calcemic humoral substances by extraosseous neoplasms (PTHRP) |
| This disorder is characterized by gray-black patches of verrucous hyperkeratosis on the skin, and patients over 40 this is seen with some forms of cancer (paraneoplastic syndrome)? | Acanthosis nigricans |
| A patient with a history of bronchogenic carcinoma of the lung comes in with joint pain. He has clubbing of the fingers, and x-rays reveal new bone formation on the distal end of his femurs, and humerus, what neoplastic syndrome is responsible? | hypertrophic osteoarthropathy |
| A patient comes in with respiratory distress, an x-ray reveals pleural effusion that is tested and is an exudate. He has recently been diagnosed with pancreatic carcinoma. What is a likely underlying problem? | Trousseau syndrome (pancreatic cancer produce mucins which stimulate clotting resulting in embolism formation >>> pulmonary embolism) |
| What is the differnece between grading and staging? | grading |
| What does TNM stand for in the staging classification? | T |
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