Malignant melanocyte tumor
|What is PTHRP?||
the actual dividing tumor
the supporting vessels, CT, and cells from the host
can be induced and manipulated by the parenchyma
lots of CT = scirrhous
Tumors can induce angiogenesis. This is essential for tumor survival.
|Capsule vs. pseudocapsule||
Capsules encapsulate benign
Pseudocapsules encapsulate malignant
benign tumors w/o a capsule
usually composed of atrophic, dead host tissue
Encapsulated (thus, usually benign) tumors that resemble normal derivatives of all three germ layers
Growths resemble normal tissue of organs (brain, hepatice, etc.)
E.g., ovarian teratoma with teeth, hair, etc.
Hyperplasia - ↑ cell numbers
Metaplasia - change of differentiated tissue to another
Dysplasia - disorderly development/differentiation; commonalities w/ malignant growth
*All of these increase the likelihood of developing neoplasia
*All of these are reversible processes
*All of these are benign, non-neoplastic processes
|Who often can go de-differentiation?||
|Where is dysplasia mainly encountered?||
|What is cachexia?||
"Wasting syndrome"- progressive loss of body fat and muscle.
Finger-like projection from an epithelial surface. Benign or malignant
pedunculated - long stalk
sessile - no or short stalk
papilloma - multiple projections
adenomatous - with glandular elements
Stalks contain mesenchyme and CT that supports the apical cells of the polyp
Lack of differentiation due to oncogenesis of pluripotent stem cells in a tissue.
pleomorphism: fewer cilia, secretory elements in a tumor for a specific tissue
unduly large nuclei
cell size discrepancy
*Benign tumors are "more differentiated" than malignant ones
|What is T0 in staging?||
|Who usually has NRAS mutation?||
|Name two groups of CDK inhibitors.||
|Using what to mesenchymal tumors metastize?||
|Are Seminomas/Hepatomas benign?||
No, despite suffix.
|Functional/biochemical features of tumor cells||
(This is not benign/malignant-specific)
These features are due to genetic changes within tumor cells.
motility (ameboid motion)
abnormal secretions (e.g., metalloproteases degraded BM)
↓ adhesion btwn cells
↓ IC communication
changes in cell-surface carbs
-oma suffix = benign tumor. (Granuloma is a notable exception)
carcinomas = malignant epthelial tumors
sarcomas = malignant mesenchymal tumors
-blastoma = neoplasms from pluripotent cells
contain mixtures of epithelial and mesenchymal elements
|What do mutant NF1/2 do?||
NeuroFibromatosis -> NeuroFibrosarcoma.
|What is an adenoma?||
Benign epithelial neoplasm- proliferation of glands, tightly arranged to create a mass, OR benign epithelial neoplasm that forms glandular patterns.
|What does cyclin D like?||
First complex created!
|What is cytokeratin?||
Type of intermediate filament- epitheloid cells.
|What is Vimentin?||
Type of intermediate filament- mesenchymal cells (muscle, cartilage, fibroblasts, endothel).
|What do you mainly use histochemistry for?||
|What is present in 100% of nasopharyngial carcinoma?||
|What is FISH?||
Fluorescence method for identifying specific DNA sequences.
|What does asbestos cause?||
Meotheliomas, bronchogenic carcinomas, GI cancers.
|Benigh vs. malignant tumors||
Malignant tumors have metastatic potential. Benign tumors do not.
Metastatis is the secondary growth of a tumor at a site separate from the primary growth
|General properties of neoplasms||
growth unrelated to host organism
atypic (structural/functional abnormality)
autonomous (indep. of growth controls)
aggressive (displace and invade host tissue)
Note that there is not satisfactory definition for neoplasm.
|What is carcinoma medullary?||
Rich epitheloid component, less stroma- soft tumor.
Diffuse, thus hard to identify, or assess real size/borders (often assessed as smaller than they are).
|What is carcinoma scirrhous?||
Significantly more stroma, often secretes a lot of collagen.
Common in gallbladder, lung, pancreas.
|What is Linitis Plastica?||
Signet-ring cell carcinoma. The stomach does not expand (=typical of lymphoma as well).
|What is grading?||
How well-differentiated the tissue is (1 is well, 3 is poorly).
Subjective, thus problematic.
|Where do you see more matrix- Fibroma or Fibrosarcoma?||
|What does p53 do?||
Stimulates transcription of several genes that mediate cell-cycle arrest (by p21, during late G1) and apoptosis (by BAX).
|What is Xeroderma Pigmentosum?||
Inhertied disorder, defective DNA repair genes (Nucleotide Excision Repair).
Patients are at increased risk for develipment of cancers of the skin when exposed to UV rays.
|What is Desmin?||
Type of intermediate filament - smooth, sometimes striated muscles.
|Where can lung carcinoma originate?||
Pneumocytes, bronchial epithelium, metastases.
|What are Teratomas?||
Neoplasms representative of more than one germ layer, usually all three- principally encountered in the gonads.
|What is the cell cycle duration in malignant cells compared to normal cells?||
|What are Polycyclic Aromatic Hydrocarbons?||
The most potent carcinogens known!
Require metabolic activation.
|What is a cystadenoma?||
Benign epithelial neoplasm that forms large cystic masses. Can be in a pattern of Papillary Cystoadenoma.
|What is pleomorphic sarcoma?||
Different types of cells- spindle, giant. All hyperchromatic.
Every mesenchymal tumor can look like this.
[you have pleomorphism in carcinoma etc as well]
Hamartomas and choristomas are neoplasms.
False - both are non-neoplastic lesions. Many are incidental and do not impede normal tissue function.
|What is VHL?||
von Hippel Lindau- the protein forms a complex that functions as ubiquitin ligase. Lack of it prevents degradation of HIF1 and is associated with increased levels of angiogenic GF.
|Where is the HPV genome in benign neoplasms? Malignant?||
|What extrinsic mechanism affect cell growth in tumors?||
Host factors- hormonal influences, blood supply (partially affected by tumor).
|What is Tamoxiphen? When is used?||
Antibody for Estrogen receptor.
Used in treatment of breast cancer, when abundance of receptors can be identified in the tissue.
|What does Aflatoxin B1 do?||
Cause HCC, by mutating p53.
|What does Vinyl Chloride cause?||
The extremely rare HemangioSarcoma of the liver.
|When is RB re-activated?||
During the M phase, by cellular phosphatases.
|Where do cells damaged by ionizing radiation arrest?||
(involves p53 and others)
|What functions as tumor antigens?||
1. Products of mutated oncogenes and tumor suppressor genes.
2. Products of other mutated genes.
3. Overexpressed cellular proteins.
4. Aberranly expressed cellular proteins (not in this tissue, only early in development).
|How does chronic inflammation promote cancer?||
1. Production of cytokines, which stimulate the growth of transformed cells.
2. Increase the pool of tissue stem cells, which become subject to the effect of mutagens.
3. Directly promote genomic instability through the production of ROS.
|After fixation, what processing is often used?||
Tissue processor that replaces water with paraffin, that solidifies in room temperature.
|In which domain of the p53 protein do most mutations occur?||
DNA binding domain!
|What features characterize familial cancers?||
1. Early age at onset.
2. Tumors arising in 2+ close relatives of the index case.
3. Sometimes, multiple/bilateral tumors.
|How does UVB light damage DNA?||
Related to formation of pyrimidine dimers.
Fixed by NER, which is faulty in Xeroderma.
|What is the hierarchy of vulnerability of different tissue to radiation induced cancers?||
1. LEUKEMIAS (except for CLL).
2. Thyroid, in the young.
Last- skin, bone, GI tract.
|Which carcinoma tends to spread in the WALLS of blood vessels?||
Renal cell carcinoma (also hepatocellular carcinoma).
|What do you see in Capillary Hemangioma?||
Cluster of tight capillaries- the younger the person, the tighter the capillaries.
What is an adenomatous polyp?
What is a papillary polyp?
Adenomatous polyp: raising of the mucous and epithelium, with many glands inside.
Papillary polyp: Raising of the mucous and epithelium, fingers-shaped.
|What does the cyclin D-CDK4 complex do?||
Phosphorylates RB, causing it to dissociate from the E2F transcription factor.
Mutations in the complex can mimic mutation in RB.
|Why are benign tumors manifest more by elaboration of hormones?||
Hormone secretion requires a decent level of differentiation.
|What do elevations of AFP level indicate?||
HCC and germ-cell tumors of the testis.
|What do you see in Cavernous Hemangioma?||
Black affliction (these can also be metastases of melanoma. Can differentiate by radioactively marking erythrocytes).
|What fixative can you use PCR on?||
Tissues that have been fixated in formaldehyde.
|Sign of infection with HPV in cell?||
Aura in cytoplasm. A result of degradation in cytoplasm.
|Why are keratin pearls markers of well differentiated tumors?||
Because it means the cell is differentiated enough to function.
|What is round-cell sarcoma? Who is typically that?||
Small abundunt cells, not a lot of cytoplasm, called "blue tumors".
Typical of Ewing, Neuroblastoma, certain carcinoma or lymphomas (Wilms tumor in kidney).
|What can you see in primary brain cancer?||
Since it originates from Glia cells, you can see a gradual transformation and not an obvious mass with normal tissue beyond it.
|What are the two manners by which cancer causes enlargement of lymph nodes?||
1. Spread and growth of cancer cells in the lymph node.
2. Reactive hyperplasia, even without cancer cells in the node (reacting to tumor cell debris/antigens),