Chapter 4 Flashcards
(34 cards)
What are neoplasms?
Uncontrolled “New growth” of cells that cannot be adequately controlled by normal regulatory mechanisms in the body.
How are human tumors classified?
Autonomous: Growing independently of normal cell growth factors and stimuli.
Excessive: Unceasing growth even in the presence of normal cellular proliferation regulators.
Disorganized: Growth not following the normal rules of tissue formation or organ development.
What are the main differences between benign and malignant tumors?
(Macro, Micro, Cellular differences)
**Benign: **Limited growth potential and good outcomes.
Macro: Clearly demarcated and usually encapsulated. Expansive growth compresses local tissue.
Micro: Differentiated, resemble the tissues from which they arose.
Cellular: Uniform features. Nucleuses might have different shapes but are around the same size. Chromatin evenly distributed.
**Malignant: **Uncontrollable growth that will eventually murder the host.
Macro: Lack capsule or clear demarcation. Invasive growth infiltrates surrounding tissue without sharp borders. Lymphatic invasion.
Micro: Undifferentiated, demonstrate anaplasia, new features not seen in the normal tissue they arose from.
Cellular: Pleomorphism, cells are heterogeneous in size, shape and function. Typically-high nuclear-to-cytoplasmic ration (N/C ratio). Hyperchromatic. Vessel invasion. Internal necrosis. Hemorrhage.
How do tumors metastasize?
- Primary tumor growth: “Normal” cancer growth
- Metastatic clone: Tumor cell becomes capable of metastasis.
- Proliferation of clone: Invades local vessel/Otherwise leaves area
- Transport by circulation (Lymph/Blood/Seeding surfaces in cavity)
- Embolization
- Invasion of tissue around embolization
- Hooray! New tumor!… wait.
List a few benign mesenchymal cells and their malignant equivalents.
Benign:
- Fibroma (Fibroblast)
- Lipoma (Fatty tissue)
- Hemangioma (Endothelial cell of blood vessel)
- Leiomyoma (Smooth muscle)
- Rhabdomyoma (Striated muscle)
- Chondroma (Cartilage)
- Osteoma (Osteoma)
Malignant:
- Fibrosarcoma
- Liposarcoma
- Angiosarcoma
- Etc Just add sarcoma
List a few benign epithelial cells and their malignant equivalents.
Benign:
- Epithelioma/Papilloma (Squamous epithelium)
- Transitional cell papilloma (Transitional epithelium)
- Adenoma (Glandular/ductal epithelium)
- Carcinoid (Neuroendocrine cells)
- Liver cell adenoma
- Renal cell adenoma
Malignant:
- Squamous cell carcinoma
- … add carcinoma.
How do carcinomas differ from sarcomas?
**Carcinoma: **Cancerous epithelial cells
**Sarcoma: **Cancerous cells of the mesenchymal
Lymphoma
Malignant lymphoid tumor
Glioma
Malignant glial cell
Seminoma
Malignant testicular seminferous epithelial cell
Teratoma
“Monster” germ line tumors that create embryonic cells that differentiate into various cell types and tissues. Skin, hair, teeth… your basic Carpenter Thing critter.
Teratoma versus mixed tumor
Mixed tumors only have one epithelial or mesenchymal neoplastic component whereas teratomas tend to have several types of cells.
Typical: Benign salivary gland mixed tumor.
Not typical: Malignant carcinosarcomas in the uterus
Eponymic tumors
Tumors that defy standard schemes and criteria so they get their own fancy names.
Ex.
Hodgkin’s lymphoma of the lymph nodes
Ewing’s sarcoma of the bones
Kaposi’s sarcoma of the skin
Difference between tumor stage and grading?
Staging: Clinically assessing extent of tumor spread. Exam, x-ray, biopsy, surgical exploration.
TNM Staging: T (tumor size), N (Lymph node involvement), M(distant metastases)
Grading: Histological exam
Grade I: Well differentiated
Grade II: Moderately well differentiated
Grade III: Undifferentiated
Both are used to decided prognosis or outcome but staging has the most predictive value. One crappy looking cell does not a death cancer make.
Are there definitive or absolute biochemical differences between normal and neoplastic cells?
No and as such there are no biochemical tests that can positively ID them as such.
What are some biochemical and structural differences between normal and malignant cells?
Pg. 76 for more detail but briefly:
Major differences are all relative and qualitative. Malignant cells are generally somewhat simpler, designed to survive on their own under unfavorable conditions and maybe have such features as:
- Fewer mitochondria
- Intercellular contact sites
- Hyperchromatin
- Free ribosomes
- CEA (tumor antigen)
- AFP (alpha-fetoprotein. Normally only seen in fetal cells)
How do tumor cells grow in vitro?
**Grow autonomously. **
Well and easily because their metabolic needs are much simpler than a normal cell. The only need a basic bath of carbs, proteins, vitamins, and essential minerals.
Tumor cells lack **contact inhibition **and will continues to try and grow despite coming on contact with vessel walls.
They also don’t exhibit anchorage dependent growth or the cell adhesion seen in normal cells.
Many also secrete their own growth hormones: **Autocrine stimulation. **
Most important exogenous and endogenous causes of cancer?
**Exogenous = Cancerogenic factors **
Chemicals/physical agents/Viruses
Endogenous: Residing in the genome of the cell
Confusing bit: **Oncogenes **cause cancer but are identical to exogenous virus genes.
How do we identify causes of cancer?
- Clinical studies
- Epi studies
- Experimental studies
Examples of chemical carcinogens and their mechanism?
Polycyclic aromatic hydrocarbons: From tar/smoke. Mimic structure of sex hormones which can induce tumors in sensitive tissues.
Aromatic amines: From dye and rubber. Excreted in urine = bladder cancer
Nitrosamines: Food additives. Procarcinogen converted by gut bacteria = Intestinal cancer
Steroid hormones: Ovary/adrenal injections. Stimulates endometrium = Endometrial carcinoma
Metals and inorganic compounds: Pesticides/ore. Skin contact/inhalation = skin/nasal cancer
How does UV light cause cancer?
DNA damage
People with xeroderma pigmentosum are extra screwed because they don’t have DNA repair enzymes
Compare oncogenic RNA and DNA viruses.
Acute-transforming RNA viruses:
Transduction: Oncogene exists in host and is incorporated by transcription into RNA viral genome. Virus enters new host cell and transduces oncogene into otherwise healthy cell.
Slow-transforming RNA viruses:
Insertion of RNA promoter gene: Viral promoter integrated into host DNA and activates oncogene in host cell.
DNA Viruses:
Integration: DNA virus genome integrated into host cell, causes host cell to become malignant. (Ex. EBV, HPV, HBV, HTLV-1)
Human DNA viruses linked to cancer?
HPV: HPV type 16 is linked to 60% of cervical carcinoma
EBV: Burkitt’s lymphoma (endemic type, Sub-Saharan African children and nasopharyngeal carcinoma.
HBV: Integrates into the DNA of neoplastic cells, implicated in liver cancer but exact mechanism is unknown (HBV does not have oncogenes).
HTLV-1: Human T-Cell Lymphoma/Leukemia Virus 1. HIV-lite that causes rare adult T-Cell leukemia
How do proto-oncogenese convert into oncogenes?
Proto-oncogenes: Normal genes that can be mutated into an oncogene.
- Point mutation: Single base sub (ex. *ras *gene)
- **Gene amplification: **Increased # of proto-oncogenes until malignant. (neuroblastoma in children)
- **Chromosomal rearrangement: **DNA gets mangled in various ways so that normally distant portions of genome touch each other. Fragment could act as a promoter for a proto-oncogene (Burkitt’s Lymphoma)
- **Insertion of the viral genome: **Typically from slow-transforming viruses, disrupts normal cellular regulation.(HBV)
