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Neoplasia by Mind Map: Neoplasia

1. Epidemiology

1.1. MCC Cancer Deaths

1.1.1. Lung

1.1.2. Breast

1.1.3. Prostate

1.1.4. Colo-recal

1.2. MCC Cancer in Men

1.2.1. lung

1.2.2. prostate

1.2.3. colo-rectal

1.2.4. hematopoietic

1.2.5. urinary tract

1.2.6. pancreas

1.3. MCC Cancer in women

1.3.1. lung

1.3.2. breast

1.3.3. colo-rectal

1.3.4. hematpoietic

1.3.5. ovary

1.3.6. pancreas

1.4. MCC Cancer in Children

1.4.1. Leukemia

1.4.2. Lymphoma

1.4.3. Brain

1.4.4. Colo-rectal

1.4.5. Bone & Soft Tissue

1.4.6. Endocrine

1.5. Change in Incidence/Death

1.5.1. decline for GI better food preservation change in dietary habits

1.5.2. decline for breast, uterine, cervical improved screening early detection

1.5.3. lung cancer reduce smoking prevalence reduce environmental smoke exposure

1.5.4. inc incidence among ethinic groups multifactorial socioeconomic environmental genetic

1.6. Factors for Cancer incidence

1.6.1. hereditary/genetic predisposition 5-10% of all cencer autosomal dominant single mutant gene point mutation in single allele mutation in second allele tumors arise in specific sites specific marker phenotype autosomal recessive defective DNA repair very rare xeroderma pigmentosum ataxia-telangiectasia bloom syndrome fanconi anemia familial cancer occur at higher frequency in famlies pattern not clearly defined siblings - 2-3x great risk no marker phenotpe early onset < 40 multiple/bilateral tumors fam hx of cx in 2 or more 1/2 degree

1.6.2. age

1.6.3. social habits

1.6.4. environmental/occupational

1.6.5. pre-existing disease states

1.6.6. chemo-radiation therapy

2. Definitions

2.1. Hyperplasia

2.1.1. inc in cell @

2.2. Hypertrophy

2.2.1. cell enlargement without division

2.3. metaplasia

2.3.1. irreversible change of one mature type to another

2.4. Neoplasia

2.4.1. new abnormal growth (tumor) proliferative uncoordinated autonomous genetically unstable composed of proliferating neoplastic parenchyma fibro-vascular supporting stroma

2.5. polyp

2.5.1. abnormal growth

2.5.2. from mucosal surface

2.5.3. attached by stalk

2.6. desmoplasia

2.6.1. dense fibrous stroma

2.6.2. seen w malignant tumors

2.6.3. invasion into ECM

2.6.4. altered stroma activated fibroblasts cytokines growth factors

2.6.5. inc collagen deposition

2.6.6. histology dense pink fibrotic desmoplasia

2.7. Benign tumors

2.7.1. Examples -oma epithelial cell of origin microscopic pattern macroscopic architecture Papilloma Hamartoma Adenoma

2.7.2. slow growing

2.7.3. well differentiated

2.7.4. localized (encapsulated margins)

2.7.5. Tx: surgical excision

2.7.6. may have lethal complications meningioma - hydrocephalus gastric leioma - hemorrhage insulin-producing pancreatic tumor insulinoma - hypoglycemia atrial myxoma - cardiac obstruction

2.7.7. exceptions capillary hemangiomas invasive margins pituitary adenomas visual disturbances

2.8. Malignant tumors

2.8.1. Nomenclature cells of origin Carcinoma

2.8.2. capable of invasion

2.8.3. capable of metastasis

2.8.4. rapid growing

2.8.5. moderate/poorly differentiated

2.8.6. desmoplastic stroma example

2.8.7. Microscopic Characteristics cellular & architectural pleomorphis loss of organized growth mitotic/apoptotic activity abnormal mitotic activity tumor necrosis example stromal & lympho-vascular invasion

3. Pathology of Neplasia

3.1. Differentiation

3.1.1. morphologic/physiologic characteristics

3.1.2. structure & function concordant

3.1.3. benign tumors well differntiatied

3.1.4. malignant tumors range of differntiation increased proliferative act variable loss of functional properties anaplasia little to no evidence of differentiation

3.2. Dysplasia

3.2.1. disordered growth

3.2.2. epithelium or mucosa

3.2.3. genetic changes

3.2.4. precursor to cancer

3.2.5. result in loss of maturation polarity architectural orientation

3.2.6. pleomorphism abnormalities in shape and size example

3.2.7. increased mitotic activity

3.2.8. carcinoma in situ premalignant/non-invasive state full epithelial thickness of dysplasia no invasion of the basement membrane

3.2.9. invasive carcinoma dysplastic cells breach basement membrane

3.2.10. example

3.2.11. example

3.3. Tumor Grade

3.3.1. level of morphologic differntation Example: Colon well moderately poorly

3.3.2. categories of evaluation size & shape nuclear:cytoplasmic ratio large nucleoli nuclear and nucleolar characteristics hyperchromasia cytoplasmic differentation mitotic activity tissue organization necrosis lymphovascular invasion

3.4. Tumor Stage

3.4.1. distribution and extent of cancer @ time of diagnosis

3.4.2. tumor characteristics tumor size location depth & extent of local invasion

3.4.3. nodal involvement

3.4.4. Metastases

3.4.5. aids in selection of therapy

3.5. Carcinogenesis

3.5.1. Agents chemical carcinogens examples radiant energy inc cutaneous cancer UVB (280-320 nm) UVC (200-280 nm) ionizing radiation oncogenic viruses & microbes Human Papilloma Virus Epstein Barr Virus Hep B Human T-Cell Leukemia (RNA) virus type 1 H. pylori in vivo mutagens in virtro

3.5.2. initiation irreversible injures DNA cellular mutation procarcinogens indirectly damage DNA following metabolic activation

3.5.3. promotion promoters stimulate division of initiated cell exogenous endogenous reversible non-tumorgenic proliferative induces tumor formation time dependent

3.5.4. progression autonomous growth genomic instability tumor heterogeneity

3.5.5. cancer invasion metastasis

3.5.6. summary carcinogenesis

4. Pathology of Tumor Growth

4.1. Rate

4.1.1. morphologic grade

4.1.2. mitotic activity

4.1.3. nature of neoplasm

4.1.4. supportive stroma & neovascularization

4.1.5. GF & hormone depenence

4.1.6. interventional treatment

4.2. Phases

4.2.1. Monoclonal proliferations growth & genetic instability Progression subpopulations

4.2.2. clonal growth and malignant change

4.2.3. local growth and angiogensis

4.2.4. regional invasion

4.2.5. metastatic spread marks a tumor as malignant 20-30% new dx have mestasis

4.2.6. growth fraction proliferating component minority of tumor cells most susceptible to cell-cycle based chemotherapy < 20% of tumor

4.3. Infiltrative Growth Margin

4.3.1. local destructive invasion

4.3.2. direct seeding body cavities peritoneal pericardial pleural example

4.3.3. lymphatic spread MC for carcinoma example

4.3.4. hematogenous spread MC for sarcoma example

4.3.5. clinical presentation most @ Site of origin 20% metastatic distant site

4.4. Development

4.4.1. Growth factors TGFbeta bFGF PDGF VEGF

4.4.2. Host factors angiogenesis

4.4.3. Proteinases digest basement membrane enable cell infiltration digest stromal matrix

4.5. Invasion

4.5.1. Invasion of Extracellular Matrix Loss of Adhesion molecules down regulation of cadherins attachment to matrix via integrins degradation of ECM detachment from solid mass move into circulation

4.5.2. Vascular Dissemination/Horning of Tumor Cells Intravasation intrxn w host immune system Dissemination bind to blood cells pass basement membrane Extravasation Micrometastasis Colonization

4.6. Metastatic sites

4.6.1. determined by anatomic vascular host-tumor paracrine effects tropism certain organs adhesion molecules for vascular bed

4.6.2. Brain lung breast kidney GI melanoma

4.6.3. Liver GI pancreato-biliary breast lung

4.6.4. bone prostate breast lung kidney thyroid testes

5. Host-Tumor Interactions

5.1. Tumor Antigens

5.1.1. Tumor specific (tumor cells only)

5.1.2. Tumor associated (tumor/normal cells)

5.1.3. classification molecular structure source

5.1.4. characteristics normal cellular proteins expressed abnormally mutated genes oncogenic viruses high levels on cancer cells altered glycolipids/glycoproteins present on cells of origin

5.2. Immunity

5.2.1. Cell mediated immunity dominant antitumor mechanism CD8+ cytotoxic T cell recognized MHCI NK cells Macrophages Antibodies

5.2.2. Immune Surveillance inc in immunocompromised host can escape immune surveillance Ag-neg variants red MHC lack co-stim immunoosuppression Ag masking CD8+ apoptosis

6. Clinical Features

6.1. clinical presentation

6.1.1. asymptomatic mass

6.1.2. pain/tenderness

6.1.3. non-healing lesino

6.1.4. persistent cough

6.1.5. abnormal bleeding

6.1.6. peforation/obstruction

6.1.7. non-specific weakness

6.1.8. fatigue

6.2. mechanisms

6.2.1. effect of compression/obstruction

6.2.2. secretory/physiological effects pituitary adenoma compress optic nerve visual disturbances hormone overexpression

6.2.3. bleeding due to ulceration

6.2.4. vascular injury

6.2.5. secondary infection

6.2.6. cachexia weakness anorexia weight loss anemia cause of 30% mortalitiy result of TNF from macrophages

6.3. endocrine/neuroendocrine tumors

6.3.1. absence of function of hormone

6.3.2. overproduction of hormone

6.3.3. suppression of hormonal activity

6.3.4. overstimulation of hormonal activity

6.4. Tumor markers

6.4.1. detection tumor cells serum effusions

6.4.2. indicators of specific cancer

6.4.3. confirm diagnosis

6.4.4. assess tumor staging

6.4.5. monitor for response to therapy

6.4.6. ID recurrent disease

6.4.7. examples PSA prostatic cancer beta-HCG gestational trophoblastic disease choriocarcinoma gonadal cancer alpha fetoprotein testicullar cancer hepatocellular cancer CEA GI Pancreato-biliary CA-125 oavarian

6.5. Paraneoplastic Syndroms

6.5.1. seconary to tumor progression

6.5.2. hormones or factors

6.5.3. earliest manifestation of occule malignancy

6.5.4. 10% of patients

6.5.5. presentation endocrinopathy hypercalcemia neuromuscular deficiency dermatologic conditions bone changes hematologic abnormalities

6.5.6. Tx: address primary deficiency

6.5.7. examples Cushing syndrome ACTH small cell carcinoma of lung pancreatic carcinoma neural tumors Syndrome of Inappropriate Antidiuretic Hormone Secretion ADH/atrial natriuretic hormone small carcinoma of lung intracranial neoplasms Hypercalcemia Parathyroid hormone related protein Squamous cell carcinoma of lung breast renal adutl T-cell leukemia/lymphoma ovarian carcinoma carcinoid syndrome Serotonin Bradykinin carcinoid tumor gastric carcinoma pancreatic carcinoma

7. Lab Diagnosis

7.1. Clinical history

7.2. physical examination

7.3. radiologic imaging

7.4. lab tests

7.5. pathologic exam

7.5.1. surgical methods Biopsy excision resection rapid frozen section at time of surgery

7.5.2. cytologic methods Pap smears Fine Needle Aspiration

7.5.3. ultrastructural methods electron microscopy

7.5.4. molecular methods immunohistochemistry technique function flow cytometry FISH PCR based on genetic makeup/expression can alter treatment more accurate testing/prognosis