ŠĻą”±į>ž’ įćž’’’ßą’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’’ģ„Į7 šæĘRbjbjUU )š7|7|ŽN7’’’’’’lvvvvvvvŠš<š<š<8(=,T=ģŠĆūöL>L>@Œ>Œ>Œ>eIeIeIBūDūDūDūDūDūDū$¹ż Ł’\hūveIÆF¶eIeIeIhūmgvvŒ>Œ>#}ūmgmgmgeI vŒ>vŒ>BūmgeIBūmgŽmgKlNīPvvBūŒ>@> `ÅóźżĀŠf;š<wSöžņtBū“ū0Ćūó05mg5BūmgŠŠvvvvŁNEOPLASM (Dr. Lena) growth progressive increase in the size of the individual multiplication of cells increase intracellular substances development increase in size of the cells (low ( higher state) differentiation increase in complexity of function fo cells & their organizational structure hamartroma disorganized mass of normal tissues "hemangioma" - considered as a form of hamartroma choristoma tumor-like mass of normal displaced tissues dysplasia disordered development same cell size at all levels anaplasia (reversionary atrophy) change from well-differentiated to embryonic - "carcinoma in situ" - earliest form of cancer of basement membrane which is not penetrated by anaplastic cells (invasive cancer if penetrated) heterotopia deviation from the natural position heterotrophic tissue - thymus neoplasia new growth neoplasm mass composing the new growth uncoordinated, purposeless growth that exceeds that of normal tissue, persisting after the cessation of stimuli, preys on the host & competes for energy & nutrition causing wasting of the individual cancer tumor where the cells adhere to the adjacent or any part of the tissue in an obstinate manner tumor benign: not life threatening malignant: life-threatening BASIC COMPONENTS OF TUMOR 1. parenchyma - proliferating neoplastic cells 2. supporting stroma - CT with blood vessel & lymphatic  abundant - soft mass depending on the scanty - firm mass supporting stroma SPREAD OF CANCER adjacent tissue lymphatics malignant cells can penetrate blood vesels organs or adjacent tissues body cavities (natural open field) transplantation (iatrogenic) BENIGN vs. MALIGNANT NEOPLASM  characteristic BENIGN MALIGNANT  differentiation well differentiated (adult-type; well differentiated to anaplastic/embryonic typical of its tissue origin) (primitive, stem or undifferentiated cells; pleomorphism with giant tumor cells, increased N/C ratio, loss of polarity)  rate of growth slow & progressive; standstill or faster (( mitoses; starts as an in situ; regress (normal mitosis & rare) unpredictable) - growth can't be tremendous, regress, stay in same size  local invasion expantile, pushing, cohesive, non- usually infiltrative or erosive (rarely cohesive) invasive, encapsulated or defined invasiveness = less cohesiveness & ( calcium cleavage  metastasis absent frequent (except H-mole & leiomyoma) (aggressive, large & rapidly growing types except basal cell carcinoma & glioma)  course usually non-fatal fatal in general (except: neuroblastoma in infants ( ganglio- neuroma or regress)  can impinge & cause hemorrhage occasionally that becomes malignant long standing types of neurons  BASIS OF DIFFERENTIATION OF TUMOR 1. differentiation 3. mode of growth 5. course 2. rate of growth 4. metastasis The spread of cancer is due to organ trophism of cancer cells which may be due to: adhesion molecules (specificity for endothelial cells of the organ) chemoattractants liberated by the organs favorable soil of growth e.g. prostatic cancer (bones) bronchiogenic carcinoma (adrenals) neuroblastoma (liver & bones) GRADING OF CANCER estimate the "aggressiveness" or "degree of malignancy" based on: 1. cytologic differentiation (poorly differentiated squamous cell carcinoma) 2. number of mitoses (smooth muscle & connective tissue tumor) STAGING OF CANCER determines the outcome based on: 1. size 2. lymph node spread 3. distant metastasis - TNM staging (accepted staging) a. tumor To - in situ T4 - extreme tumor with invasion b. node No - lymph node involvement N1 - mild N2 N3 ( higher number, higher involvement c. metastasis Mo - no metastasis M1 - distant metastasis NOMENCLATURE OF TUMORS I. BENIGN: tissue + "oma" (fibrous, fat, skeletal, etc) (exception: seminoma, melanoma, lympoma, hepatoma) II. BENIGN EPITHELIAL TISSUE 1. glandular - adenoma (liver, pancreas, kidney, etc.) 2. finger-like - papilloma/polyp 3. large cystic mass, glandular - cystadenoma 4. optic mass with finger-like projection - papillary cystadenoma 5. cystic mass with mucin producing gland - mucinous cystadenoma III. MALIGNANT EPITHELIAL TISSUE - carcinoma (adenocarcinoma, papillary carcinoma, squamous cell carcinoma, etc.) IV. MALIGNANT TUMOR FROM MESENCHYMAL TISSUE - sarcoma V. MORE THAN ONE NEOPLASTIC CELL (relate tissues) e.g. mixed tumor of salivary gland malignant mixed mulllerian tumor VI. TUMOR OF MORE THAN ONE GERM CELL - teratoma VII. UNDIFFERENTIATED MALIGNANT EPITHELIAL TUMOR - poorly differentiated or undifferentiated carcinoma teratoma benign malignant solid squamous cell carcinoma stratified cells loss of polarity cells are hyperchromatic papillary tumor arising from parotid gland & forms a cyst 9 WARNING SIGNS OF CANCER 1. change in bowel habits 2. sore that does not heal 3. unusual bleeding or discharges 4. lump in breast or elsewhere 5. indigestion or difficulty of swallowing 6. change in wart or mole 7. nagging cough or hoarseness 8. sudden unexplained weight loss 9. unexplained anemia PREDISPOSITION TO CANCER I. adults MALE FEMALE prostate breast lungs colorectum colorectum lungs urinary tract uterus lymphomas lymphomas II. children (less than 15 years old) MALE FEMALE leukemia leukemia brain & other NS brain & other NS lymphomas bone connective tissue bladder bone lymphoma FACTORS IN THE CAUSATION OF CANCER A. GEOGRAPHIC/RACIAL FACTORS e.g. gastric cancer - more on Japan than America lung cancer - more on America than Japan B. ENVIRONMENTAL FACTORS 1. cardiogenic substances coal tar (hydrocarbon) - scrotal cancer (chimney sweepers) aflatoxin - liver cancer (Aspergillus flavus) nitrosamine (preserved food) - stomach cancer betel nuts - oral cavity cancer UV rays - skin cancer alcohol - cancer in oropharynx, esophagus, larynx, liver cigarette smoking - cancer of lungs, mouth, pharynx, esophagus, pancreas, bladder asbestos - mesothelioma arsenic (fungicides, herbicides, metals) - cancer of lungs & skin hemangiosarcoma benzene (light oil, rubber, detergents) - leukemia, lymphoma cadmium (batteries, metal platings) - prostatic cancer diethylstilbestrol - vaginal adenocarcinoma ethylene oxide (ripening agents for fruits & nuts) - leukemia vinyl chloride (refrigerant, plastics) - angiosarcoma, liver cell carcinoma nickel (ceramics, batteries) - cancer of nose and lungs 2. practices sexual practices: many partners, early age of marriage exposure = cervical cancer circumcision 3. viruses HTLV - leukemia (human T-cell leukemia virus) HSV - cervical cancer (herpes simplex virus) HPV - warts (human papilloma virus) EBV-NP - lymphoma (epstein barr/Burkitt's lymphoma) 4. bacteria (Helicobacter pylori : gastric) - gastric cancer, gastritis, lymphoma (mucosa associated type) C. AGE D. HEREDITY 1. inherited cancer syndrome: inheritance of a single mutant gene increases risk of cancer (related to cancer suppressor gene) characteristics: autosomal dominant pattern of inheritance involve specific sites or tissues associated with specific marker phenotype with incomplete penetrance & variable expressibility example: retinoblastoma - most frequent familial adenomatous polyposis neurofibromatosis 2. familial cancer characteristics: early age of onset 2 or more close relatives multiple or bilateral no specific marker phenotype nuclear transmission pattern example: breast cancer ovarian cancer colonic cancer 3. autosomal recessive syndrome of defective DNA repair - associated with chromosomal or DNA instability e.g. xerodermal pigmentosum E. ACQUIRED PRE-NEOPLASTIC DISORDER condition example hyperplasia endomethelial cancer bronchial dysplasia bronchogenic cirrhosis liver cell cancer chronic atrophic gastritis gastric cancer leukoplasia mucosal cancer borderline tumor tumors of low malignant potential compared to an angel with horn or tail CHEMICAL CARCINOGENS 1. direct acting (e.g. cyclophorphoride) 2. indirect acting (procarcinogens) - should be activated - e.g. aflatoxin, nitrosamine, insecticides TARGETS OF CHEMICAL CARCINOGEN DNA (mutagenic) mutagenic effects: oncogenes - causes cancer for apoptosis cancer suppressor gene I. INITIATION PHASE (rapid & irreversible) metabolic activation - CARCINOGEN cytocchrome P450 peroxidase oxidation reduction reaction glutathione conjugation CARCINOGEN electrophilic intermediate detoxification  EXCRETION  binding to DNA: detoxification  ADDUCT FORMATION DNA repair Normal cell permanent DNA lesion: Cell death INITIATED CELL  II. PROMOTION PHASE (reversible & dose-dependent)  promoters: hormones cell proliferation  drugs altered differentiation phenols  phosphoesters preneoplastic clone  artificial sweetener (saccharin) neoplastic cells RADIATION I. UV rays (UVB & UVC) - depends on quantity & intensity mechanism: pyrimidine dimer formation on DNA transcriptional error ( cancer formation example: skin cancer (UVB) II. IONIZING RADIATION Types: electromagnetic (X-ray, gamma ray) particulate ((, (, protons, neutrons) Mechanism: chromosomal damage protein alteration enzyme inactivation cell membrane damage Example: Skin cancer, leukemia, etc. VULNERABLE TO DEVELOP CANCER WITH RADIATION infants children with DNA repair defects seen in: xeroderma pigmentosum - degradation of skin, skin tumors bloom's syndrome - mental retardation, causes several types of cancer ataxia-telangiectasia - lymphomas, uculocutaneous type fanconi's anemia - leukemia - ( RBC, ( patelet BIOLOGY OF TUMOR GROWTHS 4 PHASES: transformation growth of transformed cells local invasion/infiltration metastasis (distant spread of tumor) OBSERVATIONS A 10 ( should at least has 30 population doubling to attain 1 gram (smallest detectable size). A 1 gram tumor needs 10 doubling to attain 1 kilo (maximum size compatible with life for malignancy). Progressive growth of tumors & its rate of growth determined by excessive cell production over cell loss. Rapidly dividing cells are targets of most anti-cancer reaction but not those in the replicating pool (cell that lack nutrients = in Go-G1 phase). Doubling time is unpredictable (1 month to years). Even if monoclonal in origin, cells in the tumor are of several variants (polyclonal) - due to genetic instability? non-antigenic clone invasive metastatic clone that requires few growth factors ANGIOGENESIS caused by tumor associated angiogenic factors (produced by tumor cells/inflammatory cells) - e.g 1. vascular endothelial growth factor (VEGF) 2. basic fibroblast growh factor (bFGF) OBSERVATION: Tumors cannot be more than 1-2 mm if without blood vessel: hypoxia ( apoptosis (p53 influence) ANGIOGENESIS is a result of influence of the: angiogenic factors anti-angiogenic factors: thrombospondin 1, angiostantis, etc. CHANGES IN CANCER CELLS I. TRANSFORMATION cell & nuclear size transplantability invasion metastasis: penetration of vessel release/embolization arrest & adherence development of blood vessel & stroma ( secondary tumor Figure 1: Metastatic cascade STEP: Should be able to loosen & detach itself brought by down-regulation. "Cadherin" - bind cells together EXTRCELLULAR MATRIX INVASION detachment ("loosening up") of cell attachment to extracellular matrix (integrin) degradation of ECM (proteolytic enzyme or proteases - destroy components) migration (locomotion) - autocrine motility factor (a cytokine) - bind to receptor for motility II. CHANGES IN MEMBRANE decreased adhesiveness & cohesiveness loss of intracellular junctions increased transport of sugar & amino acid III. ANTIGENIC CHANGES fetal antigen (liver, ovarian & testicular tumor) common tumor associated antigen seen in normal tissues which elicits rejection response to tumors soluble (shed) antigen blocks antibody of cell-mediated response IV. CHANGES IN KARYOTYPE deletion gene amplification balanced translocation V. BIOCHEMICAL CHANGES alkaline phosphatase (placental type - lung cancer) aldolase (hepatoma) insulin (fibrosarcoma) FUNDAMETAL PRINCIPLES IN CARCINOGENESIS (Molecular Point of View) Cancer is due to "non-lethal damage". Three targets of genetic damage: growth promoting protooncogenes growth inhibiting cancer-suppressor genes genes regulating apoptosis Damaged gene is regulated by DNA repair genes 4th regulating gene "caretakers" 2abc - considered as "gate-keeper" Carcinogenensis is a multi-step process with genetic & phenotypic attributes (excessive growth, local invasiveness & distant metastasis) ACTIVATION OF PROTOONCOGENES change in structure of gene ( change in regulation of gene expression ( increased growth promoting proteins ( increase in number of cells POINT MUTATION involvement of a specific point e.g. RAS oncogene - pancreatic adenocarcinoma CHROMOSOMAL REARRANGEMENT translocaton results to: overexpression of protooncogenes (in Burkett's lymphoma - Cr 8 & 14)) hybrid gene formed that promotes growth promoting proteins (as in Philadelphia chromosome - Cr 9 & 22) GENE AMPLIFICATION 2 patterns: double minutes (chromosome like structure - small rounded, oval) homogeneous staining region (HSP within chromosome) ONCOGENES (cancer causing genes) e.g. 1. V-oncogene (viral oncogene) - in transforming viruses 2. C-oncogene (cellular oncogene) - result to insertional mutagenesis ONCOPROTEINS: protein products of oncogenes TYPES OF GROWTH FACTORS PLATELET DERIVED GROWTH FACTOR osteosa & fibrosarcoma fibroblast of cancer of the breast, stomach, etc. GROWTH FACTOR RECEPTOR deliver oncogenic signals activated by mutation, overexpression or gene rearrangement e.g. epidermal growth factor receptor - SCC of lung SIGNAL TRANSDUCING PROTEINS at inner leaflet of plasma membrane e.g. RAS GTP binding protein which regulates cell cycle through control of kinases NUCLEAR TRANSCRIPTION PROTEIN contain specific amino acid sequences that bind to DNA CYCLINS & CYCLIN-DEPENDENT KINASES modulators of cell cycle allow quiescent cells to enter the cell cycle mutation that dysregrate their activity favor cell proliferation TUMOR SUPPRESSOR GENES basic characteristics: regulate cell growth, do not prevent tumor formation loss of these genes ( tumor products of tumor & suppressor genes (nuclear) Rb Gene "brake" from G1 to S phase (inactivated) by phosphorylation ( brake release ( cells to S phase p53 Gene single most common target for genetic alteration in human tumor "guardian of the genome"; "molecular policeman" - prevents cancer: control in transcription of their genes specific functions: recognizes DNA damage ( arrest G1 phase for DNA repair direct cells with unrepaired DNA to undergo apoptosis BRCA - ? DNA repair transcriptional regulation; mutation ( female: cancer of ovary & breast male & female breast cancer outside the nucleus: a. genes that regulate signal transduction e.g. adenomatous?C in cytosol-inihibitor - degrades B catanin which promotes cell proliferation b. cell surface receptor e.g. epithelial cadherin gene ( cell adherence; "glue gene" loss of cell's ability to invade & metastasize GENES that regulate APOPTOSIS Characteristics: starts with letter "b" with 2 types: inhibition of apoptosis (if overexpressed) e.g. bcl 2 - in lymphoma - regulates exit of cytochrome C which help in activating caspase g favors apoptosis e.g. bad, bax, bcl-xs ratio of death antagonists to agonist = determine occurrence of apoptosis DNA REPAIRS GENE facts: defective DNA repair - reduction error repair is done by the mismatched gene e.g. during replication, instead of the normal A=T pair, it may be G=T pair ( allows mutation in other genes if there is loss of the normal repair, genes = cancer TUMOR GROWTH telomere specialized structure at the end of the chromosome, the shortening of which serves as a clock for cell division, shortening beyond certain point = cell death telomerase increased activity in cancer TUMOR ANTIGENS I. tumor specific antigen (TSA) in tumor cells source: mutation of normal cell - associated with major histocompatibility Ag, class I); recognized by CD8T cell product of oncogene & anti-oncogene II. tumor associated antigen (TTA) normal & tumor cells e.g. 1. TA carbohydrate Ag (as mucin assoc. Ag) 2. oncofetal Ag (as CEA, AFP) 3. differentiation - specific Ag (CD10-B cell type) III. semi-tumor specific antigen e.g. overexpressed Ag in tumors between tumor-associated & specific PARANEOPLASTIC SYNDROME characteristics: can't be explained by: local spread distant spread hormone production e.g. 1. Cushing's syndrome (ACTH) 2. hyperthyroidism (TSH) - bronchogenic & prostatic cancer 3. hypoglycemia (insulin) - fibrosarcoma & hepatoma 4. polycythemia (erythropoeitin) facts: No single oncogene cvan transform cells in vitro but combination is needed. Every human cancer has several genetic alterations: activation of several oncogenes & loss of 2 or more suppressor gene. Usually a gene is present in cancer that influences mutations. EFFECTS OF TUMOR ON THE HOST LOCAL & HORMONAL e.g. pituitary adenoma ( pituitary destruction ( endocrinopathy B cell adenoma ( insulin production CACHEXIA cachectin-mediated (TNF alpha, IL-1, etc.) loss of body fat, wasting, & profound weakness loss of appetite reduced synthesis & storage of fat & increased mobilization of fatty acids from adipocytes PARANEOPLASTIC SYNDROME symptoms not directly related to the spread of the tumor or elaboration of hormones indigenous to the tissue from which the tumor arose may be the earliest clinical manifestations of a neoplasm & may mimic distant spread HOST DEFENSES VIA TUMOR cytotoxic cells - vs. membrane associated tumor Ag NK cells (natural killing cells) - no sensitization needed complement activation macrophages - with cytotoxic product; Ab dependent produce reactive O2 metabolites secrete TNF ( (tumor necrosis factor) immunosurveillance - cancer cells acted on by host effector cells/host immune responses MECHANISMS TO INVADE IMMUNOSURVEILLANCE outgrowth of Ag-negative variant loss or decreases expression of class I - histocompatibility Ag (ALA) lack of co-stimulatory molecules to sensitized T-lymphocyte immunosuppression by oncogenic agents (chemical & radiation) apoptosis of cytotoxic T cells (e.g. in melanoma & hepatomas with Fas ligand) DIAGNOSIS OF TUMORS histology & cytology (biopsy, FNAB, smears) immunocytochemisry stain (keratin-carcinoma, mesothelioma; desmin) DNA flow cytometry molecular diagnosis tumor markers carcinoembyonic ( - feto protein prostatic specific antigen prostatic acid phosphatase ( - HCG thyroglobin Ca 15.3 (breast) Ca 1.25 (ovary) Ca 19.9 (pancreatic) Ca 72 (GIT cancer) IMMUNOTHERAPY adoptive cellular Tx cytokine Tx Ab-based Tx: Ab + potent toxin PAGE  PAGE 11a( PAGE  PAGE 11b(  ½¾FG\]„‘“ž«²ĖÕöū 29LM²³ƒ „ … ā ć   Į Ä Å Ę : ; „ … . / %&󟎟ӟӟȟȟȟȟȟȟȟӟӟӵźÓźµźµźó§µœµœŽœµœ€œµœ jÆšB*CJ OJQJph333 j­šB*CJ OJQJph333B*CJ OJQJph3335B*CJ OJQJ\ph333%jB*OJQJUmHnHph333u>*B*OJQJph333B*CJOJQJph333 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