Neoplasia Robbin's path


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  • FIGURE 7-6  Malignant tumor (adenocarcinoma) of the colon. Note that compared with the well-formed and normal-looking glands characteristic of a benign tumor (see Fig. 7-5 ), the cancerous glands are irregular in shape and size and do not resemble the normal colonic glands. This tumor is considered differentiated because gland formation can be seen. The malignant glands have invaded the muscular layer of the colon.  (Courtesy of Dr. Trace Worrell, University of Texas Southwestern Medical School, Dallas, TX.)
  • Well-differentiated squamous cell carcinoma of the skin. The tumor cells are strikingly similar to normal squamous epithelial cells, with intercellular bridges and nests of keratin pearls (arrow)
  • FIGURE 7-10  A, Carcinoma in situ. This low-power view shows that the entire thickness of the epithelium is replaced by atypical dysplastic cells. There is no orderly differentiation of squamous cells. The basement membrane is intact, and there is no tumor in the subepithelialstroma. B, A high-power view of another region shows failure of normal differentiation, marked nuclear and cellular pleomorphism, and numerous mitotic figures extending toward the surface. The basement membrane is not seen in this section.
  • FIGURE 7-11  Schematic representation of tumor growth. As the cell population expands, a progressively higher percentage of tumor cells leaves the replicative pool by reversion to G0, differentiation, and death.
  • FIGURE 7-12  Fibroadenoma of the breast. The tan-colored, encapsulated small tumor is sharply demarcated from the whiter breast tissue.
  • Microscopic view of fibroadenoma of the breast seen in Figure 7-12 . The fibrous capsule (right) delimits the tumor from the surrounding tissue.
  • The microscopic view of the breast carcinoma seen in Figure 7-14 illustrates the invasion of breast stroma and fat by nests and cords of tumor cells (compare with fibroadenoma shown in Fig. 7-13 ). The absence of a well-defined capsule should be noted.
  • FIGURE 7-26  Model for action of RAS genes. When a normal cell is stimulated through a growth factor receptor, inactive (GDP-bound) RAS is activated to a GTP-bound state. Activated RAS recruits RAF and stimulates the MAP-kinase pathway to transmit growth-promoting signals to the nucleus. The mutated RAS protein is permanently activated because of inability to hydrolyze GTP, leading to continuous stimulation of cells without any external trigger. The anchoring of RAS to the cell membrane by the farnesyl moiety is essential for its action. See text for explanation of abbreviations.
  • Neoplasia Robbin's path

    1. 1. Neoplasia – Images and TablesRobbin’s Pathologic basis of disease, 8th Ed Dr.CSBR.Prasad, M.D., CSBRP-July-2012
    2. 2. Colonic polyp A, This benign glandular tumor (adenoma) is projecting into the coloniclumen and is attached to the mucosa by a distinct stalk. B, Gross appearance of several colonic polyps. CSBRP-July-2012
    3. 3. This mixed tumor of the parotid gland contains epithelial cells forming ducts and myxoid stroma that resembles cartilage CSBRP-July-2012
    4. 4. Gross appearance of an opened cystic teratoma of the ovary.Note the presence of hair, sebaceous material, and tooth. B, A microscopic view of a similar tumor shows skin, sebaceous glands, fat cells, and a tract of neural tissue (arrow). CSBRP-July-2012
    5. 5. Tissue of Origin Benign MalignantCOMPOSED OF ONE PARENCHYMAL CELL TYPETumors of Mesenchymal OriginConnective tissue and derivatives Fibroma Fibrosarcoma Lipoma Liposarcoma Chondroma Chondrosarcoma Osteoma Osteogenic sarcomaEndothelial and Related TissuesBlood vessels Hemangioma AngiosarcomaLymph vessels Lymphangioma LymphangiosarcomaSynovium Synovial sarcomaMesothelium MesotheliomaBrain coverings Meningioma Invasive meningiomaBlood Cells and Related CellsHematopoietic cells LeukemiasLymphoid tissue LymphomasMuscleSmooth Leiomyoma LeiomyosarcomaStriated Rhabdomyoma RhabdomyosarcomaTumors of Epithelial OriginStratified squamous Squamous cell papilloma Squamous cell carcinomaBasal cells of skin or adnexa Basal cell carcinomaEpithelial lining of glands or ducts Adenoma Adenocarcinoma Papilloma Papillary carcinomas Cystadenoma CystadenocarcinomaRespiratory passages Bronchial adenoma Bronchogenic carcinomaRenal epithelium Renal tubular adenoma Renal cell carcinomaLiver cells Liver cell adenoma Hepatocellular carcinomaUrinary tract epithelium (transitional) Transitional-cell papilloma Transitional-cell carcinomaPlacental epithelium Hydatidiform mole ChoriocarcinomaTesticular epithelium (germ cells) Seminoma Embryonal carcinomaTumors of Melanocytes Nevus Malignant melanomaMORE THAN ONE NEOPLASTIC CELL TYPE—MIXED TUMORS, USUALLY DERIVED FROM ONE GERM CELL LAYERSalivary glands Pleomorphic adenoma (mixed tumor of salivary origin) Malignant mixed tumor of salivary gland originRenal anlage Wilms tumorMORE THAN ONE NEOPLASTIC CELL TYPE DERIVED FROM MORE THAN ONE GERM CELL LAYER—TERATOGENOUS CSBRP-July-2012Totipotential cells in gonads or in embryonic rests Mature teratoma, dermoid cyst Immature teratoma, teratocarcinoma
    6. 6. Leiomyoma of the uterus. This benign, well-differentiated tumor contains interlacing bundles of neoplastic smooth muscle cells that are virtuallyidentical in appearance to normal smooth muscle cells in the myometrium. CSBRP-July-2012
    7. 7. Benign tumor (adenoma) of the thyroid. Note the normal-looking (well-differentiated), colloid-filled thyroid follicles. CSBRP-July-2012
    8. 8. Malignant tumor (adenocarcinoma) of the colon CSBRP-July-2012
    9. 9. Well-differentiated squamous cell carcinoma of the skin. The tumor cells are strikingly similar to normal squamous epithelial cells, with intercellular bridges and nests of keratin pearls (arrow) CSBRP-July-2012
    10. 10. Anaplastic tumor of the skeletal muscle (rhabdomyosarcoma). Note the marked cellular and nuclear pleomorphism, hyperchromatic nuclei, and tumor giant cells. CSBRP-July-2012
    11. 11. Anaplastic tumor showing cellular and nuclearvariation in size and shape. The prominent cell in the center field has an abnormal tripolar spindle CSBRP-July-2012
    12. 12. Carcinoma ‘in situ’ CSBRP-July-2012
    13. 13. Schematic representation of tumor growth. As the cell population expands,a progressively higher percentage of tumor cells leaves the replicative pool by reversion to G0, differentiation, and death. CSBRP-July-2012
    14. 14. Fibroadenoma of the breastThe tan-colored, encapsulated small tumor is sharply demarcated from the whiter breast tissue. CSBRP-July-2012
    15. 15. Microscopic view of fibroadenoma of the breastThe fibrous capsule (right) delimits the tumor from the surrounding tissue. CSBRP-July-2012
    16. 16. Cut section of an invasive ductal carcinoma of the breastThe lesion is retracted, infiltrating the surrounding breast substance, and would be stony hard on palpation. CSBRP-July-2012
    17. 17. The microscopic view of the breast carcinoma seen in Figure 7-14 illustrates the invasion of breast stroma and fat by nests and cords of tumor cells (compare with fibroadenoma shown in Fig. 7-13 ). The absence of a well- defined capsule should be noted. CSBRP-July-2012
    18. 18. Colon carcinoma invading pericolonic adipose tissue CSBRP-July-2012
    19. 19. Axillary lymph node with metastatic breast carcinoma. Thesubcapsular sinus (top) is distended with tumor cells. Nests of tumor cells have also invaded the subcapsular cortex CSBRP-July-2012
    20. 20. A liver studded with metastatic cancerCSBRP-July-2012
    21. 21. Characteristics Benign MalignantDifferentiation/ Well differentiated; structure Some lack of differentiation withanaplasia sometimes typical of tissue of anaplasia; structure often origin atypicalRate of growth Usually progressive and slow; Erratic and may be slow to rapid; may come to a standstill or mitotic figures may be numerous regress; mitotic figures rare and abnormal and normalLocal invasion Usually cohesive expansile Locally invasive, infiltrating well-demarcated masses that surrounding tissue; sometimes do not invade or infiltrate may be seemingly cohesive and surrounding normal tissues expansileMetastasis Absent Frequently present; the larger and more undifferentiated the primary, the more likely are metastases CSBRP-July-2012
    22. 22. Comparison between a benign tumor of the myometrium (leiomyoma) and a malignanttumor of the same origin (leiomyosarcoma). CSBRP-July-2012
    23. 23. Cancer incidence and mortality by site and sex.Excludes basal cell and squamous cell skin cancers and in situ carcinomas, except urinary bladder CSBRP-July-2012
    24. 24. The change in incidence of various cancers with migration from Japan to theUnited States provides evidence that the occurrence of cancers is related to components of the environment that differ in the two countries. CSBRP-July-2012
    25. 25. Human Cancer Site forAgents or Groups of Which ReasonableAgents Evidence Is Available Typical Use or OccurrenceArsenic and arsenic Lung, skin, Byproduct of metal smelting; component of alloys,compounds hemangiosarcoma electrical and semiconductor devices, medications and herbicides, fungicides, and animal dipsAsbestos Lung, mesothelioma; Formerly used for many applications because of fire, heat, gastrointestinal tract and friction resistance; still found in existing construction as (esophagus, stomach, large well as fire-resistant textiles, friction materials (i.e., brake intestine) linings), underlayment and roofing papers, and floor tilesBenzene Leukemia, Hodgkin Principal component of light oil; despite known risk, many lymphoma applications exist in printing and lithography, paint, rubber, dry cleaning, adhesives and coatings, and detergents; formerly widely used as solvent and fumigantBeryllium and beryllium Lung Missile fuel and space vehicles; hardener for lightweightcompounds metal alloys, particularly in aerospace applications and nuclear reactorsCadmium and cadmium Prostate Uses include yellow pigments and phosphors; found incompounds solders; used in batteries and as alloy and in metal platings and coatingsChromium compounds Lung Component of metal alloys, paints, pigments, and preservativesNickel compounds Nose, lung Nickel plating; component of ferrous alloys, ceramics, and batteries; by-product of stainless-steel arc weldingRadon and its decay Lung From decay of minerals containing uranium; potentiallyproducts serious hazard in quarries and underground minesVinyl chloride Angiosarcoma, liver Refrigerant; monomer for vinyl polymers; adhesive for plastics; formerly inert aerosol propellant in pressurized CSBRP-July-2012 containers
    26. 26. INHERITED CANCER SYNDROMES (AUTOSOMAL DOMINANT)Gene Inherited PredispositionRB Retinoblastomap53 Li-Fraumeni syndrome (various tumors)p16/INK4A MelanomaAPC Familial adenomatous polyposis/colon cancerNF1, NF2 Neurofibromatosis 1 and 2BRCA1, BRCA2 Breast and ovarian tumorsMEN1, RET Multiple endocrine neoplasia 1 and 2MSH2, MLH1, MSH6 Hereditary nonpolyposis colon cancerPTCH Nevoid basal cell carcinoma syndromePTEN Cowden syndrome (epithelial cancers)LKB1 Peutz-Jegher syndrome (epithelial cancers)VHL Renal cell carcinomasINHERITED AUTOSOMAL RECESSIVE SYNDROMES OF DEFECTIVE DNA REPAIRXeroderma pigmentosumAtaxia-telangiectasiaBloom syndromeFanconi anemiaFAMILIAL CANCERSFamilial clustering of cases, but role of inherited predisposition not clear for each individual Breast cancer Ovarian cancer Pancreatic cancer CSBRP-July-2012
    27. 27. Chronic Inflammatory States and CancerPathologic Condition Associated Neoplasm(s) Etiologic AgentAsbestosis, silicosis Mesothelioma, lung carcinoma Asbestos fibers, silica particlesBronchitis Lung carcinoma Silica, asbestos, smoking (nitrosamines, peroxides)Cystitis, bladder inflammation Bladder carcinoma Chronic indwelling urinary cathetersGingivitis, lichen planus Oral squamous cell carcinomaInflammatory bowel disease Colorectal carcinomaLichen sclerosis Vulvar squamous cell carcinomaChronic pancreatitis Pancreatic carcinoma Alcoholism Hereditary pancreatitis Pancreatic carcinoma Mutation in trypsinogen geneReflux esophagitis, Barrett esophagus Esophageal carcinoma Gastric acidsSialadenitis Salivary gland carcinomaSjögren syndrome, Hashimoto thyroiditis MALT lymphomaCANCERS ASSOCIATED WITH INFECTIOUS AGENTSOpisthorchis, cholangitis Cholangiosarcoma, colon carcinoma Liver flukes (Opisthorchis viverrini) Bile acidsChronic cholecystitis Gallbladder cancer Bacteria, gallbladder stonesGastritis/ulcers Gastric adenocarcinoma, MALT Helicobacter pyloriHepatitis Hepatocellular carcinoma Hepatitis B and/or C virusMononucleosis B-cell non-Hodgkin lymphoma and Hodgkin Epstein-Barr virus lymphomaAIDS Non-Hodgkin lymphoma, squamous cell Human immunodeficiency virus, human carcinoma, Kaposi sarcoma herpesvirus type 8Osteomyelitis Carcinoma in draining sinuses Bacterial infectionPelvic inflammatory disease, chronic Ovrian carcinoma, cervical/anal carcinoma Gonorrhea, chlamydia, humancervicitis papillomavirusChronic cystitis CSBRP-July-2012 Bladder, liver, rectal carcinoma Schistosomiasis
    28. 28. The use of X-linked markers as evidence of the monoclonality of neoplasmsCSBRP-July-2012
    29. 29. Tumor progression and generation of heterogeneity CSBRP-July-2012
    30. 30. Flowchart depicting a simplified scheme of the molecular basis of cancer.CSBRP-July-2012
    31. 31. Category Proto-oncogene Mode of Activation Associated Human TumorGROWTH FACTORSPDGF-β chain SIS (official name PBGFB) Overexpression Astrocytoma OsteosarcomaFibroblast growth factors HST1 Overexpression Stomach cancer INT2 (official name FGF3) Amplification Bladder cancer Breast cancer MelanomaTGF-α TGFA Overexpression Astrocytomas Hepatocellular carcinomasHGF HGF Overexpression Thyroid cancerGROWTH FACTOR RECEPTORSEGF-receptor family ERBB1 (EGFR), ERRB2 Overexpression Squamous cell carcinoma of lung, gliomasFMS-like tyrosine kinase 3 FLT3 Amplification Breast and ovarian cancersReceptor for neurotrophic factors RET Point mutation Leukemia Point mutation Multiple endocrine neoplasia 2A and B, familial medullary thyroid carcinomasPDGF receptor PDGFRB Overexpression, translocation Gliomas, leukemiasReceptor for stem cell (steel) factor KIT Point mutation Gastrointestinal stromal tumors, seminomas, leukemiasPROTEINS INVOLVED IN SIGNAL TRANSDUCTIONGTP-binding KRAS Point mutation Colon, lung, and pancreatic tumors HRAS Point mutation Bladder and kidney tumors NRAS Point mutation Melanomas, hematologic malignanciesNonreceptor tyrosine kinase ABL Translocation Chronic myeloid leukemia Acute lymphoblastic leukemiaRAS signal transduction BRAF Point mutation MelanomasWNT signal transduction β-catenin Point mutation Hepatoblastomas, hepatocellular carcinoma OverexpressionNUCLEAR-REGULATORY PROTEINSTranscriptional activators C-MYC Translocation Burkitt lymphoma N-MYC Amplification Neuroblastoma, small-cell carcinoma of lung L-MYC Amplification Small-cell carcinoma of lungCELL CYCLE REGULATORSCyclins Cyclin D Translocation Mantle cell lymphoma Amplification Breast and esophageal cancers Cyclin E Overexpression Breast cancerCyclin-dependent kinase CDK4 Amplification or point mutation Glioblastoma, melanoma, sarcoma CSBRP-July-2012
    32. 32. Model for action of RAS genes CSBRP-July-2012
    33. 33. The chromosomal translocation and associated oncogenes in Burkitt lymphoma and chronic myelogenous leukemiaCSBRP-July-2012
    34. 34. Amplification of the N-MYC gene in human neuroblastomasCSBRP-July-2012
    35. 35. Schematic illustration of the role of cyclins, CDKs, and CDK inhibitors (CDKIs) in regulating the cell cycle. CSBRP-July-2012
    36. 36. Main Cell Cycle Components and Their InhibitorsCell CycleComponent Main FunctionCYCLIN-DEPENDENT KINASESCDK4 Forms a complex with cyclin D that phosphorylates RB, allowing the cell to progress through the G1 restriction point.CDK2 Forms a complex with cyclin E in late G1, which is involved in G1/S transition. Forms a complex with cyclin A at the S phase that facilitates G2/M transition.CDK1 Forms a complex with cyclin B that facilitates G2/M transition.INHIBITORSCIP/KIP family: p21, p27 Block the cell cycle by binding to cyclin-CDK complexes; p21 is induced by the tumor(CDKN2A-C) suppressor p53; p27 responds to growth suppressors such as TGF-β.INK4/ARF family p16/INK4a binds to cyclin D–CDK4 and promotes the inhibitory effects of RB; p14/ARF(CDKN1A-D) increases p53 levels by inhibiting MDM2 activity.CHECKPOINT COMPONENTSp53 Tumor suppressor gene altered in the majority of cancers; causes cell cycle arrest and apoptosis. Acts mainly through p21 to cause cell cycle arrest. Causes apoptosis by inducing the transcription of pro-apoptotic genes such as BAX. Levels of p53 are negatively regulated by MDM2 through a feedback loop. p53 is required for the G1/S checkpoint and is a main component of the G2/M checkpoint.Ataxia-telangiectasia Activated by mechanisms that sense double-stranded DNA breaks. Transmits signals tomutated arrest the cell cycle after DNA damage. Acts through p53 in the G1/S checkpoint. At the G2/M checkpoint, it acts both through p53-dependent mechanisms and through the inactivation of CDC25 phosphatase, which disrupts the cyclin B–CDK1 complex. Component of a network of genes that include BRCA1 and BRCA2, which link DNA damage with cell cycle arrest and apoptosis CSBRP-July-2012
    37. 37. Selected Tumor Suppressor Genes Involved in Human Neoplasms Tumors Associated with Tumors Assocated withSubcellular Locations Gene Function Somatic Mutations Inherited MutationsCell surface TGF-β receptor Growth inhibition Carcinomas of colon Unknown E-cadherin Cell adhesion Carcinoma of stomach Familial gastric cancerInner aspect of plasma NF1 Inhibition of RAS signal Neuroblastomas Neurofibromatosis type 1membrane transduction and of p21 and sarcomas cell cycle inhibitorCytoskeleton NF2 Cytoskeletal stability Schwannomas and Neurofibromastosis type meningiomas 2, acoustic schwannomas, and meningiomasCytosol APC/β-catenin Inhibition of signal Carcinomas of stomach, Familial adenomatous transduction colon, pancreas; polyposis coli/colon melanoma cancer PTEN PI3 kinase signal Endometrial and prostate Cowden syndrome transduction cancers SMAD2 and SMAD4 TGF-β signal transduction Colon, pancreas tumors UnknownNucleus RB1 Regulation of cell cycle Retinoblastoma; Retinoblastomas, osteosarcoma carcinomas osteosarcoma of breast, colon, lung p53 Cell cycle arrest and Most human cancers Li-Fraumeni syndrome; apoptosis in response to multiple carcinomas and DNA damage sarcomas WT1 Nuclear transcription Wilms tumor Wilms tumor P16/INK4a Regulation of cell cycle by Pancreatic, breast, and Malignant melanoma inhibition of esophageal cancers cyclindependent kinases BRCA1 and BRCA2 DNA repair Unknown Carcinomas of female breast and ovary; carcinomas of male breast CSBRP-July-2012
    38. 38. Pathogenesis of retinoblastoma CSBRP-July-2012
    39. 39. The role of RB in regulating the G1-S checkpoint of the cell cycle CSBRP-July-2012
    40. 40. The role of p53 in maintaining the integrity of the genome CSBRP-July-2012
    41. 41. The role of APC in regulating thestability and function of β-catenin CSBRP-July-2012
    42. 42. CD95 receptor–induced and DNA damage– triggered pathways of apoptosis and mechanisms used by tumor cells to evade cell deathCSBRP-July-2012
    43. 43. Sequence of events in the development of limitless replicative potential CSBRP-July-2012
    44. 44. The metastatic cascade. Sequential steps involved in the hematogenous spread of a tumorCSBRP-July-2012
    45. 45. Sequence of events in the invasion of epithelialbasement membranes by tumor cellsCSBRP-July-2012
    46. 46. Mechanisms of metastasis development within a primary tumorCSBRP-July-2012
    47. 47. Role of miRNAs in tumorigenesis CSBRP-July-2012
    48. 48. Molecular model for the evolution of colorectalcancers through the adenoma-carcinoma sequence CSBRP-July-2012
    49. 49. DIRECT-ACTING CARCINOGENSAlkylating Agents β-Propiolactone Dimethyl sulfate Diepoxybutane Anticancer drugs (cyclophosphamide, chlorambucil, nitrosoureas, and others)Acylating Agents 1-Acetyl-imidazole Dimethylcarbamyl chloridePROCARCINOGENS THAT REQUIRE METABOLIC ACTIVATIONPolycyclic and HeterocyclicAromatic Hydrocarbons Major Benz[a]anthracene Benzo[a]pyrene Chemical Dibenz[a,h]anthraceneAromatic Amines, Amides,Azo Dyes 3-Methylcholanthrene 7,12-Dimethylbenz[a]anthracene Carcinogens 2-Naphthylamine (β-naphthylamine) Benzidine 2-Acetylaminofluorene Dimethylaminoazobenzene (butter yellow)Natural Plant andMicrobial ProductsAflatoxin B1 Griseofulvin Cycasin Safrole Betel nutsOthers Nitrosamine and amides Vinyl chloride, nickel, chromium Insecticides, fungicides Polychlorinated biphenyls CSBRP-July-2012
    50. 50. Experiments demonstrating the initiation and promotion phases of carcinogenesis in mice CSBRP-July-2012
    51. 51. General schema of events in chemical carcinogenesisCSBRP-July-2012
    52. 52. Effect of HPV proteins E6 and E7 on the cell cycle CSBRP-July-2012
    53. 53. Possible evolution of EBV-induced Burkitt lymphoma.CSBRP-July-2012
    54. 54. Tumor antigens recognized by CD8+ T cells CSBRP-July-2012
    55. 55. Mechanisms by which tumors evade the immune system CSBRP-July-2012
    56. 56. Paraneoplastic Syndromes Major Forms of UnderlyingClinical Syndromes Cancer Causal MechanismENDOCRINOPATHIESCushing syndrome Small-cell carcinoma of lung ACTH or ACTH-like substance Pancreatic carcinoma Neural tumorsSyndrome of inappropriate Small-cell carcinoma of lung; Antidiuretic hormone or atrialantidiuretic hormone secretion intracranial neoplasms natriuretic hormonesHypercalcemia Squamous cell carcinoma of lung Parathyroid hormone–related Breast carcinoma protein (PTHRP), TGF-α, TNF, IL-1 Renal carcinoma Adult T-cell leukemia/lymphomaHypoglycemia Ovarian carcinoma Fibrosarcoma Insulin or insulin-like substance Other mesenchymal sarcomasCarcinoid syndrome Hepatocellular carcinoma Bronchial adenoma (carcinoid) Serotonin, bradykinin Pancreatic carcinomaPolycythemia Gastric carcinoma Renal carcinoma Erythropoietin Cerebellar hemangioma Hepatocellular carcinoma CSBRP-July-2012
    57. 57. Paraneoplastic Syndromes cont….NERVE AND MUSCLE SYNDROMESMyasthenia Bronchogenic carcinoma ImmunologicalDisorders of the central and Breast carcinomaperipheral nervous systemDERMATOLOGIC DISORDERSAcanthosis nigricans Gastric carcinoma Immunological; secretion of Lung carcinoma epidermal growth factor Uterine carcinomaDermatomyositis Bronchogenic, breast carcinoma ImmunologicalOSSEOUS, ARTICULAR, AND SOFT-TISSUE CHANGESHypertrophic osteoarthropathy Bronchogenic carcinoma Unknownand clubbing of the fingersVASCULAR AND HEMATOLOGIC CHANGESVenous thrombosis (Trousseau Pancreatic carcinoma Tumor products (mucins thatphenomenon) Bronchogenic carcinoma activate clotting) Other cancersNonbacterial thrombotic Advanced cancers HypercoagulabilityendocarditisRed cell aplasia Thymic neoplasms UnknownOTHERSNephrotic syndrome Various cancers Tumor antigens, immune CSBRP-July-2012 complexes
    58. 58. A normal cervicovaginal smear shows large, flattened squamous cells and groups of metaplastic cells; interspersed are some neutrophils. There are no malignant cells CSBRP-July-2012
    59. 59. An abnormal cervicovaginal smear shows numerous malignant cells that have pleomorphic, hyperchromatic nuclei;interspersed are some normal polymorphonuclear leukocytes. CSBRP-July-2012
    60. 60. Anti-cytokeratin immunoperoxidase stain of a tumor of epithelial origin (carcinoma) CSBRP-July-2012
    61. 61. Steps required for the analysis of global gene expression by DNA microarrayCSBRP-July-2012
    62. 62. Selected Tumor MarkersHORMONESHuman chorionic gonadotropin Trophoblastic tumors, nonseminomatous testicular tumorsCalcitonin Medullary carcinoma of thyroidCatecholamine and metabolites Pheochromocytoma and related tumorsEctopic hormones See “Paraneoplastic Syndromes” ( Table 7-11 )ONCOFETAL ANTIGENSα-Fetoprotein Liver cell cancer, nonseminomatous germ cell tumors of testisCarcinoembryonic antigen Carcinomas of the colon, pancreas, lung, stomach, and heartISOENZYMESProstatic acid phosphatase Prostate cancerNeuron-specific enolase Small-cell cancer of lung, neuroblastomaSPECIFIC PROTEINSImmunoglobulins Multiple myeloma and other gammopathiesProstate-specific antigen and prostate-specific membrane antigen Prostate cancerMUCINS AND OTHER GLYCOPROTEINSCA-125 Ovarian cancerCA-19-9 Colon cancer, pancreatic cancerCA-15-3 Breast cancerNEW MOLECULAR MARKERSp53, APC, RAS mutants in stool and serum Colon cancerp53 and RAS mutants in stool and serum Pancreatic cancerp53 and RAS mutants in sputum and serum Lung cancerp53 mutants in urine Bladder cancer CSBRP-July-2012
    63. 63. ENDCSBRP-July-2012
    64. 64. Contact:Dr.CSBR.Prasad, M.D.,Associate Professor of Pathology,Sri Devaraj Urs Medical College,Kolar-563101,Karnataka,INDIA.CSBRPRASAD@REDIFFMAIL.COM CSBRP-July-2012