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Neoplasia,[object Object],Dr Omar Chughtai,[object Object]
Neoplasia 6-3-2011
Cancer,[object Object],Uncontrolled growth of abnormal cells,[object Object]
Neoplasia 6-3-2011
Neoplasia 6-3-2011
The Study of Cancer,[object Object],[object Object]
Pathologists
Molecular Biologists and Geneticists
Diagnose:
Pathologists
Radiologists
Treat:
Oncologists
Surgeons,[object Object]
Nomenclature,[object Object],Metaplasia	Dysplasia,[object Object]
Characteristics of Neoplasms,[object Object],Differentiation and Anaplasia,[object Object],Rate of Growth,[object Object],Invasion of Surrounding Tissue,[object Object],Metastatic Potential,[object Object]
Differentiation and Anaplasia,[object Object],Differentiation:  How similar tumor cells are to normal cells ,[object Object],Benign Tumors: Well-differentiated,[object Object],Malignant Tumors: Range of differentiation,[object Object],Anaplasia: The lack of differentiation,[object Object]
Neoplasia 6-3-2011
Neoplasia 6-3-2011
Neoplasia 6-3-2011
Differentiation and Anaplasia,[object Object],Pleomorphism: ,[object Object],Variable  cell size / shape,[object Object]
Differentiation and Anaplasia,[object Object],Abnormal Nuclear Morphology: ,[object Object],Variable nuclear size / shape,[object Object],dark (hyperchromatic),[object Object],prominent nucleoli,[object Object],clumped chromatin,[object Object]
Differentiation and Anaplasia,[object Object],Mitoses: Increased in number, abnormal in shape ,[object Object]
Differentiation and Anaplasia,[object Object],Loss of Polarity: No longer arranged neatly,[object Object]
Differentiation and Anaplasia,[object Object],Tumor Giant Cells: ,[object Object]
Differentiation and Anaplasia,[object Object],Tumor Necrosis: ,[object Object]
Rate of Growth ,[object Object],Tumors are clonal,[object Object]
Rate of Growth,[object Object],[object Object]
Doubling Time is same as normal tissue or even longer
Growth Fraction:
Very high initially
Decreases as tumor size grows
Cell Loss:
Apoptosis, Lack of nutrients, Necrosis ,[object Object]
Rate of Growth ,[object Object],Slow Growing Tumors,[object Object],Low cell proliferation,[object Object],Low cell loss,[object Object],Resistant to chemotherapy,[object Object]
Local Invasion,[object Object],Benign Tumors: ,[object Object],Discrete, well-circumscribed mass,[object Object],Don’t infiltrate surrounding tissue,[object Object],Fibrous capsule,[object Object]
Local Invasion,[object Object],Malignant Tumors: ,[object Object],Poorly demarcated,[object Object],Infiltrate surrounding tissue,[object Object],No capsule,[object Object]
Metastasis,[object Object],Tumor implants discontinuous from the primary tumor,[object Object]
Metastasis – Peritoneal Cavity,[object Object]
Metastasis – Hepatic Metastasis,[object Object]
Metastasis – Lymph Node,[object Object]
Nomenclature,[object Object],BENIGN,[object Object],[object Object]
Will remain localized
Local surgical removal
Epithelial:
Adenoma
Papilloma
Mesenchymal
Fibroma
LeiomyomaMALIGNANT,[object Object],[object Object]
Potential to spread widely
Surgical removal is not enough
Epithelial: carcinoma
Adenocarcinoma
Squamous cell carcinoma
Mesenchymal: sarcoma
Fibrosarcoma
Leiomyosarcoma,[object Object]
Epidemiology,[object Object],Second most common cause of death ,[object Object],In the United States, one in five deaths is due to cancer,[object Object],In Pakistan, . . . .,[object Object]
Most Common Cancers,[object Object],Men,[object Object],Prostate,[object Object],Lung,[object Object],Colorectal,[object Object],Women,[object Object],Breast,[object Object],Lung ,[object Object],Colorectal,[object Object]
Cancer Mortality Trends,[object Object],Decreased deaths in men from,[object Object],Ca Lung: Decreased smoking,[object Object],Prostate: PSA screening,[object Object],Ca Colon: Colonoscopy screening,[object Object],Decreased deaths in women from ,[object Object],Ca Breast: Self exam, Mammography,[object Object],Ca Cervix: Pap Smear,[object Object]
Cancer Mortality Trends,[object Object],Increased deaths in men and women from ,[object Object],Hepatocellular Ca: Hepatitis C ,[object Object],Increased deaths in women: ,[object Object],Ca Lung: Smoking,[object Object]
Cancer Incidence,[object Object]
Cancer Mortality - Men,[object Object]
Cancer Mortality - Women,[object Object]
Geography and Environment,[object Object],Ca Stomach deaths are 7-8 times higher in Japan than in the US,[object Object],Ca Lung deaths are higher in the US than in Japan,[object Object]
Geography and Environment,[object Object]
Obesity and Cancer,[object Object]
Age and Cancer,[object Object]
Genetic Predisposition to Cancer,[object Object],Cancers are caused by genetic mutations,[object Object],Sporadic,[object Object],Inherited,[object Object]
Inherited Cancer Syndromes,[object Object],Person inherits one autosomal dominant mutant gene,[object Object],Carriers of the mutated gene have a significantly increased risk of developing cancer,[object Object],Familial Adenomatous Polyposis,[object Object],Retinoblastoma,[object Object]
Defective DNA Repair,[object Object],Autosomal recessive,[object Object],Cells have decreased ability to recover from DNA damage,[object Object],Xeroderma pigmentosum,[object Object],Ataxia-Telangiectasia,[object Object]
Familial Cancers,[object Object],Clustering of certain cancers in families,[object Object],Early age at onset,[object Object],Two or more first-degree relatives with the same cancer,[object Object],Siblings: 2-3 X risk of cancer,[object Object],Multiple / Bilateral tumors,[object Object],Multiple low-penetrance genes,[object Object]
Precancerous Conditions,[object Object]
Molecular Basis of Cancer,[object Object],Nonlethal Genetic Damage,[object Object],Clonal Expansion of Mutated Cell,[object Object],Accumulation of Mutations,[object Object]
Nonlethal Genetic Damage,[object Object],Proto-oncogenes,[object Object],Tumor Suppressor Genes,[object Object],Genes that regulate Apoptosis,[object Object],Genes involved in DNA repair,[object Object]
Neoplasia 6-3-2011
Neoplasia 6-3-2011
Tumor Progression,[object Object]
Accumulation of Mutations,[object Object]
Neoplasia 6-3-2011
Neoplasia 6-3-2011
Growth Factors,[object Object],Normal: Paracrine stimulation,[object Object],Cancer cells: Synthesize the same growth factors to which they are responsive (Autocrine loop),[object Object]
Growth Factor Receptors,[object Object],Normal: Receptors are transiently activated,[object Object],Mutated: Constitutive activation without the need for Growth Factor binding!,[object Object]
Signal Transducing Proteins,[object Object],Located on inner surface of plasma membrane,[object Object],Receive signals from Growth Factor Receptor,[object Object],Transmit signals to the cell nucleus,[object Object],Two most important members of this group: ,[object Object],RAS,[object Object],ABL ,[object Object]
Neoplasia 6-3-2011
RAS,[object Object],Most commonly mutated oncogene,[object Object],One of a family of small GTP/GDP binding  Proteins,[object Object],Normal activation is transient,[object Object],Upon Activation, GDP is replaced by GTP,[object Object],GTP is hydrolyzed to GDP by intrinsic GTPase,[object Object],GTPase activity is accelerated by GTPase- Activating Proteins,[object Object]
RAS,[object Object],Point mutations interfere with hydrolysis of GTP,[object Object],RAS is trapped in the activated state,[object Object],Cell ends up in a state of continuous proliferation,[object Object]
BCR-ABL Translocation,[object Object]
BCR-ABL Translocation,[object Object],ABL proto-oncogene:,[object Object],Limited tyrosine kinase activity,[object Object],Localizes to nucleus and promotes apoptosis in cells with DNA damage ,[object Object],BCR-ABL Hybrid Protein:,[object Object],Much higher, uncontrolled tyrosine kinase activity,[object Object],Can’t move into nucleus, thus can’t cause apoptosis in cells with damaged DNA,[object Object],Chronic Myeloid Leukemia,[object Object]
Signal Transducing Proteins,[object Object]
The Cell Cycle,[object Object]
Transcription Factors,[object Object],MYC proto-oncogene: ,[object Object],Induced rapidly upon signal to divide,[object Object],Activate CDK’s,[object Object],Inhibits CDKI’s,[object Object],Levels decline to baseline when cell cycle begins,[object Object]
Transcription Factors,[object Object],Mutated MYC oncogene: ,[object Object],Persistent expression / overexpression,[object Object],Leading to sustained proliferation,[object Object]
Transcription Factors,[object Object]
Cell Cycle Regulators,[object Object],Cyclins D, E, A and B appear sequentially and bind to various CDK’s,[object Object],Cyclin-CDK complexes drive the cell through the cel cycle,[object Object],CDKI’s exert negative control over the cell cycle,[object Object]

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