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neoplasm

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tumor

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tumor

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cell that has abnormal, uncontrolled growth -- benign and malignant

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benign

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not invasive (not cancer)

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malignant

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invades surrounding tissues and/or metastasize --> cancer

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Metastasis

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spread of malignant tumor cells throughout the body (typically through the blood and lymphatic system)

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carcinoma

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cancer arising from epithelial cells

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sarcoma

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cancer arising from muscle cells

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glioma

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cancer arising from cells of nervous system

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leukemia and lymphoma

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cancer arising from from hematopoietic and lymphatic cells

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Known causes of cancer

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Environmental (1-3)+genetics (4-5) 1. chemical exposure 2. radiation 3. infection 4. inherited genetic mutation 5. spontaneous sporadic mutations

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Aflatoxin B

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Slide 10 - Environmental carcinogens - Can directly reacting with on DNA and induce mutations - Is a toxin from mold that grows on grain and peanuts when stored in humid tropical conditions; - A contributory cause of liver cancer in the tropics with a characteristic mutations in TP53.

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Rous sarcoma virus (RSV)

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Slide 11 viral carcinogen (environmental)

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Germline mutations

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Slide 12 - inherited from parents - present in eggs or sperms - cause *inherited cancer-predisposing syndromes* - account for 5% of all cancers

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(Spontaneous) Somatic mutations

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- Are not heritable - Occur in specific tissues - Responsible for the majority, possibly all, types of cancers - Can occur during cell division

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Cancer is a complex genetic disease that arises from malfunction of genes: *accumulation of genetic mutations/epigenetic changes.* T/F?

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Slide 14 T

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What does accumulation of genetic mutations refer to in terms of cancer?

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Slide 15 - caused by a single mutated cell that undergoes a clonal evolution process - tumor progress with accumulation of mutations; single mutation is generally not enough to cause cancer (takes years)

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What are the three types of cancer critical genes?

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1. Proto-oncogenes and oncogenes 2. Tumor-suppressor genes 3. DNA repair genes

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Proto-Oncogenes vs oncogenes

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Slide 19 *Proto-oncogene:* genes which are involved in the promotion of cell division and proliferation, in which gain of function mutation can drive a cell toward cancer; *Oncogene*s: mutation, overactive or overexpressed forms of proto-oncogenes. *Gain of function; dominant at cellular level.*

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Functions of Cellular Proto-Oncogenes

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promote viability of cells through different methods e.g. RAS-GTPase, c-MYC, RET-Tyrosine kinase, MET-Tyrosine kinase, CD4-cell cycle, BCL2- Anti-apoptosis, BCR/ABL - Tyrosine kinase

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Tumor Suppressor Genes

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Slide 27 - Normally exerts a *negative effect* on cell division and proliferation. - *Recessive* at cellular level. - Loss of function in both alleles result in uncontrolled cell division and tumor formation - *'Loss of Heterozygosity' and 'Two Hit Hypothesis'*.

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Example of loss of function of tumor suppressor gene that results in cancer

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RB1 gene, TP53 tumor-suppressor gene, DCC, WT1, BRCA1/2

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Knudson Two Hit hypothes?s

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Inactivation of a tumor suppressor gene requires two mutations, inherited mutation and somatic mutation. LOH: Loss of Heterozygosity

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The RB1 Gene

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- Encodes Rb protein which is involved in cell cycle regulation; - mutations of Rb have also been identified in various cancers, including retinoblastoma, osteosarcomas, small-cell lung carcinomas, bladder, breast, pancreatic and prostate cancers.

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Retinoblastoma (Rb)

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*Tumor of retinal stem cell* • Average age at presentation - unilateral 26 months - bilateral 8 months • Males and Females equally affected • Occurs in familial (~40%) and sporadic (~60%) forms • Familial more likely to be bilateral, younger • RB1gene on chr13 (first tumor suppressor gene discovered) • Knudson's Two Hit Hypothesis

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TP53 tumor suppressor gene

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- In Chr. 17 and encodes a protein p53 with molecular weight 53 kDa. - 'Guardian of the genome': *Loss of function mutations in TP53 are the most common genetic changes observed in human cancer*, with mutations found in ; 50% of all tumors. - Germline mutations in TP53 cause the inherited cancer predisposing condition known as *'Li- Fraumeni syndrome'*, a rare *autosomal dominant* syndrome characterized by *neoplasms at multiple sites*, including breast cancer, soft tissue sarcomas, brain tumors, osteosarcoma, leukemia, and adrenocortical carcinoma.

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The Adenomatous Polyposis Gene, APC

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an inhibitory component of the Wnt signaling pathway.

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Familial Adenomatous Polyposis (FAP)

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*FAP* - also called *adenomatous polyposis coli (APC)* - *autosomal dominant* sub-type of colon cancer that is characterized by a large number of adenomatous polyps (;100). - caused by mutations in APC gene. - rare, less than 1% of total colon cancers *Somatic mutations in APC gene* - approximately 85% of all colon cancers Note: Colonoscopic removal of polyps could reduce the incidence of colon cancer by as much as 90%.

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DNA Repair Genes

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- Genes that ensure each strand of genetic information is accurately copied during cell division of each cell cycle - Mutations in these genes lead to an increase in the frequency of mutations in other genes (such as tumor-suppressor gene and proto-oncogene)

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BRCA 1 (Chr 17) / BRCA 2 (Chr 13)

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•BRCA1 is important for homologous recombination, cellular repair of DNA damage, and transcription of mRNA. •Mutations in BRCA1 also are involved in ovarian cancer. •BRCA2 plays a role in timing of mitosis in the cell cycle.

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BRCA1/2 in Breast and Ovarian Cancer

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•Represents 31% of cancers in women •~5% of breast cancers are hereditary, with age of onset earlier than sporadic forms (mutations at 2 alleles). •Inherited breast/ovarian cancer is an *autosomal dominant* condition and occurs as a result of mutations in DNA repair genes: BRCA1 (Chr17) and/or BRCA2 (Chr13).

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DNA *mismatch* repair genes

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mutations lead to Human Non-Polyposis Colon Cancer (HNPCC)

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Human Non-Polyposis Colon Cancer (HNPCC)

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•2-3% of all colorectal cancer (CRC) cases. •*Autosomal dominant*, high penetrance. •Typical age of cancer onset is 40-50 years. •High lifetime risk of CRC and other cancers beginning age 20. •Caused by *mutations or deletions in mismatch repair (MMR) genes MSH2, MLH1, MSH6, (PMS2) , with 90% of detectable mutations in MSH2 and MLH1* •Tumor formation *requires mutation at the second allele*. •All four genes have homologsin yeast. •DNA blood tests are available for all four genes.

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Prevention ; Diagnosis of cervical cancer

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Pap test ; HPV screening -- caused by Human Papilloma Virus Risk Factors: smoking, having many children, and human immunodeficiency virus (HIV) infection.

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Genetic testing for heritable cancer

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- BRCA1/2 in breast and ovarian cancer -APC in familial adenomatous polyposis -Sets of cancer predisposing genes

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Liver cancer prevention

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vaccine to hepatitis B; diet without cancer inducing chemicals

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Detection of colon cancer

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colonoscopy

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Prevention of lung cancer

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stay away from smoking tobacco

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General cancer targeting strategies

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- All the clinically used cancer therapeutic reagents work by inhibiting oncogenic pathways. - Activating tumor suppressor genes is currently not feasible. - Several most common onco-drivers, such as K-Ras, MYC, are very difficult to target directly by anti-cancer drugs. - Targeting specific oncogenic mutation - Some anticancer drugs and drug targets in the RTK-Ras- MAP-kinase signaling pathway - Utility of tumor's genetic instability for therapy - synthetic lethality - Many Cancers Can Be Treatable by Enhancing the Immune Response Against the Specific Tumor - Treating patients simultaneously with several drugs has potential advantages

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