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Chapter 21: Molecular Basis of Cancer
Chapter 21: Molecular Basis of Cancer

... hypermorph = increased amount / activity ...
Slide 1
Slide 1

... Genetic map ...
Causes, Risk Factors, and Prevention
Causes, Risk Factors, and Prevention

... We do not know exactly what causes most adrenal cortical tumors. Over the past several years, experts have made great progress in understanding how certain changes in a person's DNA can cause cells in the adrenal gland to become cancerous. DNA is the molecule that carries the instructions for nearly ...
Genes and Evolution - Mad River Local Schools
Genes and Evolution - Mad River Local Schools

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No Slide Title

... Oncogenes, Tumor Suppressor Genes, Programmed Cell Death Programmed Cell Death (Apoptosis) --> cell brings about its own death and lysis, signaled from outside or programmed in its genes, by systematically degrading its own macromolecules When? Development of embryo (fingers) Anti-self antibodies pr ...
Study Guide
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... MAIN IDEA: Genomics involves the study of genes, gene functions, and entire genomes. Take notes on concepts in genomics by completing the concept map below. ...
PathWay #7 - Text - The Royal College of Pathologists of Australasia
PathWay #7 - Text - The Royal College of Pathologists of Australasia

... Was there really evidence of progression at the molecular level? “By dissecting these lesions out and examining them with techniques like LOH, we were able to determine that many of the changes found in cancer cells were also there in early precancerous lesions.” They were present even in some tissu ...
Word document - Personal Genetics Education Project
Word document - Personal Genetics Education Project

... 4. Since Noah and Alexis are not identical twins, they had the same chance as any brother and sister to inherit SPR mutations from both of their parents. 5. Noah and Alexis did not show identical symptoms. This might be explained by other differences in their genetic make-up and/or environmental fac ...
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Establishment of Cell Identity in Drosophila Embryos

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epigenetics
epigenetics

... organism is the same. Because cell differentiation is epigenetic, a somatic cell can be reprogrammed to become totipotent*. If we transfer the nucleus of a body cell (e.g. skin cell) to an enucleated egg cell, the nucleus forgets that it was formerly a skin cell, and become totipotent, that is the c ...
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Oncology Newsletter_green_2Jan08.rk

... prospective, 2 year uncontrolled clinical trial to test the effects of sirolimus on angiomyolipomas and lymphangioleiomyomatosis tumors which are associated with mutations in TSC genes. The results published in NEJM showed that angiomyolipomas regressed (30% or more) during sirolimus therapy, but tu ...
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... • Essentially like 2-point mapping problem between one gene locus and the centromere. • Identify first-division segregation (may or may not be most common group) from second-division segregation. • D = 1/2(second-division segregant asci)/total. • For example, if there are 65 first-division asci and ...
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Human Genetics

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March 20, 2011 - Transcript

... Antibodies are actually large protein molecules that our own bodies make as part of our immune defense mechanisms against infectious agents, and research almost 30 years ago found that antibodies could be raised in mice and the cells making them could be harvested such that the antibodies could be p ...
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... The human genome (total composition of genetic material within a cell) is packaged into larger units known as chromosomes—physically separate molecules that range in length from about 50 million to 250 million base pairs. Human cells contain two sets of chromosomes, one set inherited from each paren ...
Note: Incomplete sections will be updated when information
Note: Incomplete sections will be updated when information

... Inheritance: pedigree symbols, patterns of inheritance (autosomal dominant and recessive, X-linked dominant and recessive, Y-linked, mitochondrial). Phenotypic characterisation: expression of a disorder (different genes, age of onset, pleiotropy, mental function) variability in expression (expressiv ...
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... Uracil, which comes about from the spontaneous deamination of cytosine or for that matter hypoxanthine (another base which comes about from the deamination of adenine) and xanthine (derived from the deamination of guanine), does not belong in DNA. A set of enzymes (base excision repair, BER) cleaves ...
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... and molecular genetics, including: prediction of genotypic and phenotypic ratios for complex crosses; mechanisms of DNA replication, recombination, transcription and gene expression. -Explaining how mutations can alter the outcomes of these processes; ATTITUDES Apply this knowledge to solving geneti ...
Gregor Mendel - father of Genetics and 18th century Austrian monk
Gregor Mendel - father of Genetics and 18th century Austrian monk

... RNA - Ribonucleic Acid RNA is an opposite copy of DNA RNA is a messenger. It takes information out of nucleus to ribosomes. Does not contain thymine, uracil ( U ) connects with Adenine ( A ) ...
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colo-rectal-kidney-cancer-risk-factors

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Bacteria Power Point File

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< 1 ... 410 411 412 413 414 415 416 417 418 ... 504 >

Oncogenomics



Oncogenomics is a relatively new sub-field of genomics that applies high throughput technologies to characterize genes associated with cancer. Oncogenomics is synonymous with ""cancer genomics"". Cancer is a genetic disease caused by accumulation of mutations to DNA leading to unrestrained cell proliferation and neoplasm formation. The goal of oncogenomics is to identify new oncogenes or tumor suppressor genes that may provide new insights into cancer diagnosis, predicting clinical outcome of cancers, and new targets for cancer therapies. The success of targeted cancer therapies such as Gleevec, Herceptin, and Avastin raised the hope for oncogenomics to elucidate new targets for cancer treatment.Besides understanding the underlying genetic mechanisms that initiates or drives cancer progression, one of the main goals of oncogenomics is to allow for the development of personalized cancer treatment. Cancer develops due to an accumulation of mutations in DNA. These mutations accumulate randomly, and thus, different DNA mutations and mutation combinations exist between different individuals with the same type of cancer. Thus, identifying and targeting specific mutations which have occurred in an individual patient may lead to increased efficacy of cancer therapy.The completion of the Human Genome Project has greatly facilitated the field of oncogenomics and has increased the abilities of researchers to find cancer causing genes. In addition, the sequencing technologies now available for sequence generation and data analysis have been applied to the study of oncogenomics. With the amount of research conducted on cancer genomes and the accumulation of databases documenting the mutational changes, it has been predicted that the most important cancer-causing mutations, rearrangements, and altered expression levels will be cataloged and well characterized within the next decade.Cancer research may look either on the genomic level at DNA mutations, the epigenetic level at methylation or histone modification changes, the transcription level at altered levels of gene expression, or the protein level at altered levels of protein abundance and function in cancer cells. Oncogenomics focuses on the genomic, epigenomic, and transcript level alterations in cancer.
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