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Neoplasia in Fish
a. In a table, compare and contrast the differences occurring in a cell undergoing hyperplasia
and neoplasia.
b. Describe in details how to diagnose a hyperplasic tissue from a neoplastic growth.
c. Discuss how the sex of an organism is a factor in the occurrence of neoplasia in fish.
d. Compare and contrast how chemical radiation and viruses causes neoplastic diseases in fish.
e. List and describe the viruses that are known to cause cancer in fish and their mode of
pathogenesis.
f. Describe the bioactivities of aflatoxin, PAH and halogenated compounds that could led to
cancer development in fish.
Step by step
Solved in 2 steps
- Genetic Diseasesa. List the differences between infectious and genetic diseases.b. Discuss the reasons why genetic diseases could hardly be diagnosed in fish.c. Describe the how albinism occur in fish and why it is considered a disease.d. List other fish species, documented to exhibit albinism.e. Elucidate the process by which melanoma or skin cancer-prone sword tail develops. Describethe genetic mechanism involved.f. Describe how domestication can lead to genetic problems in aquaculture.. Describe the general relationship that may exist between mutations and cancer. Explain what is meant by the “normalization window” for treatment of cancer with antiangiogenic therapies and conventional treatments.
- Here, Research a cancer caused by an oncogenic virus. how the virus disrupts normal cell function and causes cancer to develop. What risk factors exist that make individuals more susceptible to this type of disease? Are there any preventative measures that can be taken to mitigate the risk of contracting this disease? What therapies are available or being developed that combat this disease? what are the methods of action for all therapies available. ?1. Describe & explain the pathophysiology of cancer based on the diagram. Reference: https://www.onlinebiologynotes.com/cancer-etiology-pathophysiology-types-diagnosis-and- treatment/ Acquired (environmental) DNA damaging agents: • chemical • radiation viruses Activation of growth- promoting oncogenes NORMAL CELL DNA Damage Failure of DNA repair Mutations in the genome of somatic cells Alteration of genes that regulate apoptosis Malignant neoplasm / Successful DNA repair CANCER Inherited mutations: • Genes affecting DNA repair • Genes affecting cell growth Expression of altered gene products and loss of regulatory gene products Inactivation of cancer suppresor genes Clonal expansion Additional mutations (progression) T Heterogeneityb. Individuals with these cancers may be treated with one of the following chemotherapeutic drugs. Complete the table below about their mechanisms of action. In which cellular compartment/ structure/organelle does this process occur? Drug Drug's mechanism of action Which process is targeted first by this drug? If more than 1 location, be sure to specify ALL relevant locations. (replication, mitosis, transcription, translation, or none of the above)? A Inhibits microtubule disassembly В Inhibits elongation by RNA polymerase Inhibits eukaryotic ribosomal function D
- . Download and read the attached review article (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5836099/pdf/EMBR-19-e45440.pdf) titled: Perturbing mitosis for anti-cancer therapy: is cell death the only answer?Pick one initial of TNM cancer staging and identify what the different stages are and what they mean.Hi, can you elaborate about: 1. MyoD to be used to manipulate cancer cells at an early stage and then be used as a treatment. 2. Angiogenesis is a major function for tumor cells to grow, so if we break off the blood supply, would this result in better treatment?
- D. What is the best term for a normal INK gene? (tumor suppressor) (inactive tumor suppressor) (oncogene) (proto-oncogene) (oncogene or tumor suppressor) (beats me). E. Suppose you have cells that have permanently active ink protein as in C. The cells also have permanently active E2F or permanently active ras. (Consult texts or handouts for roles of E2F and ras.) E-1. If your cells have active E2F and active ink, then your cells should (grow normally) (fail to grow) grow uncontrollably) (can't predict). E-2. If your cells have active ras and active ink, then your cells should (grow normally) (fail to grow) grow uncontrollably) (can't predict).. Please explain the role of Ubiquitin Ligase Activity in the regulation of apoptotic cell death.Our government has finite funds to devote to cancer research.Discuss which of the following areas of research you think shouldreceive the most funding.A. Identifying and characterizing oncogenes and tumorsuppressorgenesB. Identifying agents in our environment that cause cancerC. Identifying viruses that cause cancer D. Devising methods aimed at killing cancer cells in the bodyE. Informing the public of the risks involved in exposure tocarcinogensIn the long run, in which of these areas would you expect successfulresearch to be the most effective in decreasing human mortalitydue to cancer?