Concept explainers
To explain: The finding of the experiment in which AAF causes bladder cancer in rat but not in guinea pig but does not cause cancer when bladder cells of both are grown in culture.
Introduction: The study of cancer is known as oncology. The agents which upon exposure cause cancer are called as oncogenic substances or mutagens. Cancer-causing substances can be physical, chemical or biological. The substance called 2-acetylaminofluorene is a chemical carcinogen affecting the P450 cytochrome associated with the electron transport chain.
To explain: Whether AAF is having a carcinogenic tendency for humans without the exposure of AAF to humans.
Introduction: The study of cancer is known as oncology. The agents which upon exposure cause cancer are called as oncogenic substances or mutagens. Cancer-causing substances can be physical, chemical or biological. The substance called 2-acetylaminofluorene is a chemical carcinogen affecting the P450 cytochrome associated with the electron transport chain.
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Becker's World of the Cell (9th Edition)
- Please help me with this question. More than one answer may be correct. THe graph relating to the information is included below. In the above figure, a wild-type plant and a plant with a atg5 knockout, which prevents autophagy within the cell, are examined for the number of peroxisomes per micrograph image taken of the plant's leaves. Which of the following are true. Options: The atg5 plants have elevated levels of malate The atg5 plants appear less able to destroy old organelles The atg5 plants may have a modified ability to deal with phosphoglycolate The atg5 plants may have a modified ability to deal with oxygen free radicals The atg5 plants appear more able to destroy old organellesarrow_forwardTrue or False? p21 inhibits the S-cyclin/S-Cdk complex.arrow_forwardBAX proteins stimulate apoptosis. Mutations in BAX genes can help developing cancers but not necessarily trigger a tumor. This is because mutations in BAX do not contribute to tumorigenesis, but BAX can prevent the formation of a tumor mutations in BAX may over-stimulate apoptosis mutations in BAX contribute to tumorigenesis only with other inhibitors of apoptosis mutations in BAX prevent the formation of tumorsarrow_forward
- Help with below solution. why we have not yet made much progress against lung cancer, compared to other types of cancer? .arrow_forwardDo it. how to deal with a high incidence of cancer in the area of your state where heavy industry is concentrated.?arrow_forwardCancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.arrow_forward
- TNF-alpha treatment of prostate carcinoma, LNCAP cells decreases cell survival as shown in the graph below. Which of the following would you observe in these cells treated with TNF- alpha? Select all that apply TNF-a 120 100 80 - 60 40 20 0. 24 72 (hrs) Control + TNF-a 100 ng TNFA 10 ng O Activation of extrinsic pathway of apoptosis O Activation of intrinsic pathway of apoptosis Activation of executioner caspases Recruitment of adapter protein FADD to the TNF-alpha receptor LNCAP cell viability (% of control)arrow_forwardRelatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.arrow_forward. Leukemia is a neoplastic (cancerous) proliferation of white blood cells. Clinicians are currently testing deoxycoformycin, an adenosine deaminase inhibitor, as a possible antileukemic agent. Why might one expect this therapy to be effective?arrow_forward
- Please help me with this question. More than one answer may be correct. THe graph relating to the information is included below. In the two figures, a wild-type plant and a plant with a atg5 knockout, which prevents autophagy within the cell, are compared. The first figure shows the number of peroxisomes per micrograph image taken of the plant's leaves. The bottom figure shows a comparison of 3-week seedlings of the wild-type plant and the atg5 plant at normal CO2 levels (360 ppm) and elevated CO2 (2000 ppm) Which of the following are true. Question 20 options: the atg5 knockout plants are more able to deal with photorespiration the atg5 knockout plants are less able to deal with photorespiration the inability to recycle peroxisomes through autophagy impairs a plants ability to deal with photorespiration Elevated CO2 overcomes the photorespiration impairment in atg5 plants Elevated CO2 overcomes the photorespiration impairment in wild-type plantsarrow_forward"Schematic outline of melanogenesis. UVR stimulates the expression of POMC by keratinocytes. The peptide produced is the precursor of the hormone a-MSH, that binds to MC1R in melanocytes. This union leads to an increase in cellular cyclic adenosine monophosphate (cAMP) that in turn leads to increased levels of MITF expression, which upregulates the transcription of TYR, TYRP1 and TYRP2, producing brown-black eumelanin. In the absence of a-MSH, the antagonist ASIP binds to MC1R, and phaeomelanin is synthetized instead. Melanosomes are then transferred to keratinocytes through the dendrites via a shedding vesicle system." Briefly discuss how these several aspects of the molecular and cellular biology of melanin production and melanosome transfer contribute to determine skin color. How would different mutations in the hormonal response to ultraviolet light, the melanin production signal transduction pathways, and melanosome transfer influence skin color, hair color, and eye color? Did…arrow_forwardcells undergo programmed cell death. Write out the pathway(s), noting the changes (e.g., localization, phosphorylation, activation) When mammalian cells are irradiated, they stop dividing by arresting at cell cycle checkpoint. If the damage persists, the kinase (CdK), Cdk inhibitor, cytochrome c, DNA damage, mitochondria, p53, phosphorylation, transcription. each step. Include: apoptosis, apoptosome, ATM, pro-apoptotic proteins, caspase, Checkpoint Kinase (Chk), cyclin, cyclin-dependearrow_forward
- BiochemistryBiochemistryISBN:9781305577206Author:Reginald H. Garrett, Charles M. GrishamPublisher:Cengage Learning