This Blog is dedicated to the B.Tech Biotechnology students, especially JNTU students. It will be useful even for other university students doing their B.Tech Biotechnology
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What is cancer? Explain different factors that are involved in the cancer development?
Discuss a) RB, retinivlastoma b) p53
What is a carcinogen? Expain different types of carcinogens in the development of cancer?
What is signal transduction? Explain the effects on the cell-cell signaling during the radiation carcinogenesis?
Write short notes on: a) cell cycle check points b) Cancer genes
Explain : a) Role of Plasma membrane components in metastatis. b) Role of extracellular matrix components and the basement membranes in tumor metastatis.
Can the gene expression patterns of cancer cells be used to identify targets for cancer diagnosis or therapy? - discuss.
Write short notes on : a) Recombinant anticancer drugs. b) Problems of antibody therapy in cancer.
SET : 2
What are receptors? Explain the ligand-receptor mechanism with an example?
Explain a) Skin Cancer b) Colon cancer
Define a) DNA adduct b) DNA repair c) p53 gene d) cyt P450.
Discuss : a) cellular stress response b) Gene induction during radiation exposure.
Write short notes on a) Retroviral transduction. b) Amplification of Oncogene action.
Explain : a) Tissue adhesion properties of metastatic cells b) Ability of metastatic tumor cells to escape the hosts immune response.
Write short notes on : a) combination therapies. b) cancer diagnosis and staging
Discuss : a) Recent developments in cancer therapy. b) New drugs, New targets and new approaches of cancer.
SET : 3
Explain a) Oncogenes b) Receptors c) Signaling molecules.
What is the role of diet in different forms of cancer?
What are mutations? Explain how Chemical carcinogens play a role in the development of mutations?
Define and discuss: a) Units of Radiation b) Radiation Dose
Write short notes on : a) Angiogenesis b) Tumor viruses and cancer
Explain a) Chemotactic factors in cancer cell migration. b) Role of Oncogenes in tumor metastatis
Write short notes on: a) Safety and acceptability of screening tests of cancer b) Evaluation of cancer screening.
Explain a) Assessing efficacy of drugs in clinical trials. b) cells as vehicles for cancer gene therapy.
Sunscreens contain chemicals that confer protection from the UV radiations. Mostly the sunscreen ingradients protect from UV-B light. UV-A protection is not offered by many sunscreens. Some the ingredients of sunscreens are:
PABA
PBI (Phenylbenzimidazole)
Octocrylene
Octylmethoxycinnamate
Benzophenone-3
Micronized titanium oxide and zinc oxide particles.
Most of the ingradients used offer protection against UV-B and not UV-A, which is more deadly then UV-B. UV-A causes malignant melanoma, which is responsible for 75% 0f the skin cancer related deaths, indicating the deadliness of the disease.
They are beneficail in that they provide protection against UV-B and thus prevent Squamous cell carcinoma and Basal cell carcinoma. (They are non-malignant skin cancers. The curable rate is also high for them.)
There are many disadvantages conceived with the use of sunscreens.
The titanium oxide and zinc oxide particles have cytotoxic and carcinogenic properties. The ingredients like Bezophenone, octocrylene, octylmethoxycinnamate have been shown to absorb into the skin and produce reactive oxigen species(ROC). ROC's under illumination bring about alterations in the DNA that may lead to cancer.
Many sunscreen ingredients have been shown to produce singlet [o] which damages the DNA.
Apart from the above mentioned, other potential disadvanatges with the use of sunscreens are:
Using sunscreens reduces melanin production. this makes us more susceptible to radiation damage.
The absense of UV-a filters combined with a long exposure to sun incrases the chances of melanoma.
As the wavelength is long they reach the deeper layers of the skin unlike UV-B which reaches only the stratum corneum (visible layer of the skin containing dead cells)
UV-A radiation like the other two forms destroy collagen fibres.
UV-A radiation is not at all absorbed by the ozone layer and it reaches the earth directly.
Causes sun burns quickly. It triggers the melanocytes to produce melanin responsible for the color of the skin burn lesions.
The lesions later transform into melanoma, a malignant form of skin cancer.
This is due to uncontrolled division of the melanocytes.
The effects of UV-A radiation is due to indirect effects unlike the UV-B radiation.
UV-A radiation leads to the generation of highly reacting species like hydroxyl and free oxygen radicals, which damages the DNA leading to cancerous growth.
Sunscreens donot usuallly contain protectants for UV-A. Recently materials like titanium oxide that confer protection against UV-A radiation are being incorporated into the sunscreens.
UV-B and its carcinogenecity
Wavelength range: 280-320 nm
It reaches the stratum corneum of the skin (visble layer of the skin with dead cells)
Even UV-B radiation causes skin burns. but it tkaes 2 days of latent period for the lesions to appear. The melanocytes produces melanin thats responsible for the color.
Melanin is a photoprotectant. It absorbs the radiation and releases the energy in the form of heat.
The carcinogenecity of UV-B radiation is due to the direct DNA damage. UV-B radiation excite the DNA molecules leading to the formation of covalent bonds between the adjacent CC residues in the same DNA strand. When the Replication process commences, this CC dimer is read as AA. This results in a TT residue in the daughter strand. This mutation is referred to as 'classical C-T mutation'. The mutations leads to cancerous growth.
Sunscreens contain protectants that confer protection from UV-B radiation.
UV-C and its carcinogenecity: Wavelength Range : 100-280 nm This is high energy radiation like the UV-B radiation. It is completely absorbed by the earthds atmosphere. But artificial sources are the causes for UV-C exposure. Like the UV-B radiations it may directly damage the DNA molecules leading to cancerous growth.
Activated RAS oncogenes were identified in human skin cancer cells. Most of the mutations in the RAS gene were found in pyramidine rich residues. this indicates that pyramidines are the targets of UV induced mutations. P53 helps in removing the damages caused by radiation
The above mentioned factors are naturally occurring but they are even released/generated human activities.
Asbestos is a naturally occurring mineral fiber, but its a human enhanced physical carcinogenic agent. The reason for this is that though it is occurring naturally we are getting exposed to it thru mining activities and thru commercial products. (It is a naturally occuring mineral but exposure to it is not a natural one. we humans are responsible for that)
Low frequency electric,magnetic fields, hyperthermia are also considered to be associated with carcinogenesis.
a)Experiment 1 – G1 cells fused with S cells entered into S – Phase.
b)Experiment 2 – G2 cells fused with S cells did not enter into S – Phase.
Provide a correct explanation for the results observed in the two experiments.
2.Name any three DNA viruses that induce cancers.
Discuss the mechanism of induction of cancers.
3.Why Rb gene is called a tumor suppressor gene? Support your answer.
4.Which chemical carcinogens are involved in the induction of skin cancers? Name the source of these carcinogens.
5.Write short notes on any two of the following :
a)UV – A light and the carcinogenic activity.
b)UV – B light and the carcinogenic activity.
c)UV – C light and the carcinogenic.
6.List the food components that could associated with carcinogenic activity.
List the food components that could give protection against carcinogenic activity of other compounds.
7.Compare the two techniques – Biopsy & Papsmear with reference to technical ease, results obtained, tissues to be screened and risk factors. Are they mutually exclusion techniques?
8.What properties of the tumors are considered in planning radiation dose? Why are radiation doses split over a period of time including the daily dose also being fractionated?
SET : 2
1.Rb along with E2F acts as a molecular switch critically regulating gene expression and cell cycle regulation. Describe the mechanism.
2.How does Ras protein control cell cycle? Majority of C – Ras oncogenes obtained from cancerous tissue have mutations in codon 12, 13, 59 or 61 in the coding sequence. Suggest an explanation.
3.Define familial retinob;astoma.
4.What are xenobiotics? Describe the mecganism involved in metabolism of xenobiotics.
5.Discuss in detail the role of DNA repair enzyme in repairing mutagenic damage induced by carcinogenic agents.
6.The American Cancer Society has listed some very common warning signals as cautions. List these signals. Why is it important to check for these signals? Discuss.
7.On what principles does ultrasonography work?
Cancers in which suspected parts of the body are screened by ultrasonography?
8.Name the major conventional therapies for cancer. Summarize the role of each in cancer treatment.
SET : 3
1.Define and differentiate START and Restriction Point.
What are the factors and mechanisms controlling passage of cells through these points?
2.How does Ras protein control cell cycle? Majority of C – Ras oncogenes obtained from cancerous tissue have mutations in codon 12, 13, 59 or 61 in the coding sequence. Suggest an explanation.
3.Why Rb gene is called a tumor suppressor gene? Support your answer.
4.Discuss the role of deletion and duplication in cancer induction.
Taking a specific example, show the mechanism involved in induction of deletion and duplication.
5.What are sunscreens made of and what potential do they pose in terms of cancer induction? What role does P53 gene play in removing UV induced damage in skin?
6.Write short notes on any two of the following :
a)invasion
b)Intravasion
c)Metastatic colonization.
7.Write short notes on the usefulness of the following in cancer diagnosis :
a.anisography
b.isotope Scan
c.ultrasonography
d.mammogram.
8.Describe the 2 main types of radiation treatments, their source and the conditions that are considered for their implantation.
SET : 4
1.Describe the molecular mechanism of CdK regulation. Suppourt your answer with a diagram.
2.Name any 3 oncogenes which function as receptors and the protein encoded by their protooncogene. Discuss the role of one oncogene in inducing cancer.
3.Name the 2 different types of Retinoblastomas. Discuss the genetic basis for each.
4.Describe Ames Test in detail. Which chemicals are subjected to this test?
5.Name the different units that measure radiation energy.
Describe the rate of release of energy and its biological effects.
6.Cancer development is a multistep process. Discuss a specific example to support this concept.
7.Tumors of which part of the body can be diagnosed by endoscopy? Can any other techniques be used for diagnosis of tumor in these parts of the body? Comment.
8.Name the major conventional therapies for cancer. Summarize the role of each in cancer treatment.
1.Define and differentiate START and Restriction Point.
What are the factors and mechanisms controlling passage of cells through these points?
2.Name one proto oncognene that functions in signal transduction pathway controlling cellular proliferation and its oncogenic protein leading to malignant transformation.
3.Explain why individuals who develop non – hereditary retinoblastoma usually have tumors in only in one eye where as those with hereditary retinoblastoma usually develop tumors in both eyes.
4.Discuss the molecular basis of cancer induction by chemical carcinogens.
5.Write short notes on any two of the following :
a)UV – A light and the carcinogenic activity.
b)UV – B light and the carcinogenic activity.
c)UV – C light and the carcinogenic activity
6.The international comparison of clinical staging is standardized in 1959 under “TNM” system. Explain in detail the method followed in staging the cancer by the TNM method.
7.What are Microarray assays? How useful are they in tumor diagnosis? Comment.
8.What is the main purpose of palliation (surgery) and in what type of cancer is it recommended?
SET : 2
1.Enumerate in detail the pathway by which Ras protein checks cell cycle progression in response to environmental factors.
2.Define transformation of cells.
Define the changes produced when cells in normal tissue culture are transformed by tumor viruses.
3.Describe the function of the normal Rb gene in controlling cell cycle progression.
4.Which chemical carcinogens are involved in the induction of skin cancers? Name the source of these carcinogens.
5.Discuss on every day exposure of human population to radiations from natural and artificial sources and proportions contributed by each. Correlate these exposures with cancers in the present era.
6.What is invasion and describe the mechanism of invasion.
7.What is the main difference between normal Radiographic Imaging and Magnetic Resonance Imaging? Which is superior in diagnosis and why?
8.Provide the importance of discussing the psycho – sociological aspects of the patients as a pre – treatment preparation.
SET : 3
1.Write short notes on any two of the following :
a)TGF-
b)Family of E2F
c)MPF
d)Cyclins.
2.Define transformation of cells.
Define the changes produced when cells in normal tissue culture are transformed by tumor viruses.
3.Describe Rb gene locus and the possible mutations that repress the activity of Rb protein which induces cancer.
4.Which chemical carcinogens are involved in the induction of skin cancers? Name the source of these carcinogens.
5.What are the 3 types of UV light? Describe in detail the specific mutagenic actions produced by each and mention their carcinogenic potentials.
6.Summarize the steps involved in metastasis.
7.What is aspiration biopsy? Describe in the technique, its usefulness and the risk involved.
8.Write short notes on the following :
a)Hypoxic cells
b)Radiation effect on cell
c)Cell repair
d)Repopulation following radiation treatment
SET : 4
1.Enumerate in detail the pathway by which Ras protein checks cell cycle progression in response to environmental factors.
2.Define transformation of cells.
Define the changes produced when cells in normal tissue culture are transformed by tumor viruses.
3.What type of mutation causes proto oncogenes to convert them to oncogenes? Give one specific example.
4.Discuss the different sources of carcinogens that enter our environment and the proportion contributed by each of these sources towards the development of human cancers.
5.Write short notes on any two of the following :
a)UV – A light and the carcinogenic activity.
b)UV – B light and the carcinogenic activity.
c)UV – C light and the carcinogenic.
6.Environmental factors including diet play a very important role in developing cancer. Distinguish the dietary factors associated with carcinogens showing the association of food with a specific cancer.
7.What is the main difference between normal Radiographic Imaging and Magnetic Resonance Imaging? Which is superior in diagnosis and why?
8.Provide the importance of discussing the psycho – sociological aspects of the patients as a pre – treatment preparation.
1.Describe the phase of cell cycle and the events that 0ccur in each. Name the important phases that check cell cycle progression.
2.Write short notes on any two of the following viruses as causative agents for human cancer :
a)Hepatitis B virus
b)SV 40
c)Adenovirus
d)Papilloma virus.
3.P53 is designated as the guardian of the genome. Support the concept.
4.Discuss the role of different environmental substances as causative agents of cancers providing some specific examples.
5.What are ionizing radiations and what type of damages could they produce in the DNA molecule? Discuss in detail.Correlate DNA damage with carcinogenesis.
6.The international comparison of clinical staging is standardized in 1959 under “TNM” system. Explain in detail the method followed in staging the cancer by the TNM method.
7.What is the main difference between normal Radiographic Imaging and Magnetic Resonance Imaging? Which is superior in diagnosis and why?
8.What are alkylating drugs? What is their basic mechanism of action to suppress or kill cancer cells? Name some of the most commonly used drugs of this category mentioning their specificity against selected cancers.
SET : 2
1.Describe the phases of cell cycle and the events that occur in each. Name the important phases that check cell cycle progression.
2.Mutation in proto oncogenes that change them to oncogenes are dominant. Provide a correct explanation with suitable examples.
3.Describe the function of the normal Rb gene in controlling cell cycle progression.
4.Describe the tests commonly used in screening chemicals for their carcinogenic potentials.
5.Briefly discuss the different agents that could be possible carcinogens.
Mention the source of these agents that enter human environment.
In general, what biological effects can these agents cause?
6.The American Cancer Society has listed some very common warning signals as cautions. List these signals. Why is it important to check for these signals? Discuss.
7.Enumerate the different biopsy techniques with reference to their specific usefulness.
8.What is the basis of gene therapy in cancer treatment? It is expected to be more potent and specific against specific cancers – discuss this in the light of available information and trail phases of the treatment.
SET : 3
1.Describe the phases of cell cycle and the events that occur in each. Name the important phases that check cell cycle progression.
2.Name any three different types of proteins that control growth in mammalian cells.
Describe oncogenes resulting from mutations in these protein coding genes. Name the tumors they induce.
3.Which gene involvement is indicated in patient with breast and ovarian carcinomas?
Discuss in detail the mechanism controlling the induction of these cancers.
4.Name a few base analogues and the mechanism of action of mutagenesis.
5.Name the different units that measure radiation energy.
Describe the rate of release of energy and its biological effects.
6.The American Cancer Society has listed some very common warning signals as cautions. List these signals. Why is it important to check for these signals? Discuss.
7.Name the tests useful in early detection & staging of cancer. Briefly describe them.
8.Describe the different types of radiations and their sources that are used in radiotherapy for the treatment of cancers. Also describe the radiation units that measure the dose.
SET : 4
1.Enumerate in detail the pathway by which Ras protein checks cell cycle progression in response to environmental factors.
2.Write short notes on any 2 of the following oncogenes :
a)erb A
b)erb B
c)H – ras
d)Src
3.Discuss the relationship between BCL – 2 & P53 genes and how does mutation in either of them effect the normal cellular process.
4.Discuss the role of different environmental substances as causative agents of cancers providing some specific examples.
5.Briefly discuss the different agents that could be possible carcinogens.
Mention the source of these agents that enter human environment.
In general, what biological effects can these agents cause?
6.The American Cancer Society has listed some very common warning signals as cautions. List these signals. Why is it important to check for these signals? Discuss.
7.What is aspiration biopsy? Describe the techniques, its usefulness and the risk involved.
8.Cyclophosphamide (Endoxan) is the most commonly used drug, the drug of choice.
Support your answer by giving its special activity and its broad spectrum usage.
