question

what is cancer

answer

Cancer is a multistage disease which is invovle accumulation of mutiple DNA mutation

question

How does the DNA demage alter cell normal regulation which cause cancer

answer

1. Alter the cell prolifertion 2.differentiastion paterns. 3. The tissue from the cell loose orgainzation then eventually travel

question

What are the Exogenous genotoxic carcinogens that can cause cancer when exposure.

answer

1. Radition 2. Chemicals 3. Tobaco smoke 4.viruses 5. aflatoxin and other food-derived carcinogens 6.detoxfication and repair system failure

question

What are the things that happen to the DNA of the cell which cause cancer

answer

1. Mutiple DNA mutation

question

What occur when proto onco or tumor suppressor gene are mutated and why that occur

answer

1. Uncontrollable growth, cell prolifilation, transformation 2. excape Apoptosis 3. This occur because they are not responding to ligand that tell it when to turn on and off or sometime death signal

question

What is the charateristic of cancer cell

answer

1. Proliferation without a stimulus 2. Ignore growth restriction signal 3. Ignore stimulus for apoptosis 4. They modify cell-cell and matrix interaction 5. abnormal shape 6. abnormal ploidy or number of chromasom 7. promote angiogensis 8. Invade surrounding tissues and metastasize

question

What factors that may cause cancer

answer

1. stimulus or exposure, Carcinogens, Hormones, Viruses 2.These cause genetic DNA demage of the cell 3. excessive growth and proliferation 4. Transformation

question

Are All tumors are cancer and what are they

answer

1. No 2. Benign tumor and Maligannt tumor

question

What is a Benign tumor and how are the cells differ from Malignant tumor cell and how are they samilar or differ from normal cell

answer

1. it a mass of cells that have a phenotype and differentiated state which is very close to normal cells 2. low proliferation rate and dont metastasize 3.They have cell-adhesion molecule that hold the tumor cells together..

question

What example of Benign tumor

answer

birthmarks, warts, mole

question

What is Malignant tumor and how are they Malignant and how are they samilar or differ from normal cell

answer

1. it a mass of cells that dont have a phenotype like normal cell 2. They prolifarate quickly and fail to die 4. They metastasize

question

What example of Malignant tumor

answer

1. A mast of cancer cells

question

How does a tumor cell become matastasize once become malignant

answer

1. The secrete protease that degrade the basal lamina

question

What is the multiple hit model of cancer

answer

This just stating that cancer is a result of mutiple mutation of a cell.

question

What is the multiple hit model of cancer mechanisim

answer

1. Cell is mutated this allow it to proliferate 2. 2nd mutation the cell avade apoptosis 3. 3rd mutation cell the cell profilarate uncontrolibly and creating protease 4. protease is secreated then you have invasion

question

What are the type of cancers

answer

1.carcinoma 2. sarcoma 3. Leukemia 4. Lymphoma 5.blastomas

question

Where is carcinoma derived from and where can you find it

answer

1.They are derived from epithelial cells both endoderm and ectoderm 2 They are Colon, breast , pancreas, lung, bladder, prostate

question

Where does Adenocarcinoma derived from

answer

1. Secreting epithelium

question

Where does Teratocarcinoma from

answer

1. Embryonic tissue

question

Where does sarcoma derived from and what are they

answer

1. mesoderm example muscle, blood, and connective tissue 2. Osteosarcoma, rhabdomyosarcoma, leiomyosarcoma

question

Where does leukemia derived and what does mean it from Myelogenic or Lymphocytic

answer

1. White blood cells in the bone marrow 2. Myelogenic means it is from a myelocyets cell (neutrophils esoinophils and basophils) 3. Lymphocytic this means it is from a precursor of a lymphocytes(T vs B)

question

Where does Lymphoma derived from and what are they

answer

1.They are derived from lymphocytes and plasma cell in the lymph nodes 2. Hodgkin disease, myeloma

question

What are Blastomas and what are they

answer

1. Cancer cells that have lost their differentiation characteristic 2. Nephroblastoma, and retinoblastoma

question

What are the step of Carcinoma how much of the epithelium is being invade by the cancer cells

answer

1.Normal epithelium The epithelium and the connective tisue is normal. 2. Low-grade intraepithelial noeplasia this is when the cancer cell is form and starting to invade the some of the epithelium tiussue 3. high-grade Intraepithelial Neoplasia This is when the cancer cells divide and invade all the epithelial tissue. 4. Invasive carcinoma the cell are invading all the eptithelial and the connective tissue

question

What is the 6 Important things that make the hallmark of cancer

answer

1. Self-sufficency in growth signal 2. Insensitivity to anti-growth signals 3. limitless replication signal 4. Tissue invasion and metassis 5.sustain angiogenis 6. Evading apoptosis

question

What are the three steps tumors must follow to progress

answer

1. Iniatiation 2. promotion 3. progression

question

What is a tumor microenviroment and why is it important?

answer

1. This is the cell to cell interaction between cancer cells and their neighbor stroma cell, inflammatory cell, and the basal lamina 2. These interaction is important in driving tumor cell proliferation and tissue invasion and metastasis.

question

What are 8 ways to inhibit tumors

answer

1. EGF inhibitors 2.cyclin dependent kinase inhibitors 3. Immune activating anti-CTLA4 mAb 4. Telomerase inhibitors 5. Selective intiflamatory drugs 6 inhibitors of HGF/c-met 7. inhibitors of VEGF 8. PARPS inhibitors 9.Proapoptotic BH3 mimic 10. Areobic glycolysis inhibitor

question

Why EGF inhibitor are bad for cancer cell

answer

1. it help them sustain proliferate signal

question

Why cyclin dependent kinase inhibitors are bad for cancer cell

answer

1. Cancer cell need CDK for growth

question

Why Immune activating anti-CTLA4 mAb is bad for cancer cells

answer

1. it use to target cancer cells by the immune system CTLA4 mAb

question

Why Telomerase inhibitors is bad for cancer cell

answer

1. Cancer cell use Telomerase to enable replicative immortality or avoid death

question

Why Selective int-inflammatory drugs is bad for cancer cell

answer

1. Tumor cells used Imflammation to grow

question

Why inhibitors of HGF/c-met is bad for cancer cell

answer

1. Cancer cell use it to activate metastasis and invasion

question

Why inhibitors of VEGF is bad for can cancer cell

answer

1. Cancer cell use it to induce angiogenis by targeting endothelia cells

question

Why PARPS inhibitors is important in preventing cancer cell

answer

PARPS inhibit DNA demage repair in tumor cell

question

Why Proapoptotic BH3 mimic is bad for can cancer cell

answer

1. Because tumor cell ignore regular apoptotic signal

question

Why Areobic glycolysis inhibitor is bad for cancer cells

answer

1. This important because cancer cell deregulate cellular energies.

question

What are ECM proteins and cells

answer

1. Laminin 2. type 4 collagen 3. perlecan 4. hyluronan 5.decorin 6. fibronectin 7.fibrillar collagen 8. nidogen 10. aggrecan 11. mast cell and macrophage

question

what is the mechanism of angiogensis

answer

1. the tumor cell growth to it limit size 2nm 2. The middle of the tumor is experincing hypoxia because of lack ot O2 3. hypoxia stimulate hypoxia inducible factor-1(HIF-1) 4.(HIF-1) activate VEGF 5. VEGF act on the endothelial cells that create blood vessels 6. This cause the endothelia cells to budd out and sprout 7. New blood vessel are form

question

Why is it important for tumor to activate angiogenesis

answer

1. To provide more O2 for growth 2. This also open path way for the tumor cell to metastasis

question

What are the tumor growth factors that promote angiogenesis

answer

1. bFGF(basic Fibroblast Growth Factor) 2. TGF alpha (Transforming Growth Factor) 3.VEGF(Vascular Edothelial Growth Factor)

question

Why is (HIF-1)Hypoxia Inducible Factor-1 important beside causing angiogenesis

answer

1. HIF-1 stimulate glucose anaerobic metabolism 2. This is important because it increase the chance of survival in a hypoxic enviroment or low O2

question

How does the tumor cells break through the basal Lamina and how they navigate once that occur

answer

1.tumor cell produce protease that degrade the basal lamina supporting tissue 2.ECM molecules

question

1. What are the steps for a tumor cell to metastasis

answer

1. tumor cell produce protease that degrade the basal lamina supporting tissue 2. The tumor cells will penetrate the vessel wall by producing proteases. 3. Matrix metalloproteases dissociate the ECM of small arteries. 4. Now they are in the blood stream 5. once the tumor cell travel in the blood stream to a specific location 6. the cancer cell adhere to the endothelium of a capillary and cross tissue

question

Why is the LIver or the bone marrow are usual site of metastasis

answer

1. Because they have very rich vascularization. 2

question

Due to the multiple steps what is the chance a tumor cell will metastasize

answer

1/10000

question

What cytokeleton element tumor cell use to migrate

answer

Actin cytoskeleton

question

Why is the Microenvironment important

answer

1. This is important for signalling tumor growth and progression

question

How does carcinoma cell degrade the basment membrane

answer

1. They used invadopodia

question

How does carcinoma cell promote tumor inflmmation

answer

1. They prouduce CSF-1 or ILB1B which then stimulate tumor promoting inflamammatory cells. 2.Tumor promoting inflammatory cells will then secrete EGF wich will act on the cell

question

What is the function of upa ligand and it associate receptor

answer

1. When uPa bind to it receptor it will activate the cell to make protease

question

What is the Multi-Hit mutation model

answer

1. Is the the stipulate that cancer cell originate from several successive genetic mutations.

question

in the Multi-Hit mutation model what doe the first mutation does to the first cancer cells

answer

1. Give growth advantage create 2. it create a close or progeny

question

In the Multi-Hit mutation model what does a second mutation to clone that from the parent with the first mutation does?

answer

1. Resistance to apoptosis 2. grow faster from the 2. A become a begign tumor

question

n the Multi-Hit mutation model what does a third mutation does.

answer

1. the tumor growth accelerate further 2. production of proteases 3. penetration of adjacen tissue

question

n the Multi-Hit mutation model what does the fourth mutation does to the cell.

answer

1. allow further protease production 2. Metastasis

question

Give example of cancer that follow the Multi-Hit mutation model of cancer

answer

1. A mole become a melanoma 2. A polyp can become adenocarcinoma in the colon

question

what are the step in colorctal carcinoma and what are the name of the stages

answer

1. You have a normal cell 2. mutation loss of APC is called hyperplastic epithelium *Early adenoma* 4.Mutation that cause activation of K-ras * intermediate adenoma* 6. Mutation that cause loss or smad 4 and other tumor suprresors. * late adenoma* 8. Mutation that cause the loss of the activity of p53 *carcinoma*

question

What are the 1st three experimental that support Muti-Hit Model of cancer.

answer

1. patern of of epigenetic. All the cell in women tumor have inactivated x chromosome this suport clonality. 2. Aging. Cancer incidence increase with age this becuase it take time to acumulate mutations 3. Cumulative mutation. people that drink alcohol or people that smoke risk of esophagus cancer is increase sligtly however those that do both increase tremendously.

question

What is the second experimental that support Muti-Hit Model of cancer.

answer

1. mutation that cause both the protooncogene myc and Ras into oncogen together wich will cause over expression of both will atomatically lead to transformation

question

What does the over expression of the oncogene Myc and Ras cause

answer

Automatic lead into transformation

question

What are two thing pro-oncogene myc promote

answer

1. Proliferation or apoptosis

question

What does pro-oncogene Ras due

answer

1. Absence of death and senescence by inhibiting one of the cell cycle proteins

question

What are two method to find the progression of intestinal cancer

answer

1. endoscopies 2. Bioscopies

question

What does of the tumor suprressor APC in the intestine due

answer

1. Inhibit cell proliferation

question

What does the activation of mutated RAS due in the colon

answer

1. This allow the cell to grow forming polyps 2. this result adenoma a benign tumor

question

What does the loss of the two tumor suppressor DCC and P53 does

answer

1. This cause uncontrollable proliferation 2. Results malignant carinoma

question

What is Myc mechanism to inactivated Rb

answer

1. Myc sit on the DNA net to Cyclin D regulatory protein 2. Cyclin D increase 3. Cyclin D bind to G1-CDK creating Cyclin D-Cdk4 4. Cyclin D-Cdk4 phosporylate Rb and inactivate it. 5. This increase trancrition of E2F cell enter S phase

question

What is Myc mechanism to activate SCF subunit gene

answer

1. Myc sit on the DNA next to SCF subunit gene 2. this cause phosphorylation and degradation of P27 G1 S-CDK inhibtor. 3. G1/S-Cdk is activated and bound to cyclin E creating cyclin E-CDK2 4. More phosphorylation of Rb protein 5. This increase trancrition of E2F cell enter S phase

question

What is Myc mechanism to activate E2f gene

answer

1. 1. Myc sit on the DNA next toE2F subunit gene 2. This increase trancrition of E2F cell enter S phase

question

What are the mechanism of cancer in colon and stage

answer

1. Loss of APC tumor supress gene on chromosome 5 *** small growth call polyp forms in the colon wall*** Benign tumor 2.Activation of K ras on chromosome 12 **class two Adenoma*** Chromosome grows. 3. Lost of tumor repressor DCC on chromosome 18 *class 3 Adenoma*** benign grows. 4. Loss of tumor surpressor P53 on chromosome 17 ***maligment carcinoma***

question

What are three categories of genes once mutated cancer can start.

answer

1. Proto-oncogenes 2. Tumor suppressors 3. Caretaker genes..

question

What those three catogories of gene control for them to cause cancer

answer

1. Growth 2. Cell proliferation

question

What are example of the three catogories of genes and what they promote

answer

1. Ras, Myc, rb, AKT, Rb.(Proto-oncogenes) 2. TGF beta, P53, APC, Tumor suppressors 3. P53 Caretaker genes

question

what happen when Ras and Myc turn on together.

answer

1. Transformation

question

Between Ras and Myc which one more affectively would create a tumor

answer

Ras

question

What is transformation

answer

1. This is a alteration of a cell genome that cause change in the type in it protein express.

question

What are oncogene

answer

1. It a mutated (proto oncogne) gene that normally promote the activation of the cell cycle, this lead to production of a protein that is hyper-active (onco protein)

question

What do they call the oncogen hyper-active protein

answer

onco-protein

question

What is called for mutation that occur to proto oncogene

answer

1. gain-of-function

question

What are ways proto oncogene become oncogene

answer

1. deletion or point mutation in coding sequnce which cause hyperactive. 2. Gene aplification this cause normal protein to be greatly over produce 3. chromosome rearragenement this cause nearby regulatory DNA seqeunces cause normal protein to be over produce 3. Fusion to actively transcribed gene produce hyperactive fusion protein

question

how does pro-oncogene point mutation occur give example of one gene

answer

1. A single aminoacid substitution makes the protein hyper-active. 2. Ras

question

how does pro-oncogene chromosomal trans location with a new promoter control mechanism cause cancer and example

answer

1. The new coding sequence of the proto oncogene becomes under the control of a very active promoter. 2. Myc become under control of the Ig promoter creating lymphomia. IG is a very active promoter

question

how does pro-oncogene mutation that cause chromosomal trans location with fusion mechanism cause cancer

answer

1. Two fused gene creatate a hybrid, and abnormal oncoprotein 2.example bcr-abl

question

How does amplification of proto-oncogene translation occur

answer

1. This cause by increase of the copy of a DNA of the gene

question

Which of the two mechanism that produce oncogene create a new protein

answer

1. Point mutation 2. Chromosomal translocation with fusion

question

Which of the two mechanism that produce oncogene that do not create a new protein however the prot-oncogene is produce excessive amount and why

answer

1. Chromosomal translocation with a new promoter 2. Amplification of proto-oncogene

question

What does the proto onco gene Myc cause in the cell cycle

answer

G1-S phase prograsion

question

Why does IG promoter is bad if it take ove control of Myc

answer

IG is a active promoter

question

How does the Mitogen receptor is affected to over produce Myc protein and give the short mechanism

answer

1. The receptor become mutated so it is activated without a mitogen binding. 2. this active MAP kinase in the cytosol 3. Active Myc in the cytosol 4. Myc go to the nucleus and active it protein

question

What other things that can cause tumor and cancer

answer

Viruses

question

What type of virus that can cause cancer

answer

1. Retrovirus

question

how does Retrovirus work which can cause cancer

answer

1. Their RNA genome are reversed transcribe into DNA then is it is inserted into the host genome or eukaryotic genome

question

how does Retrovirus DNA insertion might cause a oncogne.

answer

1. When the virus proliferates it incooprates a proto-oncogene on the host genmone and further mutation of this proto oncogene lead to oncogene

question

how does Retrovirus DNA insertion might cause a oncogne.

answer

1. The virus genome is inserted close to the site of the host proto-oncogene which cause a over expression.

question

What is the only Retrovirus that cause human tumors

answer

1. The human Tcell leukemia/lymphomia virus (HTLV)

question

What viruse that can do extreme demage to a tissue which can increase the risk of getting cancer.

answer

Hepatitis B,C

question

What other viruses that also can include oncogene and incoporated in host DNA beside Retrovirus and what it cause

answer

1. DNA viruses 2. This will lead to permanent transformation of the cell which lead to a benigh tumor further mutation cancer

question

What is a example of a DNA viruses and what it can do

answer

1. Human papillomavirus 2. It can induce papillomas or benigh warts which can degenerate into cervical cancer

question

What are example of DNA virus

answer

1. Papovavirus family cause warts, and uterine cervix carcinoma 2. Hepdadmavirus family (hepatitis b and C) liver cancer and hepatocellular carcinoma 3. Hepesviruse family(epstein-barr) virus family they can cause bukitt lyphoma cancer of lyphocyte and nasopharyngeal carcinoma

question

Retrovirus family

answer

1.Human T-cell leukemia virus cause adult T-cell leukemia lymphoma 2. Hiv this cause Kaposi sarcoma

question

Where do you find the DNA viurs Papovavirus

answer

Worldwide

question

Where do you find the DNA viurs Hepdadmavirus family (hepatitis b and C)

answer

1. B south east Asia, and tropical africa 2. C Worldwide

question

Where do you find the DNA Hepes viruse family (epstein-barr)

answer

1. west africa Papua ne guinea 2. southern china, greenland

question

where do you find Retrovirus HTLV-1 found

answer

1. Japan, West Indies 2. central and souther africa

question

What is the check point between G1 and S phase call

answer

1. R check point

question

Why are the cell cycle check point are important

answer

1. it control the timing and monitor DNA synthesis accuracy, and ensure the correct chromosome segragation

question

1. What are three things that can active p53

answer

1. Hyperproliferation signal 2. DNA demage 3. Telomere shortening 4. hypoxia

question

What the are three action which can happen if p 53 is activated

answer

1. Cell cycle arrest 2. enescene 3. Apoptosis

question

how does p53 suppresses cell division

answer

1. it does that by turning on the CDK inhibitor P21

question

What is the mechanism of turning on the CDK inhibitor P21 to inactivate G1/S-Cdk

answer

...

question

What is is predisposition of cancer

answer

1. The liability or the susceptibility or the likely to catch cancer.

question

what is inherited predisposition

answer

1. This is the likely hood of offspring catching cancer because it inherited a mutated allele.

question

What happen to a offspring inherited one mutated allele and why

answer

1. The offspring have a higher probability to catch cancer 2. If a single mutation occur to the second allele will be enough to cause transformation

question

What is called when a single allele is mutated which can induce cancer

answer

1. lost of heterozygosty

question

What are the gene that is know to have lost of heterozygosty mutation

answer

1. Rb+/+ 2. APC+/+ 3.BRAC+/+

question

What happen when Rb+/+ have a single mutation Rb+/-

answer

1. Mutation into Rb+/- will predispose or increase the likely hood to catch retinoblastoma 2. Rb+/+ block G1 phase

question

What happen when APC+/+ have a single mutation APC+/-

answer

1. Mutation into APC+/- will predispose or increase the likely hood to catch colon cancer 2. APC control cell cycle progression

question

What happen when BRAC+/+ have a single mutation BRAC+/-

answer

1. Mutation into BRAC+/- will predispose or increase the likely hood to catch breast cancer

question

What is hereditary retinoblastoma

answer

1. one somatic retinal cell that is carring one mutated rb allele Rb+/- then a somatic mutation occur then it become homozygous Rb-/- for the mutation and gives rise to tumor of the retina

question

What is sporadic retinoblastoma

answer

1. Both of the somatic retinal cell Rb is normal Rb+/+ one somatic mutation occur making it heterozygous for that mutation. A second mutation occur making it homozygous which give rise to tumor in the retina

question

What can cause heterozygosity mutation

answer

1. Nundisjuction. Mis-segragation of the chromosomes durring mitosis 2. Recombination error. Recombination between mutated allele and normal ones 3. Chromosome deletion including normal allele

question

What are 4 example of oncogenic mutation

answer

1. Oncogenic receptor 2 Consecutively active signal transducer 3. Growth inhibiting signaling pathways 4. Cell cycle controls

question

How are mutated receptor become oncogenic and able to dimerize without a ligand and example

answer

1. This occur by a change of the base pair which create glutamine instead of valine this allow the receptor to dimerize without a ligand. 2. EGF receptor-2 or (Her-2) mutated to Neu oncoprotein in breast cancer

question

How are mutated receptor become oncogenic which can lead it to be consecutively active and example

answer

1. The ligand binding domain is deleted leading the receptor to be consecutively active 2. EGF receptor converting into ErbB

question

How are normal receptor become cancerous and example

answer

1. A mutation that cause over-production of a normal receptor making the cell hyper-sensitive to a ligand. 2. EGF recptor-2 (Her-2) being over express in breast cancer.

question

What is some cause of a abnormal receptor and example

answer

1. Chromosomal translocation 2. Trk receptor in colon carcinoma

question

What is the name of Her-2 or a EGF receptor that is mutated by the deletion of a base pair which cause it to dimerize

answer

1. Neu oncoprotein

question

What is a EGF receptor that have a deleted ligand binding domain called.

answer

1. ErbB oncoprotein

question

Where are most oncogene are derived from and example

answer

1. They are derive from protein involved in transduction of signaling pathway promoting growth and proliferation. 2. Ras, and C-abI

question

What is Ras and how is it active

answer

1. Ras is a small GTPase 2. active when GTP bound inactive when GDP bound

question

What is a short mechanism of the Ras path way

answer

1. Ligand bind to the RTK 2. The activated RTK induce shift GDP to GTP in RAS 3. Ras is activated. 4. The Activated Ras activate MAP kinase 5. MAP kinase stimulate transcription of involved in growth and cell cycle and proliferation

question

how the activity of Ras can become cancerous

answer

1. Any muation of glycine a the position 12 slow down GTPase activity of Ras 2. This lead it to be consecutively active. 3. cancer bladder, colon, breast, lung, skin, leukemia

question

What is the Bcr-AbI

answer

1. It is the translocatin of the c-abi and Bcr chromosome causin the fusion of the genes creating a chimeric onco protein

question

what is the function of c-abi

answer

1. it encode tyrosine kinase that control cell shape and movement through polymerization of the actin filament

question

what is the function of Bcr

answer

1. Unknown

question

What happen when Bcr and c-abi fuse to create a chimeric on co protein Bcr-AbI

answer

1. They form a tetramer which continuous activate abI activities. 2. This cause phosphorylation which activate substrates that are not normally phosphorylated by c-abI 3. Example Jak/stat patway of cell growth

question

How to detect Bcr and c-abi fusion and translocate to create a chimeric onco protein Bcr-abl what is it called

answer

1. The present of the philadelphia Chromosome one the karyotype

question

What happen when Bcr and c-abi translocation occur in hematopoietic cells (bone marrow)

answer

1. excessive but slow proliferation of white blood cell 2. this called Acute myelogenous leukemia

question

What is myelogenous leukemia

answer

1. It is a excessive but slow proliferation of white blood cell which cause by Bcr and c-abi translocation in hematopoietic cells (bone marrow)

question

What is the breaking point

answer

This on the gene where the trans location take place

question

What is the mechanism of creating Bcr-AbI

answer

1. Mutation 2. This cause ABL and BCR chromosome to trans locate with each other at the breaking point 3. This allow the gene to fuse 3. This create the philadelphia chromosome 4. The transcription of the gene 5. This fuse the mRNA Bcr/Abl 6. This create Bcr-Abl fusion protein

question

What drug that blocks the activity of Bcr-Abl protein

answer

1. (Imatinib)GLEEVEC BLOCKS

question

What is the mechanism of Bcr-Abl activating cell proliferation and survival and eventually into leukemia.

answer

1. ATP bind to Bcr-Abl kinase binding domain and activated it 2. Bcr-Abl phosphorylate it substrate protein 3. It substrate protein activate cell signal for proliferation and survival and eventually into leukemia.

question

How does GLEEVEC block Bcr-Abl activity

answer

1. It bind to it ATP binding site or it kinase domain inhibiting it from phosphorylation Bcr-Abl

question

Why is Bcr-Abl fusion protein are easy to targeted with specific inhibitors

answer

1. it create a new protein

question

What is kind of cancer (Imatinib)Gleevec treat

answer

1. Chronic myelogenous leukemia with the philadelphia chromosome

question

Why do cancer cell resist (Imatinib)Gleevec

answer

1. Due to cancer cell genetic instability they can develope additional mutations that can make them resistance to gleevec

question

What path ways mutation can affect

answer

1. Growth-promotin patways 2. Growth inhibiting pathways

question

What pathway which can be affected by mutation which can be cancerous

answer

1. Transforming growth factor-beta(TGFBeta)

question

What is the function of Transforming growth factor-beta(TGFBeta)

answer

1. Inhibtor of cell growth in epithelia in immune system 2. Promote Apoptosis

question

What is a short mechanism of Transforming growth factor-beta(TGFBeta) pathway

answer

1. Transforming growth factor-beta(TGFBeta) ligand bind to one receptor. 2. This cause another receptor to come and dimerisze with the first receptor. 3. The first receptor will phospholate the second receceptor at it serine/threonin kinase domain. 4 This will recruit Smad3 and smad3 will bind to the receptor that been phosphorylated 5. The phosphorylated TGFBeta receptor will phosphorylated smad3. 6. Smad3 will desociate from the receptor and oligeomerize with smad 4 and go in the nucleus to activate the expression of many genes

question

What gene and function does Smad activate by the activation of from the activation of TGFBeta receptors

answer

1. p15 this inhibit the cell cylce 2.PAI This inhibitor of proteiase, thereby inhinbiting ECM degradation.

question

What does the mutation of TGFBeta cause

answer

1. this cause the incresed of proliferation by blocking P15 2. Increase the risk of metastasis by blocking PAI

question

what is the cell cycle

answer

1. growth factors G1 2. CDK4,6 activated and bind to cyclin D G2 3. CDK2 bind to cyclin E S 4. CDK2 bind to cyclin A G2 5.Cdk1 bind to cyclin A M 6. CDk1 bind to cyclin B

question

what is CIP/KIP

answer

????

question

What aid progression through the cell cycle

answer

Cyclin

question

What is the most important inhibitory of the cell cycle which CDKs have to phophorylate from G1 to S phase

answer

rb

question

What is the most comon cause of cancer

answer

1. Mutation that cause over production of cyclin 2. loss rb or p15/16 fucntions 3. these cause excessive proliferation

question

What does p16 does

answer

1. it bind to Cyclin D and CDK4 complex inhibiting it from phosphorylating Rb

question

What are Carcinogens

answer

1. They are natural or sythetic chemical that cause cancer by DNA mutation

question

What are tow class of carcinogen that can form mutation

answer

1. Direct carcinogens. they directly react with the N & O atom on the DNA 2. Indirect carcinogens. Non polar chemicals which can become reactive after they are modified by cellular enzyme example cytochrome p450 adding OH groups the non polar chemical to make them more soluble for excretion

question

What are non chemical mutagens

answer

1. Non chemical mutagen Radiation..UV creating melanoma and X-ray creating leukemia

question

What half of cancer cells have

answer

1. Inactivate p53

question

What activate and function of p53

answer

1. P53 activated by DNA demage 2. G1&G2 arrest , DNA repair, if all this fail Apoptosis

question

What are know carcinogen that cause cancer by binding to DNA base

answer

1. Afltoxin 2. vinyl chloride and benzene, asbestos

question

What is the mechanism of tumor growth

answer

1. Initiation exposure to carinogen one cell become mutated but it growth are restrain 2. Promotion mutated cell proliferate and further mutation occur

question

What are two point you must have to have tumor growth

answer

1. Initiation 2. Promotion

question

What is one compound if not dextoxifide by in enzyme propely it will bind to DNA and become a carcinogen

answer

Benzo pyrne

question

What cooking method can cause colon cancer

answer

Over coking meat

question

What take care of carcinogen mutation or repair and prevent DNA demage

answer

1. Care taker genes

question

How many DNA demage can a normal cell response to in the daily basis

answer

1. 20,000

question

What does the defect of the DNA repair system cause

answer

1. herediatary cancer predisition. 2. risk of cancer is much higher 3. Tumor progression is faster

question

What cancer is form when there is a genetic demage to the incision repair machinery

answer

1. Xeroderma pigmentosum(XP) 2. patient are highly sensitive to UV light

question

What cancer is form where there is a genetic demage to the mismatch-repair system

answer

1. Hereditary nonpolyposis colorectal cancer(HNPCC) 2. This cause rapid progressive of polyp into colon cancer.

question

Where does PAI bind to prevent protease activation

answer

1. UPA

question

What are three genes genetic demage occur on to cause cancer

answer

1.Proto Oncogenes 2.Tumor suppressor gene 3.Care Taker genes

question

What is the function of Proto Oncogenes and what is ti call when mutated

answer

1. They regulate cell growth 2 oncogene

question

What happen when a Proto oncogne is mutated and what the name of the mutation

answer

1. This create excessive activity of them 2. Gain function mutation

question

What example of Proto onco gnes

answer

1. AKT 2. Ras 3. EGF receptor

question

What is the function of a Tumor Supress or gene

answer

1. They suppress growth and proliferation

question

What happen when a Tumor supressor genes is mutated and what the name of the mutation

answer

1. They are inactive so cell can growth and proliferation any time 2. Loss of function mutation

question

What example of Tumor supressor genes

answer

1. PTEN 2. TGFB 3.P53

question

What is the function of the Care take gene

answer

1.Protect the integrity of the genome from DNA demage

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What happen when a Care Taker genes is mutated and what the name of the mutation

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1. The risk of mutation and tumor drastically increase

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What does Carcinogens do

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1. They increase the risk of mutations in the three gene categories.

question

What must be done once a tumor cells is in the blood stream.

answer

1. It must Adhere to the endothelium of the capillary and cross into specific tissue.

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