I'm Aware of Cancer Team Work

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PHYSICAL STUDENTS ACTIVITY AND Gökdeniz.AKDAGMTAL, ZEHRA ZUMTAL, CEREN ONMTAL, ÖYKÜ CANCER Demet AKSOY ONMTAL, İlayda NBS, ENES Nurullah AKBULUT AKDAGMTAL, RAVZA Ayşe USLU İBNİSİNA, FATİH.OFL, Teachers SELENAY.OFL CCAHNECMEI RCAALNSD EGE.OFL Altun KARABATAK, Mehmet Harun TOPAY Selahattin.AKDAGMTAL, and Tuba ÖZALP BURÇİN ZUMTAL, Melisa NBS, Teachers SEVDA ONMTAL, KEREM AKDAGMTAL, MELİKE İBNİSİNA, AYŞENUR.OFL, BAHADIR.OFL, ARDA.OFL Nazlı.AKDAGMTAL, MELİHA ZUMTAL, ROJİN ONMTAL, İrem NBS, YAMAN AKDAGMTAL, İREM İBNİSİNA, ASUDE.OFL, RAHİME.OFL CANCER AND ALEYNA ZUMTAL, NUTRITION Emre.AKDAGMTAL, Gordana Jordeva, BAHAR ONMTAL ,SELİN Valentina Bogojovska ONMTAL, Hatice NBS, Teachers and Nesrin Reyyan NBS, EREN ALTINKARGI Teachers AKDAGMTAL, ARDA İBNİSİNA, FATİHCAN.OFL, HATİCE.OFL, MUHAMMED.OFL

Cancer Awar Cancer an Ülkü Kıvanç Oltu Nenehatun MTAL

reness Handbook nd Genetics Yusuf Kartal Oltu Fen Lisesi

STUD ENTS CEREN ONMTAL ÖYKÜ ONMTAL FATİH.OFL SELENAY.OFL EGE.OFL Gökdeniz.AKDAGMTAL ZEHRA ZUMTAL İlayda NBS ENES AKDAGMTAL RAVZA İBNİSİNA



WHAT IS All organs in our body are made up of cells. Hea have the ability to divide. They use these abilit tissues (inside and outside the body). They are n it will divide where and as much as necessa consciousness, begin to divide uncontrollably a tumors (masses), tumors can compress, infiltrate the tumor where they formed, they can travel to circulation. They form tumor colonies where cancer to other parts of the body Battle of cancer cells (pink

CANCER? althy body cells (except muscle and nerve cells) ties to regenerate dead cells and repair injured not infinitely divisible. A healthy cell knows that ry. On the other hand, cancer cells lose this and multiply. Cancer cells accumulate and form e or destroy normal tissues. If cancer cells leave o other parts of the body via the blood or lymph they go and continue to grow. The spread of y in this way is called metastasis. ), lymphocytes (yellow).

Cancer cells have many features that normal ce have.  Receptors on the cell surface receive signal frequently  They have their own signaling system that e uncontrolled reproduction  It does not stop dividing after contact wit adjacent cell and continues to grow and mu  While healthy cells can use all types of nut cancer cells can only use glucose from glycolys take sugar from the blood about 100 times mo normal cells and provide energy by producing (Warburg effect).  They can form new vascular systems by influe stroma around them to receive the necessary n and oxygen. They can replicate and multiply indefinitely b their telomeres or maintaining telomerase ac  They can enter the circulatory system and m distant place and start cancer by settling in a n  They can escape apoptosis  They are not genetically and epigenetically

ells do not ls more ensures th the ultiply. trients, sis. They ore than g lactate encing the nutrients y fixing ctivity. move to a ew place. y stable

Causes of C There are two groups of risk factors for can on lifestyle, age, gender, and family hist fact smoking alcohol use, Being under the sun for long and dangerous hours, Overdose of X-ray exposure, Some chemicals some viruses Air pollution radiation exposure, bad eating habits

Cancer? ncer. Risk factors for cancer vary depending tory. Another risk group is environmental tors.

Cancer Genetics All cancers are caused by some abnormalities in the DNA sequence. It is thought that 10- 15% of cancers are hereditary, that is, inherited by genes from parents, and the remaining 85- 90% is shaped by the exposure of DNA in living cells to mutagens throughout life, mild progressive changes in cell DNA and errors in replication.



Since the division and control of c cancer is basically a disease related are tightly packed, and physical or ch directly affect cell function. Althoug the function of the gene due to da always achieved. In this case, inc proteins, which are the products o cellular fu

cells is under the control of genes, d to genes. Genes on chromosomes hemical changes on these genes can gh DNA repair systems try to restore amage to the gene, success is not complete or faulty production of of genes, leads to deterioration in unctions.

REGULATION OF THE CELL CYCLE AND C The cellular events that occur in the process from one c the next form the cell cycle. The interphase phase of the cell cycle is the process be divisions. ¤ Meanwhile, the cell grows and copies its D During G1, the cell prepares for DNA synthesis by acc enzymes and molecules necessary for DNA replication. G1 is followed by the S phase, in which the cell's chrom is copied. During G2, the cell continues to grow and prepare for During the M phase, the duplicated chromosomes are sister chromosomes separate to opposite poles, and th in two.

CANCER cell division to etween mitotic DNA. cumulating . mosomal DNA division. condensed, he cell divides

RHEHÜGÜCUCRLREAETDDIÖOÖNNNGGÜOÜSFSÜÜTNHNÜEÜNNCDEDÜLÜZLZECENYNLCLEELNNEMMAEENSSDİİVCV Cells that divide continuously do not exit the cell cycle, through the G1, S, G2, and M stages until they receive signals to stop their growth. If the cell stops proliferating, it enters the G0 phase of During G0, the cell is metabolically active but cannot g However, cancer cells do not have the ability to enter t Abnormal cell surface receptors or cytoplasmic signal t molecules send continuous growth signals to the nucle absence of external growth signals. The cell cycle is regulated by the interactions of genes or suppress the cycle. Mutation or misexpression in any controls the cell cycle contributes to the development many ways. For example, if the genes controlling the G checkpoints are defective, the cell can continue throug without repairing the DNA damage. This may lead to the accumulation of more mutations i thus uncontrolled proliferation and metastasis.

VCVEAEKNKACANENSRSEERR , but progress the necessary f the cell cycle. grow or divide. the G0 phase. transduction eus even in the that promote y gene that of cancer in G1/S or G2/M gh the cycle in genes and

Before the cell division stage, DNA where damage is prevented and/or repa stages are included. The phases of this c growth factors, cytokines, oncogenes cyclins, proteins such as CDK and MP (with Maturation Promoting Factor) being organized, in any of the phases When there is disruption (DNA damage), the suppressor genes immediately is stopping. The synthesized DNA is damag if not replicated, loop goes to M phas It is stopped at the G-2 phase before it ente DNA damage detected is moderate. p21 by the tumor suppressor gene (p53 protein is synthesized. Cyclin G-D is inhibited by inhibiting the cyclin CD being stopped in phase 1 or G-2, or is suspended. If DNA damage is too mu If it is large, p53 will cause the cell to undergo causes.

ired cycle s, F s e tumor ged or se ers. G-1 3). DK complex. uch apoptosis.

\"genetic cancer\" or \"hereditary Being hereditary of cancer is not the sam inherited. In some cases, the harmful geneti cause cancer is passed from the mother or fa baby. The child is born with this mutation, people develop cancer in later ages. These a cancers\". Because other cancers that are not develop in the person over time are also “g constitutes most of the non-hereditary and ca 80-90%

y cancer\"? me thing as being ic mutation that will ather to the newborn and some of these are called \"hereditary t hereditary and that genetic” after all. It ancer diseases, about

What does cancer gene mean With the completion of the Human Gen in 2003, it was found that most of th mutations (changes) that cause cancer body, that is, in the somatic cells. Such are called somatic mutations. That damages are not passed on to offs inheritance. However, mutations that frequently in reproductive cells are pass offspring and increase the risk of can mutations are called germline/inherited Cancers are genetically divided into Sporadic cancers (caused by somatic Hereditary cancers (occur as a result mutations) Familial cancers (genetic background Epigenetics

n? According to 2018 data nome Project worldwide he genetic 18.1 million occur in the new cases of cancer and h mutations 9.6 million people is, these from cancer spring by lost his life t occur less is indicated. sed on to the ncer. Such d mutations. o 4 groups: c mutations) of germline d unclear)

Sporad Sporadic cancers are caused by en approximately 80 percent of all cance occur as a result of DNA damage ac characteristics of sporadic cancers, w ages. The probability of finding an in l Even if there is more than one cancer cancer, this does not indicate that t heredity. Today, we know that we can positive life Familia With hereditary cancers, this individ category if he is diagnosed with canc person, the environment and lifestyle Hereditary cancer syndromes are no occurs in

dic cancers nvironmental influence and constitute ers. In other words, they are cancers that ccumulated over time. If we look at the we see that the disease occurs at certain nherited mutation in genetic tests is very low. r case in the family of the individual with the transmission has occurred through n largely prevent sporadic cancers with a estyle change. al cancers dual is considered in the familial cancer cer. The general genetic structure of the determine the risk of developing cancer. ot seen in this type of cancer. It usually middle age.

Epigen Mechanisms called supragenetic inhe this type of cancer. Environmental in play a role in the formation of these cancers is between 10-15 perce Waddington in 1942 as the science t genes that make up a certain pheno how the genotype affects the p Etymologically, it can mean above g epigenetics examines the factors th DNA sequence, but cause c Hereditar As a result of heredity of damage (m cancer types occur in offspring. It oc cancers. This type of cancer is less c tumor in different parts of a tissue o relatives of people with damaged ge the same damage. The incidence

netics eritance are thought to be effective in nfluence and genetic predisposition e cancers. The incidence of familial ent. Epigenetics was defined by that studies the relationship between otype and these gene products, and phenotype during development. genetics or beyond genetics. Today, hat do not cause any changes in the changes in gene regulation. y cancers mutations) in certain genes, specific ccurs at an earlier age than sporadic common and is usually multifocal (a or in different organs). First-degree enes have a 50 percent risk of having e of hereditary cancers is 5-10%.







genes and they cause diseases

There are 3 gene groups that have the These are oncogenes, tumor suppress oncogenes, which are normal genes tha can become active and turn into oncog expression, gene duplications and/or c of the most known oncogenes a

biggest role in the formation of cancer. or genes and DNA repair genes. Proto- at enable cell growth and differentiation, genes due to mutations, increased gene chromosomal rearrangements. Examples are genes such as RAS, Erk, MYC.

Cancer cells show chromosomal abnorm mutation rates Cancer cells often show specific chromo the type and stage of cancer. For exam patients with chronic myelogenous leuk CM

malities, genomic instability, and higher s than normal. osomal errors that are used to identify mple, leukemic white blood cells from kemia (chronic myelogenous leukemia: ML)

WHY DO CANCER CELLS METASTASIS The main cause of cancer-related de metastasis of the cancer. The cancer cel circulation, goes to another organ or t forming a secondary tumor there. This i human cancers are hereditary, 93% of th non-hereditary env

S TO CERTAIN TISSUES OR ORGANS? eaths is not the cancer itself, but the ll reaches the blood vessel and joins the tissue in the body and metastasizes by is not a random event. While only 7% of hem occur as a result of interaction with ironmental factors.

DNA damage According to Halliwell, two There is a mechanism: The first is directly DNA formed by the hydroxyl radical chain breakage, base modification and deoxyribose fragmentation. Latter, endonuclease resulting from oxidative stress DNA fragmentation by inactivation is to occur.

In summary, every factor that causes cancer Regardless, ultimately the cell's genetic deterioration of the material occurs. Single rather than a mutation in a gene, in several genes damage caused plays a role in cancer formation. Genes altered in cancer tissue homeostasis and cell three major biological pathways that regulate growth (cell cycle, apoptosis and differentiation) effects. Disruptions on a road, may have profound consequences in the other.

REFEREN Geoffrey M. Cooper , Robert E. Hausma Edition, 2016, Sunderla Türkiye Kanserle Savaş Vakfı http://www.kanservakfi.org/ https://hsgm.saglik.gov.tr/tr/kanser- Baykara O. Horizons in Cancer Resea Developments in Cancer Treatmen Hiroto S. Nova Science Publishers, N ADÜ Tıp Fakültesi Dergisi 2008; 9(3)

NCES an. The Cell, A Molecular Approach Seventh and, Massachusetts U.S.A. -istatistikleri). arch vol.57. Current Therapies and Latest nt, s.105-156, 2015. Editor: Watanabe, New York, ABD. ISBN: 978-1-63482-498- 9 : 51 – 61 Hücre Siklusu ve Kanser

Nakayama K. I, Nakayama K. (200 And Cancer Campbell, Reece Biyoloji 6. Baskı Seo, J. Y., Park, Y. J., Yi, Y. A., Hw H. ve Seo, D. G. (2015). Epige implications for oral health. Resto 1 Gürel Ç. ve ark. 2016.Epigenetik v Oncol-Specia Balikesir Saglik Bil Derg Cilt:5 Say

06, May). Ubiquitin Ligases: Cell-cycle Co r. Nature Revıews, Vol 6. ang, J. Y., Lee, I. B., Cho, B. H., Son, H. enetics: general characteristics and orative Dentistry ve Endodontics, 40(1), 14-22. ve Kanser.Türkiye Klinikleri J Radiat al Topics. 2(1). yı:3 Aralık 2016

PHYSICAL A AND CA

ACTIVITY ANCER

What is physica Physical activity is de movement that uses sk and requires more e resting. Physical activi walking, running, dan swimming, performin chores, exercising, and sports activi

al activity? efined as any keletal muscles energy than ity can include ncing, biking, ng household d engaging in ities