PENYULUHAN TENTANG DETEKSI DINI KANKER SERVIKS

Abstract

Cervical cancer is cancer with number incident number four the most what happens to women

The whole world and cancer most freguently within the country low income (Mustafa dkk 2016) cervical cancer is a malignity caused by exists language cell growth ephithelium cervix Uncontrollable(mirayashi 2013).according to cervical cancer 99,7% caused by human papillomavirus (hpv) oncogene that attacks the uterus cervical cancer is most malignant tumor

Which grow inside cerviks that is lowest part womb attaced at the top female genitals (hartati dkk 2014).based on the exposure cervical cancer or which known as cancer cerviks is tumor

Most malignant  is cerviks caused by human papillomavirus the main cause cervical cancer is

Human papilloma virus (HPV)more than 90% cancer cerviks womb is sguamous is  wich contain DNA virus human papilloma virus (HPV) and 50% cervical cancer associated with human papilloma  virus type 16. Virus HPV can spread through contact sexual especially in relationships sexual which is not safe. The HPV virus attacks the membranes in the mouth  and esophagus and anus .and will cause the formation  of precancerous cells in the long term.(ridayani 2016).the HPV virus will attach to the cell surfare reseptor by means of an attachment virus that spreads or the survace of the virus.HPVthat will attach to the cell surface receptors will penetrate , the existence of a wound makes it easier for the virus to enter the cell.the virus enters and releases the genome after which the capsit is destroyed afte the virus enters the cell nucleus, the virus performs transcription by turning its DNA into MRNA.(Yanti , 2013),the mechanisme of cervical cancer is related to the cell cycle expressed by HPV.the main proteins associated with carcinogens are E6 and E7. The silkular HPV geno form if integrated will become linear and truncated between the E2 and E1 genes . integration between the HPV genome and human DNA causes the E2 gene to malfunction so that it stimulates E6 to bind to p53 and E7 to bind to prb.