致癌基因

癌基因[編輯]

 

 

癌基因（英語：Oncogene，亦稱為致癌基因）是細胞遺傳物質的一部分, 它們參與細胞從正常生長狀態到腫瘤的過程。它們通過誘導或突變被激活。

原癌基因[編輯]

原癌基因(proto-oncogene)是參與細胞生長、細胞分裂和細胞分化的正常基因。但當其發生突變後，例如基因序列被改變，就會變成致癌基因。也就是說，原癌基因是致癌基因的前體。它們會在諸如放射性物質，化學物質和病毒的作用影響下過渡成引發癌症的形式。截至2004年，已經發現超過100種的原癌基因。

原癌基因根據其編碼的蛋白質被分類：

• 生長因子
• 生長因子受體蛋白
• G蛋白,例如由Ras原致癌基因編碼的
• 非受體-蛋白激酶,例如胰蛋白酶激酶
• 核酸轉錄因子
• 致癌的染色體畸變
• 病毒來源的致癌基因

很多影響細胞生長的因子都可被視為原癌基因。如果這些基因發生突變，通常隻會使編碼的蛋白質喪失原有功能，細胞分裂停止，進而引發程序性細胞死亡（細胞凋亡）。這並不會對機體產生影響，因為附近有分裂能力的正常細胞可以通過有絲分裂替代凋亡的細胞。

但突變也可能會產生致癌基因並推動細胞分裂，甚至不受控製。這樣，致癌基因就會導致癌症的形成。

 

Oncogene

From Wikipedia, the free encyclopedia

 

 

For the journal, see Oncogene (journal).

 

Illustration of how a normal cell is converted to a cancer cell, when an oncogene becomes activated

An oncogene is a gene that has the potential to cause cancer.^[1] Intumor cells, they are often mutated or expressed at high levels.^[2]

Most normal cells undergo a programmed form of death (apoptosis). Activated oncogenes can cause those cells designated for apoptosis to survive and proliferate instead.^[3] Most oncogenes require an additional step, such as mutations in another gene, or environmental factors, such as viral infection, to cause cancer. Since the 1970s, dozens of oncogenes have been identified in human cancer. Many cancer drugs target the proteins encoded by oncogenes.^[2][4][5][6]

 

Contents

  [hide] 

• 1 History
• 2 Proto-oncogene
  • 2.1 Activation
• 3 Classification
• 4 See also
• 5 References
• 6 External links
•  

 

Classification[edit]

There are several systems for classifying oncogenes,^[16][17] but there is not yet a widely accepted standard. They are sometimes grouped both spatially (moving from outside the cell inwards) and chronologically (parallelling the "normal" process of signal transduction). There are several categories that are commonly used:

Category	Examples	Cancers	Gene functions
Growth factors, or mitogens	c-Sis	glioblastomas, fibrosarcomas,osteosarcomas, breast carcinomas, and melanomas[18]	induces cell proliferation.
Receptor tyrosine kinases	epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor (PDGFR), andvascular endothelial growth factor receptor (VEGFR),HER2/neu	Breast cancer, gastrointestinal stromal tumours, non-small-cell lung cancer and pancreatic cancer[19]	transduce signals for cell growth and differentiation.
Cytoplasmictyrosine kinases	Src-family, Syk-ZAP-70family, and BTK family of tyrosine kinases, the Abl gene in CML - Philadelphia chromosome	colorectal and breast cancers, melanomas, ovarian cancers, gastric cancers, head and neck cancers, pancreatice cancer, lung cancer, brain cancers, and blood cancers[20]	mediate the responses to, and the activation receptors of cell proliferation, migration, differentiation, and survival [21]
CytoplasmicSerine/threonine kinases and their regulatory subunits	Raf kinase, and cyclin-dependent kinases (throughoverexpression).	malignant melanoma, papillary thyroid cancer, colorectal cancer, and ovarian cancer[22]	Involved in organism development, cell cycle regulation, cell proliferation, differentiation, cells survival, and apoptosis [23]
Regulatory GTPases	Ras protein	adenocarcinomas of the pancreas and colon, thyroid tumors, and myeloid leukemia[24]	involved in signalling a major pathway leading to cell proliferation.[25]
Transcription factors	myc gene	malignant T-cell lymphomas and acute myleoid leukemias, breast cancer, pancreatic cancer, retinoblastoma, and small cell lung cancer [26]	-They regulate transcription of genes that induce cell proliferation.

More detailed information for the above Table:

• Growth factors are usually secreted by either specialized or not specialized cells to induce cell proliferation in themselves, nearby cells, or distant cells. An oncogene may cause a cell to secrete growth factors even though it does not normally do so. It will thereby induce its own uncontrolled proliferation (autocrine loop), and proliferation of neighboring cells. It may also cause production of growth hormones in other parts of the body.
• Receptor Tyrosine Kinases add phosphate groups to other proteins to turn them on or off. Receptor kinases add phosphate groups to receptor proteins at the surface of the cell (which receive protein signals from outside the cell and transmit them to the inside of the cell). Tyrosine kinases add phosphate groups to the amino acid tyrosine in the target protein. They can cause cancer by turning the receptor permanently on (constitutively), even without signals from outside the cell.
• Ras is a small GTPase that hydrolyses GTP into GDP and phosphate. Ras is activated by growth factor signaling (i.e., EGF, TGFbeta) and acting like a binary switch (on/off) in growth signaling pathways. Downstream effectors of Ras include three mitogen-activated protein kinases Raf a MAP Kinase Kinase Kinase (MAPKKK), MEK a MAP Kinase Kinase (MAPKK), and ERK a MAP Kinase(MAPK), which in turn regulate genes that mediate cell proliferation.

所有跟帖： 

• 腫瘤抑製基因: "廣東瘤"的研究 -26484915- ♂ (48872 bytes) () 09/29/2014 postreply 14:32:54