Cancer tissue has a very distinctive morphological features when observed with a microscope. Among a large number of cells undergoing mitosis, variations in the number and size of the nucleus, variations in size and shape of the cell, there were no distinctive features of cellular, mobile coordination does not occur normally visible in normal tissue and there were no clear network boundary.
Immunohistochemistry and other molecular methods used to find morphological features typical of cancer cells / tumor, as the referral diagnosis and prognosis.
Hahn and colleagues used an ectopic expression of telomerase reverse transcriptase combined with h-ras oncogene and T antigen of SV40 virus to induce conversion tumorigenik on fibroblast cells and human epithelial cells, which occur due to disruption of intracellular metabolic path. Phenotype characteristic of cancer cells after experiencing a transformation from normal cells, among others:
Immunohistochemistry and other molecular methods used to find morphological features typical of cancer cells / tumor, as the referral diagnosis and prognosis.
Hahn and colleagues used an ectopic expression of telomerase reverse transcriptase combined with h-ras oncogene and T antigen of SV40 virus to induce conversion tumorigenik on fibroblast cells and human epithelial cells, which occur due to disruption of intracellular metabolic path. Phenotype characteristic of cancer cells after experiencing a transformation from normal cells, among others:
Transformation in vitro
• There were changes in cytology, such as in cancer cells in vivo that increased cytoplasmic basophils, increased number and size of nuclei
• A change in cell growth characteristics:
a. difficult to have undergone differentiation to death despite repeated
b. that does not stop growing, although it has been squeezed by the surrounding cells, so that cancer tissue has a high density
c. require serum and growth factors less
d. no longer need the interface layer to multiply, and can grow as a free colony in semi-solid medium.
e. has no control over the cell cycle
f. difficult experience apoptosis
• Changes in the structure and function of cell membranes, including the increase due to lectins herbal aglutinabilitas
• Changes in the composition of the interface cell, glycoproteins, proteoglycans, glycolipid and mucin, tumorik antigen expression and increased absorption of amino acids, and nucleoside heksos.
• No interaction matrix cells and cell-extracellular, so there is no decrease in the rate of differentiation
• Cancer cells do not respond to stimulation of substances that induce differentiation, because the interface changes in the composition of the cell, including the molecular composition of substances concerned.
• Changes in cellular signal transduction mechanisms, including the track that is very fundamental, in addition to regulations that control the trajectory function of growth factors, levels of phosphorylation and defosforilasi.
• The ability to induce tumors in the model. This capability is a sine qua non that defines the word "fierce" in transformation in vitro. However, cancer cells that do not have the ability like this, still has the character "tumorigenik" on other models.
• There were changes in cytology, such as in cancer cells in vivo that increased cytoplasmic basophils, increased number and size of nuclei
• A change in cell growth characteristics:
a. difficult to have undergone differentiation to death despite repeated
b. that does not stop growing, although it has been squeezed by the surrounding cells, so that cancer tissue has a high density
c. require serum and growth factors less
d. no longer need the interface layer to multiply, and can grow as a free colony in semi-solid medium.
e. has no control over the cell cycle
f. difficult experience apoptosis
• Changes in the structure and function of cell membranes, including the increase due to lectins herbal aglutinabilitas
• Changes in the composition of the interface cell, glycoproteins, proteoglycans, glycolipid and mucin, tumorik antigen expression and increased absorption of amino acids, and nucleoside heksos.
• No interaction matrix cells and cell-extracellular, so there is no decrease in the rate of differentiation
• Cancer cells do not respond to stimulation of substances that induce differentiation, because the interface changes in the composition of the cell, including the molecular composition of substances concerned.
• Changes in cellular signal transduction mechanisms, including the track that is very fundamental, in addition to regulations that control the trajectory function of growth factors, levels of phosphorylation and defosforilasi.
• The ability to induce tumors in the model. This capability is a sine qua non that defines the word "fierce" in transformation in vitro. However, cancer cells that do not have the ability like this, still has the character "tumorigenik" on other models.
Transformation in vivo
Transformation in human cells requires the accumulation of genetic changes that lead to genomic instability, such as:
• Increased expression of oncogene protein as a result of translocation, amplification and mutation on the chromosome.
• There was no protein expression of the gene "tumor suppressor".
• Changes in DNA methylation.
• There is a transcription of genetic disorders that cause overproduction of growth supporting substances, such as IGF-2, TGF-α, tumor angiogenesis factor, PDGF, and hematopoietic growth factors such as CSF and interleukin.
• There was no genetic balance, which becomes increasingly uncontrolled proliferation, increased the likelihood of metastasis.
• Changes in patterns of enzymes and increased enzymes that play a role in the synthesis of nucleic acids and enzymes that are lytic, such as protease, collagenase and glikosidase.
• Production onkofetal antigens, such antigens plasentis karsinoembrionik and hormones (eg, chorionic gonadotropin), or phosphatase isoenzymes as alkalina plasentis.
• The ability to avoid the host antitumor response.
Of the various genetic changes, in tumors in humans, frequently found chromosomal translocation that produces the product kimerik transformation into cells with the ability of tumor / cancer or change the expression of oncogenes.
Transformation in human cells requires the accumulation of genetic changes that lead to genomic instability, such as:
• Increased expression of oncogene protein as a result of translocation, amplification and mutation on the chromosome.
• There was no protein expression of the gene "tumor suppressor".
• Changes in DNA methylation.
• There is a transcription of genetic disorders that cause overproduction of growth supporting substances, such as IGF-2, TGF-α, tumor angiogenesis factor, PDGF, and hematopoietic growth factors such as CSF and interleukin.
• There was no genetic balance, which becomes increasingly uncontrolled proliferation, increased the likelihood of metastasis.
• Changes in patterns of enzymes and increased enzymes that play a role in the synthesis of nucleic acids and enzymes that are lytic, such as protease, collagenase and glikosidase.
• Production onkofetal antigens, such antigens plasentis karsinoembrionik and hormones (eg, chorionic gonadotropin), or phosphatase isoenzymes as alkalina plasentis.
• The ability to avoid the host antitumor response.
Of the various genetic changes, in tumors in humans, frequently found chromosomal translocation that produces the product kimerik transformation into cells with the ability of tumor / cancer or change the expression of oncogenes.
Source: http://id.wikipedia.org/wiki/Kanker
