Benign and malignant tumors are both referred to by the same word that ends in oma. Cancers that are made up of layers of cells are called carcinomas, and cancers that arise in connective tissue or blood vessels are called sarcomas
An outline of tumors in animals
The characteristic of animal tissues is the regulated and limited growth of cells. In a rare phenomenon, a cell can break free from the constraints of normal regulation and divide uncontrollably, creating an abnormal mass of tissue. Such masses are called tumors.
Tumors are classified according to how they develop into two groups: benign and malignant. The group that does not invade surrounding tissue is called benign, they develop by displacing adjacent cells and rarely kill the body except when they occur in the brain. Malignant tumors called cancer to invade and kill surrounding cells as they grow, they also release into the bloodstream and lymphatics cells that have the ability to form new tumor sites called metastases.
Benign and malignant tumors are both referred to by the same word that ends in oma. Cancers that are made up of layers of cells are called carcinomas, and cancers that arise in connective tissue or blood vessels are called sarcomas. Many cancers are named after the specific cells they form. Examples include hepatoma from hepatocytes in the liver, melanoma from melanocytes in the skin, and lymphoma from lymphocytes. An exception is when leukemia arises in the bone marrow to form white blood cells.
Tumor viruses were first discovered by V. Ellerman and O. Bang in 1908 when they demonstrated that avian leukemia (ALV) could be transmitted to other chickens by the filtrate of blood cells. In 1911, P. Rous discovered that chicken sarcoma could also be transmitted in a similar way and confirmed that the causative agent was a virus, now called Rous's sarcoma virus (RSV), a retrovirus.
At first the discovery of the tumor virus in chickens received little attention, but in 1932 when R. Syope showed that papilloma in rabbits was also caused by a virus, interest increased. Interest increased in 1936 when J. Bitter demonstrated that the murine mammary gland virus (MTV) could be transmitted through milk from mother to pups. Bitter's work helps us understand many important aspects of cancer viruses: an animal infected with a cancer virus in childhood may not develop a tumor until adulthood, a tumorigenic virus does not always. In tumor formation, many factors such as the surrounding environment and host physiology are also important. Female mice infected with MTV at a young age develop tumors with a high frequency during pregnancy.
Tumor viruses discovered so far are mostly DNA viruses: poxvirus, adenovirus, herpesvirus, papovavirus, hepatitis B virus, and only one RNA virus group, Retrovirus, has been found. But after the retrovirus infects the cell, the RNA is transcribed into DNA and then integrated into the cell's chromosomes. One can therefore assume that tumorigenesis is a property related to viral DNA.
Tumor DNA virus
Currently, no virus has been confirmed to be a human tumor virus because it is not possible to experiment with a human tumor virus. However, some viruses have epidemiological, serological or detectable genomic or antigenic evidence from human tumor cells.
The virus is so named because when injected into newborn mice, it gives rise to many types of tumors. They are found widely in wild and laboratory rat populations and are transmitted by secretions and secretions.
Polyomavirus is a member of the family Polyomaviridae, with a cuboidal symmetry, 42-45 nm in diameter, containing a double-stranded DNA molecule. This virus is found in monkey kidney cell cultures, it induces tumors in molluscum contagiosum and transforms yellow terrapin cells in vitro.
Several other members of the Polyomavirus family, such as BK virus (BKV) and JC virus (JCV), cause infection in pregnant women, congenital infections, and reactivation in kidney and bone marrow transplant patients. , the donor can be a source of infection. JCV causes progressive multifocal leukoencephalopathy (PML) that may be associated with lymphomas or malignancies.
Virus diagnosis can stain damaged tissue (kidney, brain), isolate virus from urine or diseased tissue, serological diagnosis for specific antibodies.
Human papilloma virus (HPV)
The papillomavirus belongs to the family Papillomaviridae, the virion structure of the papillomavirus is similar to the polyoma virion but is slightly larger and also contains a 2-stranded DNA molecule. Currently, there are at least 60 known types.
Members of the human papillomavirus (HPV) form benign papillomas (warts) in many animals including humans, human warts often disappear spontaneously, but can also develop into skin carcinomas, especially those with the compromised immune systems. Papillomavirus types 16 and 18 are considered to cause cancer in the female reproductive organs, such as in the vaginal wall, external vagina, cervix. In men, HPV causes penile cancer.
In terms of diagnosis, DNA hybridization is now commonly used to identify the virus on the lesional tissue.
Epstein-Barr virus (EBV)
Discovered in 1964 by Epstein et al. in cell culture of a Burkitt lymphoma. EBV is a human B-lymphocyte-directed Herpesvirus, widespread worldwide. EBV is considered the cause of various cancers:
Burkitt Lymphoma is a B-cell lymphoma that occurs especially in children. It is an endemic disease in Central Africa and New Guinea and occurs sporadically around the world. In vitro, lymphoma cells develop into a lymphoblastic cell line that retains stem cell properties. EBV DNA and antigen have been found in Burkitt lymphoma cells.
EBV DNA and antigen are found in Burkitt lymphoma cells, only a short fragment of EBV DNA integrates, while most of the viral DNA is closed-loop and exists in the cell cytoplasm. The difficulty to prove that EBV causes cancer in humans is that in endemic areas there is a very high prevalence of EBV infection, but a very low rate of cancer. In terms of pathogenesis, EBV infection depresses immunoregulatory, B-lymphocyte proliferation associated with c-myc gene activation. There is a translocation of the c-myc gene from chromosomes 8 to chromosomes 14, 22, or 2, which brings the cell tumorigenic gene to the edge of the promoter of the immunoglobulin gene. , deregulation of genes, activation of c-myc leads to proliferation and non-differentiation of Burkitt lymphocytes.
Infectious lymphocytosis: common in children over 10 years of age and young adults with latent viral infection in childhood in Western countries, does not cause epidemics. Some cases of the disease occur in older children and middle-aged people with primary EBV infection (who have not been infected with EBV since childhood) through kissing (the virus is present in the salivary glands) or by blood transfusion, organ transplantation. when the donor is infected with the virus.
Lymphoma in immunocompromised individuals: latent EBV infection in seropositive individuals is controlled by cell-mediated immunity. In organ transplant recipients or AIDS as a result of this loss of control, asymptomatic “reactivated infection” occurs, in some cases causing EBV-associated leukocytosis.
Hodgkin's Disease: In recent years, there has been evidence that EBV plays a role in Hodgkin's disease. 60% of Hodgkin's patients have viral DNA and proteins in the Reed-Sternberg and reticular cells of the tumor. However, it is not enough to prove that EBV is the etiology of Hodgkin's disease, and more research is needed on this link.
T-lymphoma: EBV DNA is found in variable rates in different types of T-lymphoma. Until now, it was well established that EBV can cause T-cell infection, but the role of the virus in the pathogenesis of T-cell lymphoma is still controversial.
Nasopharyngeal carcinoma: this is common cancer in men of several ethnic groups in China. The patient had a high anti-EBV titer. The tumor consists of lymphoid infiltrates. EBV is present in epithelial cells. It induces lymphoma when injected into squirrel monkeys or owls.
In addition, there have recently been reports on the association between EBV and some other cancers such as thymic carcinoma, salivary gland cancer, gastric cancer, especially smooth muscle cancer. However, this relationship needs to be studied further.
Herpes simplex virus (HSV)
HSV type 2 (HSV-2) is considered a probable human carcinogen based on two main types of evidence:
Epidemiology: Women with HSV-2 urinary tract infections have a higher rate of cervical cancer than those without HSV-2. In women with this disease, anti-HSV titers are generally higher than those without HSV-2.
Molecular biology: HSV-2 DNA and proteins have been found in cervical cancer cells. HSV-2 can induce cell transformation in vitro. Most of these findings can be explained by the hypothesis that HSV-2 causes latent infection in patients with early sexual activity in infancy.
Hepatitis B virus ( HBV)
Primary hepatocellular carcinoma (hepatoma) is more common in people with HBV infection than in uninfected people. This association is evident in Africa and Asia, where rates of HBV infection and primary liver cancer are high. HBV has paved the way for hepatocellular carcinoma, although some HCC patients have no evidence of HBV infection. HBV DNA and HBV surface antigen can be found in liver cancer cells. HBV DNA integration presumably activates the cell's oncogenes.
Tumor RNA Virus: Retrovirus
Retroviruses contain an enzyme called reverse transcriptase that converts RNA into DNA. Many retroviruses cause sarcoma, leukemia, lymphoma, and carcinoma in chickens and mammals. In addition, Retroviruses include non-tumor members.
In terms of structure, Retrovirus has the same characteristics as the HIV virus. Virion is enveloped and ether-sensitive, about 100 nm in diameter, cubic symmetric capsid containing single-stranded RNA. A genome is a molecule of 8000 to 10,000 nucleotides. The peculiarity of Retrovirus is that after infecting cells, single-stranded RNA is transcribed into complementary double-stranded DNA (cDNA). Once formed, additional DNA integrates into the cell's chromosomes and is called a provirus, which contains the genes necessary for viral replication. Viruses are copied simultaneously with chromosomes, so the viral genome is passed on to daughter cells, so an infection in an organism can last a lifetime. When provirus is expressed, viral RNA and protein components appear in the cytoplasm and then accumulate in the cell membrane, where the virus is formed, budded, and exited the cell.
Retrovirus causes human tumors
These viruses, in addition to the genes necessary for replication, contain one or more additional genes. One of these extra genes, called tat (transacting transcriptional activator), encodes a protein that induces changes in other viral genes and possibly some cellular genes. Another feature of the human retrovirus is its T4 helper lymphocyte (CD4) cytotoxicity. Although other cells may be infected, helper T4 is preferentially selected and disease is associated with this cell population.
Up to now, two types of retrovirus that cause leukemia and lymphoma have been isolated in humans, HTLV I and HTLV II. Both of these viral diseases are associated with leukemia (leukemia) and lymphoma (lymphoma).
HTLV I (or HTLV1)
Most HTLV I-induced leukemias or lymphomas are related to T4 lymphocytes: T4 lymphocytes have a giant multinucleated or multilobular form, in some cases without obvious morphological changes. In vitro, infection with HTLV I causes normal T-lymphocytes to change or lose immune function. Leukemia or lymphoma caused by HTLV I often carries a special form of cancer called adult T cell leukemia/lymphoma (ALT) that has an infiltrating, often leukocytosis hemophilia, opportunistic infections, half of cases due to leukocyte infiltration. HTLV I is also associated with T-cell leukemia/lymphoma of a chronic course (15-20%). Typical ALT cases are almost always HTLV I positive.
HTLV II (or HTLV 2)
HTLV II was first isolated from a cell line in a patient with a dendritic leukemia variant and differentiated from HTLV I by competitive radioimmunoassay. Subsequently, the virus was isolated in many patients with a more chronic form of cell carcinoma. Overall, HTLV II has 55% nucleotide homology with HTLV I with only slight biological differences. Serological tests cannot distinguish antibodies to the two viruses. In many parts of the United States, the predominant HTLV virus in addicts is HTLV II.