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2357
Advances in Environmental Biology, 5(8): 2357-2360, 2011
ISSN 1995-0756
This is a refereed journal and all articles are professionally screened and reviewed
ORIGINAL ARTICLE
A Review on Cancer Genetic
Sharrif Moghaddasi Mohammad
Islamic Azad University,Saveh Branch, İran.
Sharrif Moghaddasi Mohammad: A Review on Cancer Genetic
ABSTRACT
From the time Boveri observed that chromosomal changes are a feature of cancer, it has been thought to
be a disease caused primarily by alterations in the genome of the affected cells. Today, the notion of cancer
being a consequence of genetic alterations, is almost intuitive and the advances in molecular biology and
genomics have given us many tools to understand and possibly to combat cancer. Since science has always
existed in a continuum, the genetic alterations in cancer have to be understood in the context of cellular
organization, differentiation, tissue organization host response and susceptibility angiogenesis etc.
Key words: Cancer, Genetic, chromosom, genome, lymphoid.
Introduction
for medicines genetic and genetically consultation.
The cancer is one of the usual and critical
maladies in bed-head medicine. The statistics show
Cancer Identification Existence:
us that cancer outbreak the most of
1
3
population.
It is cause of 20 percent of deceases and in the
developed countries allocates most of 10 percent total
medical expenditures for itself. The cancer always
killer if it didn't treat.
Prematurity and proper distinction has vital and
identification of privates in risk of affection to cancer
before creation, constitute the important objective of
cancer's researches.
In this chapter, we emphasis that cancer is a
genetics’ illness basically. (Point to the inside cadre's
matters).
We describe gens that interfere in cancer
creation and mechanisms that by contravention them,
gens can caves to illnesses.
We explain a few of cancer's syndromes with
potency of heritage and show that how recognition
outcome their pathogenesis become clear us the
public foundation of cancer and we will pay off to
explanation of difficult that these syndromes bring
Cancer isn't unity illness but rather it's a name
that utilize for many kind of neoplasia. It is the
illness processes that result from uncontrolled
multiplication of cells that terminate to neoplasm pile
or tumor. For treatment that one neoplasm, treat
cancer, has to malignant. It means that the tumor has
invasion potency to neighbor tissue and the extension
to farther region. (Metasaz giver) (The tumor that
doesn’t give Metasaz, isn't cancer. But freat as
benign tumor, but its size and position of location
may not much benign for patient). Cancer has there
chief shape that include: Sarkoms, that tumor in them
appear from mezanshim's tissues like as bone, muscle
and even bind. Carcinomas that origin from sheeting
epithelial like as clothing garbage cells, exogenous
and running of mamma and finally malignity’s
connected to blood originator (Hematopoietic) and
lymphoid like as losemis and lymphomas that spread
completely in marrow, lymphoid system and
environmental blood.
In every one of groups, we grouping tumor on
basis of location, the kind of tissue, the view of
Corresponding Author
Sharrif Moghaddasi Mohammad, Islamic Azad University,Saveh Branch, İran.
E-mail: [email protected]
Adv. Environ. Biol., 5(8): 2357-2360, 2011
histology degree of malignity. Neoplasms, unnatural
cells accommodation.
Had been outbreak because of imbalance
between cells duplication and disappear. Them cell's
duplication outcome during the cell's cycle and with
Mitoz performance. Anyway disappearing them,
because of planned cell's death, during a natural
process of DNA segmentation and happened because
of cell's felo-de-se presented to Apoptosis.
Enhancement of perturbation’s degrees
accompany with gradual disappearing of tumor’s
repressor gens from a few chromosome and hot up
proto-ANKO gens with or without coincide defect in
DNA restore action. Example, Monogamy cancer
with DNA restoration defects. Has fewer out break
that cancers without unnatural without restoration but
when they engender, their improvement's way to final
common point namely malignity, they are different
but parallelism.
2358
creation with cell's growth set. Disappear the
operation of coding proteins by tumor repressor gens
lead to cells division and unnatural and unmoral cells
growth or defective apoptosis. Often jumping happen
in the division very of cells (See chapter B) and
Ankogens and repressive gens of tumor haven't more
ability of jumping hereditary. Kinship of other gens.
Whatever that distinguished cancer’s jump from
another kind of jumps is intensive reinforcement of
cells multiplication and or remains preclusion cells
from jump. This is exactly the phonotype of one
cancer cell. As the same its name, intensive
multiplication finally facility to a jumping cell to
change a tracker illness. Converse that, jumps that
cause to a cell lose it's operation between great
numbers of cell or dead and it hasn't any phenotype’s
effect none. Because in one organ, losing a cell by
many great health cells had cover.
Cancer in Families:
Genetic Roots of Cancer:
Cells division process and cell's death set by
spread spectrum of gens. Vast studies in a few past
decades show us that, occurrence of mutation in
duplication controller and cell's death is the cause of
cancer. In most of cancer, jumping in one singular
somatic cell happen and then had divide and going
to make a cancer. In one rarely case, when cancer
out break as one part of a syndrome that is
hereditary cancer syndrome, the first carcinogen
jump, heritage by series of fundamental cells. And so
there is all part of body cells before. Cancer by
starting with every mechanism, with aggregate other
genetic damages, in manner of jumping in coder gens
in cell's system that recovery the damage DNA and
keep the sitogenic's health, full-fledged and
progressing Damage of these gens have worse
circulation of jumping that affected on cell's
duplication controlling and DNA damage restoration.
So, real colon of Neoplastic cells can change to sub
series of humorous cells with different degree of
malignity that everyone comport jumping that every
one is different from others. But be transferred with
jumps in another subseries have commensurability
with each others.
Grouping interference gens in cancer for two
group is very good, They are include: Ankogens and
repressive gens-tumor. Often, Ankogens are activate
allels, on series of natural gens of cell namely protoAnkogens but they can gens such as telomerase
coder or gens that can discontinue Apoptosis, too.
Ankogenz, often, outcome jumping obtain actuality
(See chapter11) that facilitate changing to malignity
with mechanism as like as persuasion of cells
duplication, multiplication in transmitting blood to
tumor and halter of Apoptosis. Repressor gens-tumor,
as like that it's name showing, prevent from tumor
Much kind of cancers have most top break out
in patient's relatives toward normal population.
Between these kind of families’ cancer, nearly, there
is 50 model inelegant that in them the risk of cancer
is very high , it means that, in some canvers,
occurrence of jump in one singular gen can origin
helper agent for create a sick. The rats studies of
knowing epidemic, show us that some families even
without clear Mandalian heredity from cancer, they
have the risk of cancer upper than the normal limit.
For example, increase in detection of cancer, 2 or 3
double in the first relative of patients. It means that,
often, cancers have complex adjectives that due to
genetically and environmental agents (See chapter
15). So, the history of cancer between first or second
degree of patient's family have to increase the
doctor's guess’s about additional risk of cancer in
patient. Some people talented fewer than 5 percent of
all the cancers patient. The knowing of genetic of
illness is very important. First of all, the families of
person with strong hereditary potential, that is for
jump in one singular gens, mostly, we can test and
council them and depend to test result, ready the
giving certainty and intensive control and treatment
about them. Secondly, as like as many of widespread illness, the knowing about hereditary defect in
illness will give us precise sight about illness
mechanism.
If for create a malignity we need a group of
jump, a hereditary jump in every one of necessary
gens can influence on aptitude affection of conveyors
to cancer and can responsible noticeable part of
cancers, conveyors of these gens can responsible for
majority of cancers cases that we don't recognite
them as "families".
Adv. Environ. Biol., 5(8): 2357-2360, 2011
Ankogens:
Ankogen include a include a jumping gen that
it's operation or changing lead to unnatural actuation
division and cell's multiplication.
Activate jump can in ankogen, in its setting
element, and or even in number of genocidal version
of it lead to operation with out control or major
expression Ankogen production. Ankogens in cells
segment have clear effect. It means that when it
activates or express very much, a singular jumpping
allel is enough to change the phenotype from cell
from normal situation to virulent form.
Noroblastom MYCN in 40 percent of cases of
progressed stages, to 200 duble strengthening.
Contrarily of invasion treatment only 30 percent of
patients that suffering the progressed form of illness
will live. Contrary that, reinforcement of MYCN only
find 4 percent of first stage of Noroblastom and the
living fortune for 3 years is for this stage is 90
percent. Reinforcement of coder gens that are aims
of chemical drug proposed as a mechanism for create
a drug resistance in patients that improved with
chemical treatment before.
Cancer and Environment:
The risk of affection to cancer between different
population and different environment show us
different kind example, the volume of spread stomach
cancer between Japanese that live in Japan
comparison with Japanese that live in Losangeles or
Havaee are most 3 double. So, it seems that
noticeable park of risk to cancer depend to existence
of carcinogenic environmental. Environmental
careinogenic's nature, evaluation surplus age risk due
to accost with these materials and ways for
populations keeping contrast these damage are cases
that very noticeable for people. The root contents of
this chapter emphasis upon that cancer is genetically
but with knowing the environment's role on cancer,
it isn't contrast with this subject. Environmental
agents act such as jumping material and cause the
somatic jumps. Somatic jumps is cancer's agent.
According to some results that often is base of data’s
that collect after Hiroshima and Nokazaki's atomic
bombardment, it seems that 75 percent risk of cancer
has environmental origin.
Outcome:
Cancer is genetically derangement that natural
control of cell's growth in that is ruined. The basic
mechanism in all of cancer jump, in dodemany's cell
natal, and with most amplitude in somatic cells.
About genetically process of cancer and
environmental agents that with changing DNA lead
to malignity, there are many points yet, that have to
clear. New horizon about basilar roles of DNA
2359
changes in cancer lead to improvement and
innovation of special ways for prevent and treatment
of malignity illnesses in near future probably.
References
1.
American Cancer Society. Cancer facts and
figures, 1999.
2. American Cancer Society 1-800-ACS-2345,
www.cancer.org
3. Burt, R.W., G.M. Petersen, 1996. Familial
colorectal cancer: diagnosis and management. In:
Young G.P., Rozen, Levin B. Prevention and
early detection of colorectal cancer. London:
Saunders, 171-194.
4. Bussey, H.J.R., 1975. Familial polyposis coli.
Family studies, histopathology, differential
diagnosis, and results of treatment. Baltimore:
Johns Hopkins University Press.
5. Bulow, S., 1987. Familial polyposis coli. Dan
Med Bull, 34: 1-15.
6. Facing Our Risk of Cancer Empowered, Inc.
(FORCE)
1-866-824-7475,
www.facingourrisk.org
7. Giardiello, F.M., 1995. Gastrointestinal polyposis
syndromes and hereditary nonpolyposis colorectal
cancer. In: Rustgi A, ed. Gastrointestinal
cancers: biology, diagnosis, and therapy. New
York: Ravin, 367-377.
8. Groden, J., A. Thliveris, W. Samowitz, M.
Carlson, L. Gelbert, H. Albertsen, G. Joslyn, J.
Stevens, L. Spirio, M. Robertson, L. Sargeant,
K. Krapcho, E. Wolff, R. Burt, J.P. Hughes, J.
Warrington, J. McPherson, J. Wasmuth, D.
LePaslier, H. Abderrahim, D. Cohen, M.
Leppert, R. White, 1991. Identification and
characterization of the familial adenomatous
polyposis coli gene. Cell, 66: 589-600.
9. Lindor, N.M., M.L. McMaster, C.J. Lindor, et
al., 2008. Concise handbook of familial cancer
susceptibility
syndromes - second edition. J.
Natl Cancer Inst Monogr, (38): 1-93.
10. Laurent-Puig, P., C. Beroud, T. Soussi, 1998.
APC gene: database of germline and somatic
mutations in human tumors and cell lines.
Nucleic Acids Res., 26: 269-270.
11. Laken, S.J., G.M. Petersen, S.B. Gruber, C.
Oddoux, H. Oster, F.M. Giardiello, S.R.
Hamiliton, H. Hampel, A. Markowitz, D.
Klimstra, S. Jhanwar, S. Winawer, K. Offit,
K.W. Kinzler, B. Vogelstein, 1997. Familial
colorectal cancer in Askenazim due to a
hypermutable tract in APC. Nat Genet, 17: 7983.
12. N.L.M., 2005. National Library of Medicine's
Health Technology Assessment Information
Resources.http://www.nlm.nih.gov/nichsr/ehta/ch
apter10.htm.
Adv. Environ. Biol., 5(8): 2357-2360, 2011
13. N.C.I., 2005. The Early Detection Research
Network: Translational Research to Identify
Early Cancer and Cancer Risk. 2005;Third
Report.
14. National Cancer Institute 1-800-4-CANCER,
www.cancer.gov
15. National Society of Genetic Counselors, Inc., 1312-321-6834, www.nsgc.org
16. Romans, K., L.M. Hylind, S.V. Booker, J.D.
Brensinger, K. Johnson, J. Bacon, M. Choti, K.
Kinzler, B. Vogelstein, G. Petersen, F.
Giardiello, 2000. Hereditary colorectal cancer
website, www.Hopkinscoloncancer. org..
2360
17. Secretary's Advisory Committee on Genetic
Testing., 2000. Department of Health and
HumanServices. Request for public comment on
a proposed classification methodology
fordetermining level of review for genetic tests.
Federal Register; 65(236): 76643-45.
18. Tarn, C., A.K. Godwin, 2006. The molecular
pathogenesis of gastrointestinal stromal tumors.
Clin. Colorectal Cancer (Emerging Trends in the
Management of Gastrointestinal Stromal Tumors)
6(1): S7-S17.
19. Wennstrom, J., E.R. Pierce, V.A. McKusick,
1974. Hereditary benign and malignant lesions of
the large bowel. Cancer, 34: 850-857.