CANCER
GENETICS
David Vaíllo García
David Vaíllo García
INTRODUCTION
A single mutation is not sufficient to transform a normal cell into a malignant cell forming a tumor. If it were enough, the cancer
would be much more frequent than es.La incidence of most cancers increases
exponentially with age.
CONCEPTS FOR CANCER
The high level of genomic instability observed in cancer cell is called a mutator phenotype. Genomic instability in cancer
cells is manifested in large defects such as translocations, aneuploid cells,
chromosomal loss, DNA amplification and chromosomal deletions.
· Example of specific translocation: chronic myelogenous leukemia (CLM)
The C-ABL gene on chromosome 9 is translocated within the BCR gene from chromosome 22. This translocation creates a structure known as the Philadelphia chromosome. The BRC-ABL fusion gene encodes a chimeric protein BRC-ABL.Normal ABL protein kinase is a protein which acts in signal transduction pathways, transferring the signals of growth factors from the external environment to the nucleus.
BRC-ABL protein molecule is an abnormal signal transduction in cells CLM, which constantly stimulates these cells to proliferate.
· Example of DNA repair: xeroderma pigmentosum (XP)
It is a rare inherited disease characterized by extreme sensitivity to UV light and other carcinogens often patients with XP develop malignant skin cancer. Cells from XP patients unable to perform nucleotide excision repair and mutations in any of seven genes whose gene products are necessary to carry out DNA repair. XP cells lack the ability to repair DNA damage such as thymine dimers induced by UV light.
The normal regulation of cell proliferation involves a large number of gene products that control cell cycle phases programmed cell death and cell response to external growth. In cancer cells, many of the genes that control these functions are mutated or aberrantly express themselves, leading to uncontrolled cell proliferation.
In the cell cycle checkpoints can be found in G1 / S, G2 / M and M. In addition to these regulatory checkpoints of the cell cycle, there are two classes of proteins that regulate cell cycle progress: the cyclins and cyclin-dependent kinase (CDK). When there is a cyclin that binds to a specific CDK, stimulating the activity of CDK-cyclin complex. Then these compounds selectively phosphorylate and activate other proteins that in turn make the necessary changes for the cell progresses through the cell cycle.
Example: in the G1 phase cdk4/cyclin D complexes activate proteins that stimulate transcription of groups of genes whose products are required for DNA to replicate during S phase.
If replication or DNA repair, or assembly of aberrant chromosomes are, the cell stops its progression through the cycle until this condition is corrected. This reduces the number of mutations and chromosomal abnormalities that accumulate in the proliferating cells. If the DNA damage or chromosome is so grave that can not be repaired, the cell can initiate a second line of defense called apoptosis or programmed cell death.
Apoptosis is genetically controlled, so that the regulation of specific gene products such as proteins and BAX bcl2 can stimulate or prevent apoptosis.
The molecules responsible for initiating apoptosis and digested intracellular components with a group of proteases called caspase. By removing the damaged cells, programmed cell death reduces the number of mutations that spreads to the next generation, including genes that cause cancer.
Proto-oncogenes are genes whose products promote cell growth and division. Encode transcription factors that stimulate the expression of other genes, molecules which stimulate signal transduction cell division and cell cycle regulators which make the cell progresses through this cycle.
When a proto-oncogene is mutated or improperly expressed and contributes to cancer development, now called oncogene (cancer-causing gene). A single mutated allele of a proto-oncogene mutated or improperly expressed is sufficient to stimulate uncontrolled growth. So oncogenes confer a dominant cancerous phenotype.
The tumor suppressor genes are those whose products regulate under normal conditions, the control points of the cell cycle and initiate the process of apoptosis.When they are mutated or are inactive, the cells can not respond normally to the points of cell cycle control, or are unable to perform programmed cell death if DNA damage is too important.
There are more than 200 oncogenes and tumor suppressor genes.
· The ras protooncogenes
These genes are mutated in most human tumors. The ras gene family encodes signal transduction molecules that are associated with the cell membrane and regulate cell growth and division. Typically, ras proteins transmit signals from the cell membrane to the nucleus, stimulating a cell to divide in response to external growth factors. Ras bound to GTP when it is active when bound to GDP is inactive.
When a cell is a growth factor, receptors for growth factors from the cell membrane bind to them, which results in autophosphorylation of the receptor cytoplasmic portion. This results in the recruitment of proteins known as nucleotide exchange factors in the plasma membrane. These factors make it flush release GDP and GTP binds to activating.
The active form of ras bound to GTP signals through cascades of protein phosphorylation in the cytoplasm. The end of these cascades is the activation of transcription factors that stimulate the expression of genes whose products drive cells quiescent state of the cell cycle. Once sent their signals to the nucleus, hydrolyzes GTP to GDP and becomes inactive.
Mutations in ras proto-oncogene become an oncogene ras protein prevent hydrolyze the GTP to GDP, while maintaining the ras protein in its active conformation, which constantly stimulates the cell to divide.
Comparison of the amino acid sequence of ras proteins between normal and cancer cells reveals that oncogenic ras proteins have a single amino acid substitution at position 12 or 61. Each of these amino acid changes may be generated by one nucleotide substitution in the ras gene.
· Protooncogene cyclin D1 and cyclin D.
· The tumor suppressor gene RB1.
· The p53 tumor suppressor gene.
The gene is mutated more frequently in human cancers, over 50% of all cancers, the p53 gene. This gene encodes a nuclear protein that acts as a transcription factor repressing or stimulating transcription. The protein p53 is often linked to another protein called mdm2, which prevents phosphorylation and acetylation of p53 protein that convert the inactive form in the active.
To arrest the cell cycle at the G1 checkpoint / S, activated p53 protein stimulates the transcription of the gene encoding the p21 protein. 21 inhibits protein complex which cdk4/cyclin D1 prevents the cell passes from phase G1 to S phase The activated p53 protein also regulates expression of genes which retard the progress of DNA replication. Activated p53 can also direct the damaged cell to commit suicide by apoptosis. It does this by activating the BAX gene transcription and repressing the activity of the bcl-2. In normal cells form dimers BAX and bcl-2, when p53 stimulates transcription of the gene BAX, BAX homodimers are formed leading to the cell to self-destruction. In cancer cells lacking functional p53, a BAX protein level is not increased and does not form homodimers so that apoptosis cannot occur.
Cells lacking functional p53 are unable to stop the cell cycle checkpoints or cause the cell to enter apoptosis in response to DNA damage.
· Example of specific translocation: chronic myelogenous leukemia (CLM)
The C-ABL gene on chromosome 9 is translocated within the BCR gene from chromosome 22. This translocation creates a structure known as the Philadelphia chromosome. The BRC-ABL fusion gene encodes a chimeric protein BRC-ABL.Normal ABL protein kinase is a protein which acts in signal transduction pathways, transferring the signals of growth factors from the external environment to the nucleus.
BRC-ABL protein molecule is an abnormal signal transduction in cells CLM, which constantly stimulates these cells to proliferate.
· Example of DNA repair: xeroderma pigmentosum (XP)
It is a rare inherited disease characterized by extreme sensitivity to UV light and other carcinogens often patients with XP develop malignant skin cancer. Cells from XP patients unable to perform nucleotide excision repair and mutations in any of seven genes whose gene products are necessary to carry out DNA repair. XP cells lack the ability to repair DNA damage such as thymine dimers induced by UV light.
The normal regulation of cell proliferation involves a large number of gene products that control cell cycle phases programmed cell death and cell response to external growth. In cancer cells, many of the genes that control these functions are mutated or aberrantly express themselves, leading to uncontrolled cell proliferation.
In the cell cycle checkpoints can be found in G1 / S, G2 / M and M. In addition to these regulatory checkpoints of the cell cycle, there are two classes of proteins that regulate cell cycle progress: the cyclins and cyclin-dependent kinase (CDK). When there is a cyclin that binds to a specific CDK, stimulating the activity of CDK-cyclin complex. Then these compounds selectively phosphorylate and activate other proteins that in turn make the necessary changes for the cell progresses through the cell cycle.
Example: in the G1 phase cdk4/cyclin D complexes activate proteins that stimulate transcription of groups of genes whose products are required for DNA to replicate during S phase.
If replication or DNA repair, or assembly of aberrant chromosomes are, the cell stops its progression through the cycle until this condition is corrected. This reduces the number of mutations and chromosomal abnormalities that accumulate in the proliferating cells. If the DNA damage or chromosome is so grave that can not be repaired, the cell can initiate a second line of defense called apoptosis or programmed cell death.
Apoptosis is genetically controlled, so that the regulation of specific gene products such as proteins and BAX bcl2 can stimulate or prevent apoptosis.
The molecules responsible for initiating apoptosis and digested intracellular components with a group of proteases called caspase. By removing the damaged cells, programmed cell death reduces the number of mutations that spreads to the next generation, including genes that cause cancer.
Proto-oncogenes are genes whose products promote cell growth and division. Encode transcription factors that stimulate the expression of other genes, molecules which stimulate signal transduction cell division and cell cycle regulators which make the cell progresses through this cycle.
When a proto-oncogene is mutated or improperly expressed and contributes to cancer development, now called oncogene (cancer-causing gene). A single mutated allele of a proto-oncogene mutated or improperly expressed is sufficient to stimulate uncontrolled growth. So oncogenes confer a dominant cancerous phenotype.
The tumor suppressor genes are those whose products regulate under normal conditions, the control points of the cell cycle and initiate the process of apoptosis.When they are mutated or are inactive, the cells can not respond normally to the points of cell cycle control, or are unable to perform programmed cell death if DNA damage is too important.
There are more than 200 oncogenes and tumor suppressor genes.
· The ras protooncogenes
These genes are mutated in most human tumors. The ras gene family encodes signal transduction molecules that are associated with the cell membrane and regulate cell growth and division. Typically, ras proteins transmit signals from the cell membrane to the nucleus, stimulating a cell to divide in response to external growth factors. Ras bound to GTP when it is active when bound to GDP is inactive.
When a cell is a growth factor, receptors for growth factors from the cell membrane bind to them, which results in autophosphorylation of the receptor cytoplasmic portion. This results in the recruitment of proteins known as nucleotide exchange factors in the plasma membrane. These factors make it flush release GDP and GTP binds to activating.
The active form of ras bound to GTP signals through cascades of protein phosphorylation in the cytoplasm. The end of these cascades is the activation of transcription factors that stimulate the expression of genes whose products drive cells quiescent state of the cell cycle. Once sent their signals to the nucleus, hydrolyzes GTP to GDP and becomes inactive.
Mutations in ras proto-oncogene become an oncogene ras protein prevent hydrolyze the GTP to GDP, while maintaining the ras protein in its active conformation, which constantly stimulates the cell to divide.
Comparison of the amino acid sequence of ras proteins between normal and cancer cells reveals that oncogenic ras proteins have a single amino acid substitution at position 12 or 61. Each of these amino acid changes may be generated by one nucleotide substitution in the ras gene.
· Protooncogene cyclin D1 and cyclin D.
· The tumor suppressor gene RB1.
· The p53 tumor suppressor gene.
The gene is mutated more frequently in human cancers, over 50% of all cancers, the p53 gene. This gene encodes a nuclear protein that acts as a transcription factor repressing or stimulating transcription. The protein p53 is often linked to another protein called mdm2, which prevents phosphorylation and acetylation of p53 protein that convert the inactive form in the active.
To arrest the cell cycle at the G1 checkpoint / S, activated p53 protein stimulates the transcription of the gene encoding the p21 protein. 21 inhibits protein complex which cdk4/cyclin D1 prevents the cell passes from phase G1 to S phase The activated p53 protein also regulates expression of genes which retard the progress of DNA replication. Activated p53 can also direct the damaged cell to commit suicide by apoptosis. It does this by activating the BAX gene transcription and repressing the activity of the bcl-2. In normal cells form dimers BAX and bcl-2, when p53 stimulates transcription of the gene BAX, BAX homodimers are formed leading to the cell to self-destruction. In cancer cells lacking functional p53, a BAX protein level is not increased and does not form homodimers so that apoptosis cannot occur.
Cells lacking functional p53 are unable to stop the cell cycle checkpoints or cause the cell to enter apoptosis in response to DNA damage.
CONTRIBUTE TO CANCER VIRUS
- The proviral DNA can integrate by chance near one of the normal cell protooncogenes.Promoters or enhancers of the provirus U3 and U5 encourage higher amounts of proto-oncogene transcription, or will at the wrong time, leading to stimulation or proliferation of the host cell.
- A retrovirus can grab a copy of a proto-oncogene and integrated into the host genome.The new viral oncogene can mutate during the transfer process to the virus, or can be expressed in abnormal amounts since it is under the control of a viral promoter.
An oncogene carried by a retrovirus called v-onc, the normal version of this gene called c-onc. Retrovirus carrying the v-onc these genes can infect and transform normal cells into tumor cells.
In humans has not identified any acute transforming retroviruses. However, RNA viruses and DNA contribute to the development of human cancers in various ways. The viruses that most contribute to the development of cancers are human papillomavirus (HPV 16 and 18), the human leukemia virus (HTLV-1), the hepatitis B virus and Epstein-Barr.
GENÉTICA DEL CÁNCER
David Vaíllo García
David Vaíllo García
INTRODUCCIÓN
Una única mutación no es suficiente para transformar una
célula normal en una célula maligna formadora de un tumor. Si fuese suficiente
con ello, el cáncer sería mucho más frecuente de lo que es.La incidencia de la
mayoría de cánceres crece exponencialmente con la edad.
CONCEPTOS SOBRE EL
CÁNCER
El alto nivel de inestabilidad genómica observado en las
células cancerosas se conoce como fenotipo
mutador. La inestabilidad genómica en las células cancerosas se manifiesta
en grandes defectos como translocaciones, aneuplodías, pérdidas
cromosómicas, amplificación del DNA y deleciones cromosómicas.
·
Ejemplo
de translocación específica: leucemia mielogena crónica (CLM)
El gen C-ABL del cromosoma 9 se ha translocado dentro del gen
BCR del cromosoma 22. Esta translocación genera una estructura conocida como
cromosoma Filadelfia. El gen fusionado BRC-ABL codifica una proteína BRC-ABL
quimérica. La proteína ABL normal es una proteína quinasa que actúa en rutas de
transducción de señales, transfiriendo las señales de factores de crecimiento
del medio externo al núcleo.
La proteína BRC-ABL es una molécula anormal de transducción de señal en las células CLM, que estimula constantemente estas células para que proliferen.
·
Ejemplo
de reparación del DNA: xeroderma pigmentosum (XP)
Es una enfermedad hereditaria poco frecuente que se
caracteriza por una sensibilidad extrema a la luz UV y a otros carcinógenos a
menudo los pacientes con XP desarrollan cáncer maligno de piel. Las células de
los pacientes con XP no pueden realizar la reparación por escisión de
nucleótidos y presentan mutaciones en cualquiera de los siete genes cuyos
productos génicos son necesarios para llevar a cabo la reparación del DNA. Las
células XP no tienen la capacidad de reparar lesiones de DNA como los dímeros de timina inducidos por la
luz UV.
La regulación normal sobre la proliferación celular implica
un gran número de productos génicos que controlan las fases del ciclo celular
la muerte celular programada y la respuesta de las células a las señales
externas de crecimiento. En las células cancerosas, muchos de los genes que
controlan estas funciones se encuentran mutados o se expresan de manera
aberrante, lo que conduce a una proliferación celular incontrolada.
En el ciclo celular se pueden encontrar puntos de control en
G1/S, en G2/M y en M. Además de la regulación en estos puntos de control del
ciclo celular, hay dos clases de proteínas que regulan la marcha del ciclo
celular: las ciclinas y las quinasas dependientes de ciclinas (CDK). Cuando hay
un a ciclina, esta se une a una CDK específica, estimulando la actividad del
complejo CDK-ciclina. Entonces estos compuestos fosforilan y activan
selectivamente otras proteínas que a su vez realizan los cambios necesarios
para que la célula progrese por el ciclo celular.
Ejemplo: en la fase G1 los complejos CDK4/ciclina D activan las proteínas que estimulan la transcripción de grupos de genes cuyos productos se requieren para que el DNA se replique durante la fase S.
Si la replicación o la reparación del DNA, o el ensamblaje de
los cromosomas son aberrantes, la célula detiene su progresión por el ciclo
hasta que se corrige esta condición. Esto reduce el número de mutaciones y de
anomalías cromosómicas que se acumulan en las células en proliferación. Si el
daño en el DNA o en los cromosomas es tan grave que no se puede reparar, la
célula, puede iniciar una segunda línea defensiva denominada apoptosis o muerte
celular programada.
La apoptosis está genéticamente controlada, de modo que la regulación
de productos génicos específicos como las proteínas bcl2 y BAX puede estimular
o evitar la apoptosis.
Las moléculas responsables de iniciar la apoptosis y de
digerir los componentes intracelulares con un grupo de proteasas denominadas
caspasa. Al eliminar las células dañadas, la muerte celular programada reduce
el número de mutaciones que se propaga a la siguiente generación, incluidas las
de los genes que causan cáncer.
Los protooncogenes
son genes cuyo producto promueven el crecimiento y la división celular.
Codifican factores de transcripción que estimulan la expresión de otros genes,
moléculas de transducción de señales que estimulan la división celular y
reguladores del ciclo celular que hacen que la célula progrese a través de este
ciclo.
Cuando un protooncogén está mutado o se expresa
incorrectamente, y contribuye al desarrollo de un cáncer, pasa a denominarse oncogén (gen que causa cáncer). Un solo
alelo mutado de un protooncogén mutado o expresado de manera incorrecta es
suficiente para estimular un crecimiento incontrolado. Por eso los oncogenes
confieren un fenotipo canceroso dominante.
Los genes supresores
de tumores son aquellos cuyos productos regulan en condiciones normales,
los puntos de control de ciclo celular, e inician el proceso de apoptosis.
Cuando están mutados o son inactivos, las células no pueden responder
normalmente a los puntos de control del ciclo celular, o son incapaces de
realizar muerte celular programada si el daño del DNA es demasiado importante.
Se conocen más de 200 oncogenes y de genes supresores de
tumores.
·
Los protooncogenes ras
Estos genes se encuentran mutados en más de los tumores
humanos. La familia génica ras codifica moléculas de transducción de señales
que están asociadas a la membrana celular y que regulan el crecimiento y la
división celular. Normalmente, las proteínas ras transmiten señales de la
membrana celular al núcleo, estimulando a la célula a dividirse en respuesta a
factores de crecimiento externo. Ras cuando esta unido a GTP está activo y cuando
está unido a GDP está inactivo.
Cuando una célula encuentra un factor de crecimiento, los
receptores de los factores de crecimiento de la membrana celular se unen a
ellos, lo que provoca la autofosforilación de la porción citoplasmática del
receptor. Esto provoca el reclutamiento de proteínas conocidas como factores de
intercambio de nucleótidos en la membrana plasmática. Estos factores hacen que
ras libere GDP y se una a GTP activándose.
La forma activa de ras unida a GTP envía señales a través de
cascadas de fosforilaciones proteicas en el citoplasma. El final de estas
cascadas es la activación de factores de transcripción que estimulan la
expresión de genes cuyos productos conducen las células del estado de
quiescencia al ciclo celular. Una vez ha enviado sus señales al núcleo,
hidroliza GTP a GDP y se vuelve inactivo.
Las mutaciones que convierten el protooncogén ras en un
oncogén evitan que la proteína ras hidrolice el GTP en GDP, manteniendo siempre la proteína ras
en su conformación activa, lo que estimula constantemente la célula a
dividirse.
La comparación de la secuencia aminoacídica de las proteínas
ras entre células normales y cancerosas revela que las proteínas ras
oncogénicas tienen sustitución de un único aminoácido en posición 12 ó 61. Cada
uno de estos cambios aminoacídicos puede generarse por una sustitución
nucleotídica en el gen ras.
·
Protooncogén ciclina D1 y ciclina D.
·
El gen supresor de tumores RB1.
·
El gen supresor de tumores p53.
El gen que se
encuentra mutado con más frecuencia en los cánceres humanos, en más del 50% de
todos los cánceres, es el gen p53. Este gen codifica una proteína nuclear que
actúa de factor de transcripción reprimiendo o estimulando la transcripción. La
proteína p53 suele estar unida a otra proteína denominada mdm2, que evita las
fosforilaciones y las acetilaciones que convierten la proteína p53 de la forma
inactiva en la activa.
Para detener el ciclo celular en el punto de control G1/S, la
proteína p53 activada estimula la transcripción del gen que codifica la
proteína p21. La proteína 21 inhibe el complejo CDK4/ciclina D1 lo que evita
que la célula pase de la fase G1 a la fase S. La proteína p53 activada también
regula la expresión de genes que retardan el avance de la replicación del DNA.
P53 activada también puede ordenar a la célula dañada que cometa suicidio por
apoptosis. Esto lo consigue activando la transcripción del gen BAX y
reprimiendo la actividad del gen bcl-2. En las células normales se forman dímeros
de BAX y bcl-2, cuando p53 estimula la transcripción del gen BAX, se forman
homodímeros de BAX conduciendo a la célula a la autodestrucción. En células cancerosas que carecen de p53
funcional, los niveles de proteína BAX no se incrementan y no se forman
homodímeros por lo que la apoptosis no se puede producir.
Las células que carecen de p53 funcional son incapaces de
detener el ciclo celular en los puntos de control o de hacer que la célula
entre en apoptosis en respuesta a daños en el DNA.
LOS VIRUS CONTRIBUYEN
AL CANCER
Los virus que provocan cáncer en animales son virus de RNA
conocidos como retrovirus. Se habla de provirus a la copia de DNA integrada del
RNA retrovírico. Un retrovirus puede provocar cáncer de dos maneras diferentes:
-
El
DNA provírico se puede integrar por casualidad cerca de uno de los
protooncogenes normales de la célula. Los promotores o intensificadores U3 y U5
del provirus estimularán cantidades más altas de transcripción del
protooncogén, o lo harán en un momento inadecuado, lo que conduce a la
estimulación o proliferación de la célula huésped.
-
Un
retrovirus puede coger una copia de un protooncogén del huésped e integrarla en
su genoma. El nuevo oncogén vírico puede mutar durante el proceso de
transferencia al virus, o puede expresarse en cantidades anormales puesto que
se encuentra bajo el control de un promotor vírico.
Un oncogén transportado por un retrovirus se denomina v-onc;
la versión normal de ese gen se denomina c-onc. Los retrovirus que transportan
estos genes v-onc pueden infectar células normales y transformarlas en células
tumorales.
En humanos no se ha identificado ningún retrovirus de
transformación aguda. Sin embargo, los virus de RNA y de DNA contribuyen al desarrollo de cánceres humanos
de diversas maneras. Los virus que más contribuyen al desarrollo de cánceres
son los papilomavirus (HPV 16 Y 18), el virus de la leucemia humana (HTLV-1),
el virus de la hepatitis B y el virus de Epstein-Barr.
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