examen 1 biomedicas

Descripcin de los exmenes

Cada examen tiene dos secciones: una de opcin mltiple y otra para llenar espacios; a cada seccin le corresponde un texto. El nmero de reactivos puede variar pero cada examen tiene entre 30 y 40 reactivos.Cada reactivo tiene tres opciones para responder. Slo una respuesta es correcta y para acreditar el examen se debe obtener mnimo el 60% de aciertos











OncogenesInstrucciones: Lee cuidadosamente el siguiente texto y escoge en la seccin correspondiente la opcin que mejor exprese lo dicho en l.

During the past few years, we have witnessed an explosion in the understanding of basic cellular and molecular biology. With advances made possible by recombinant DNA and monoclonal antibody technology, some insight has been gained into how normal cells regulate their growth and differentiation and how abnormal cells, capable of multiplying and accumulating without the usual developmental constrains, are generated. Emerging from this work is the central concept of proto-oncogenes and oncogenes: normal cellular genes (proto-oncogenes) controlling growth, development, and differentiation that somehow become misdirected (i.e. converted to oncogenes) in the neoplastic cancer cell.

The seminal discovery leading to this concept was made in the laboratories of Drs. J. Michael Bishop and Harold Varnus at the University of California, San Francisco. These scientists showed that the transforming gene src of the Rous sarcoma virus shared sequences with normal cellular genes. Subsequently they proposed that other viral oncogenes were homologous to normal cellular "proto-oncogenes" and that when these normal genes are perturbed, neoplasia eventually results hence the labeling of such genes as "enemies within."

The term "cancer" actually encompasses many different diseases, all of which are characterized by uncontrolled cell growth. Malignant cells are capable of spread or metastasis by both local invasion of adjacent normal tissue and lymphatic or hematogenous dissemination to distant sites.Theyhave somehow escaped constrains that confine normal cells to proliferate within closely defined patterns.

Our better understanding of cancer had been hampered by lack of fundamental knowledge of how normal cells become transformed. Although the mechanism of transformation is not known with certainty for any cancer, certain etiologic and predisposing actors have been well defined. Chemical carcinogens are associated with skin, lung, and bladder tumors. Radiation exposure predisposes to hematological malignancies, leukemia and lymphoma, as well as to solid tumors such as thyroid carcinoma. Hormones influence cancer cell growth as in breast and uterine tumors. Viruses have been implicated in both human and non-human T cell malignancies as well as sarcomas and epithelial neoplasms in animals.

Genetic predisposition has been noted with childhood tumors, e.g., retinoblastoma and Willms' tumor, and associated with rare familial neoplasias such as polyposis coli, neurofibromatosis, and the multiple endocrine neoplasia syndromes. Familial clustering, implying underlying genetic factors, has been reported for nearly every common malignancy including breast and colon carcinoma and the acute and chronic leukemias. Finally, syndromes characterized by chromosomal instability and ineffectual DNA repair, including Bloom's syndrome and xeroderma pigmentosum, predispose to skin cancer and other malignancies. All of these agents share the common denominator of affecting DNA, the genetic material.

Concurrent with studies of carcinogenesis have been studies of normal cellular growth and differentiation. Normal genes can be divided roughly into two categories: structural and regulatory. Originally defined for simple prokaryotes and later shown to hold for even most advanced eukaryotes, structural genes determine RNA or protein sequences used to build and run a cell, and regulatory genes govern the temporospatial expression of structural genes and other regulatory genes. In 1969 Huebner and Todaro proposed the concept that in multicellular organisms genes responsible for regulation of normal development could go awry. The result could be the misregulated growth typical of cancer. The term "oncogene" was introduced to describe such genes. And the concept became known as the oncogene hypothesis.

The oncogene hypothesis is attractive from several perspectives. First, it defines the genetic basis for cancer. Second, it links normal cellular functions of growth and differentiation (due to the actions of the oncogenes). And third, it provides the unifying theory whereby the ability of carcinogens and other genetic disturbances to contribute to oncogenesis can be explained.

This theory demands that perturbations of normal genes are necessary for cancer to emerge. Experimental evidence has confirmed the presence of a variety of genetic perturbations in human neoplasia. With human leukemias, and colon and bladder cancers, a single base pair substitution in a ras gene converts a normal allele to a transforming one. With chronic myelogenous leukemia, theshufflingof chromosomal material leads to the expression of a novel transforming protein which is the result of the fusion of two unrelated genes. Overexpression of an intact c-myc allele is seen in Burkitt's lymphomas due to an interruption of normal elements that control gene expression. Lastly, the loss of an inhibitor of transformation has been described in retinoblastomas. Furthermore, an examination of the evidence will demonstrate that an abnormality of a single gene is often insufficient to induce the fully transformed phenotype, but that, two or more genetic lesions are necessary.

Though the oncogene hypothesis has contributed greatly to the conceptual framework used in the current study of cancer, many questions have since emerged. Oncogenes as ras, src, and ski transform certain types, but induce differentiation of others. Since these are opposite processes for a cell, one must speculate the presence of cellular factors that modulate the effects of these oncogenes. Thus oncogene-cellular gene interactions as well as oncogene-oncogene interactions may play important roles in determining the final phenotype of a cancer cell.Selecciona la opcin correcta.El primer prrafo plantea

la idea de que las clulas normales regulan su crecimiento por medio de los protooncogenes y las clulas anormales guan el suyo por los oncogenes.que en los ltimos aos la comprensin de cmo las clulas regulan su crecimiento y desarrollo permite la modificacin de los oncogenes en las clulas neoplsicas.los avances hechos en la tecnologa de los anticuerpos monoclonales y el ADN recombinante propician la comprensin y la regulacin del desarrollo celular.

Los doctores Bishop y Varnus

plantearon que la secuencia de los genes normales poda alterarse y transformarse en cncer.propusieron que los genes de clulas normales compartan secuencias enteras con los genes de diferentes virus del Sarcoma.manifestaron que las neoplasias eran el resultado de genes homlogos a los de los virus carcinognicos.

En el prrafo 3 la palabra"They"se refiere a:

metstasis.clulas malignas.diferentes enfermedades.

Cul de las siguientes causas de cncer no se menciona en el prrafo 4?

Carcinognesis qumica.Exposicin a elementos radiactivos.Mutacin por radiacin solar.

Los carcinomas

de orgen gentico se manifiestan unicamente al ocurrir una reparacin del ADN.que muestran predisposicin gentica incluyen neoplasias comunes como la Histocitosis.con componente gentico subyacente se expresan principalmente en leucemias agudas y crnicas.

Huebner y Todaro

propusieron la hiptesis de que los genes se dividen en dos categoras principales, los estructurales y los regulatorios.plantearon la idea de que los genes responsables de la regulacin del crecimiento celular pudieran salirse de control.propusieron que los genes estructurales dirigen la secuencia proteica y los regulatorios ordenan la secuencia temporoespacial.

De las siguientes opciones escoge la afirmacin que ms se apega a la teora de los oncogenes.

La teora explioca el papel fundamental y exclusivo de los oncogenes en el desarrollo del cncer.Esta es una teora unificadora que asocia los diferentes carcinognicos con los trastornos genticos comunes.Esta teora esclarece la asociacin entre la diferenciacin, el crecimiento y la transformacin celular para explicar la oncognesis.

En relacin a la teora de los oncogenes hay evidencia experimental de que:

la transformacin de una protena nueva es el producto de genesnorelacionados.la sustitucin de una sola base en dos pares de bases convierte un alelo normal en uno que se transforma.la anomala de un solo gen es suficiente para inducir la completa transformacin del fenotipo.

En el prrafo 8 la palabra"shuffling"es cercana en significado a:

reordenamiento.arrastre.impulso.

Cul de los siguientes enunciados no forma parte de la hiptesis de los oncogenes?

Las diferentes interacciones de los oncogenes determinan el fenotipo final del cncer.Esta hiptesis contribuye a cuestionar los mltiples estudios sobre el cncer.Cierto tipo de oncogenes transforman las clulas e inducen cambios celulares.Assays : Tools of the New Biology

Instrucciones :Lee el siguiente artculo y escoge de la lista de palabras presentadas la que corresponde a cada espacio en blanco.

Technical advances in molecular biology and tissue culture have permitted the detailed study of specific genes in the pathogenesis of cancer. Assays have been designed to examine the major macromolecules of a cell: DNA, RNA, and proteins. In addition, cell culture techniques and the use of genetically defined experimental animals allow for the identification of factors necessary for transformation.

In general, the power of these_____1_____lies first in their ability to sort and_____2_____specific macromolecules among a large population of like_____3_____, and second in their capacity to expand and purify to a_____4_____degree a macromolecule of interest , such that structural and functional_____5_____can be performed. Methods for analyzing DNA require the_____6_____to cleave DNA at specific sites, to sort the difference fragments according to a_____7_____characteristic (e.g. , size), and to identify pertinent fragments that include DNA_____8_____of interest. This is accomplished by restriction endonuclease digestion, agarose gel electrophoresis, and Southern blot hybridization. DNA fragments can be_____9_____and expanded for more detailed studies by employing_____10_____whereby individual fragments are_____11_____into separate bacteria or phage. A "library" of these fragments can be_____12_____which may cover the entire genome and from this_____13_____, pertinent clones can be identified and expanded. Once significant quantities of_____14_____DNA are obtained, then direct DNA_____15_____of the segment can be determined through_____16_____developed by Sanger or Maxam and Gilbert. Similar techniques for sorting , probing, and isolating RNA (Northern blotting, cDNA cloning) and proteins (monoclonal and polyclonal antibodies, Western blotting) also have been_____17_____.

Cell culture techniques have been invaluable in_____18_____those factors necessary for cell growth, and for_____19_____a difference between normal and transformed cells. Immortalized cell_____20_____, both transformed and non transformed, have permitted study of the cellular_____21_____of oncogenes and their gene products. The ability to isolate or clone individual cells yielding a homogenous_____22_____for experimentation, and the capacity to_____23_____this cell population in order that sufficient material is made available for study are further benefits afforded by these techniques. The study of oncogenes depends, therefore, on the integration of knowledge obtained utilizing all these techniques.Mostrar las preguntas una a unaSelecciona la opcin correcta. Cuando termines, haz clic en el botnTerminar Examen.

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examen 1 biomedicas

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