Oncogenes and Leukemia
Oncogenes and Leukemia
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In recent years, major progress has been made in the fields of cancer research. These advances have begun to elucidate the cytogenetic mechanisms responsible for neoplastic change. Several oncogenes have been implicated in the etiology of leukemia. The work is providing new insight into the pathogenesis of these diseases. Cell growth and cell differentiation are dynamic processes. The physiologic mechanisms involved result in enormous diversity of cellular structure and function. In higher organisms this diversity is necessary for normal homeostasis. When the processes malfunction, however, the result is often cancer. Cancer can be characterized as a disorder of cell proliferation. It occurs in many different forms and may result from a variety of factors. These diseases represent a significant threat to human health; they are currently responsible for inestimable suffering. Moreover, the incidence of cancer could be reduced. The development of different cell types is highly regulated (62:3). Normal tissue homeostasis is achieved through properly timed cell growth. Cells must respond appropriately to both external and internal signals (42:23). In cancer, control of these events is disrupted. As a response to changes in their genetic material, cells simply continue to proliferate. In the early stages of the disease, cancerous cells merely accumulate in excessive numbers at their site of origin (18:16). The simples
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in the unregulated proliferation of morphologically identical small to medium size lymphocytes. Surface immunoglobulin and glucose6phosphate dehydrogenase isoenzyme studies have revealed that these cells are monoclonal in origin. In addition, although they may appear fully mature, the cells are generally only of intermediate differentiation. Thus, malignant CLL cells actually exist in a state of developmental arrest. As they multiply, they accumulate in the peripheral blood, bone marrow, lymph nodes, and spleen.
CLL symptoms include a slowly progressive lymphocytosis, lymphadenopathy, and splenomegaly. With lymphadenopathy, the lymph nodes are typically soft, painless, discrete, and rubbery. As the disease progresses though, lymphocytic infiltration of their capsules may cause the nodes to stick together and form large masses. In advanced splenomegaly cases, the organ may grow to over 1,000 grams.
In general though, CLL tends to be an indolent neoplasm. Survival times are variable, ranging from 1 to 15 years. Advanced disease is marked by extensive replacement of the bone marrow. These patients may have compromised immune systems, neutropenia, anemia, thrombocytopenia, and hypogammaglobulinemia. In persons who d
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Some common words found in the essay are:
HTLVI HTLVI, Cancer Society, CML AML, Cancer Cell, Ph+ AML, Finally Ph, L3 Acute, Nras Initially, Normally Bcell, Chromosome Abnormalities, bone marrow, tcell receptor, chromosomal abnormalities, cml patients, abl gene, exon 2, chromosome 9, chromosome 22, growth factors, growth factor, breakpoint cluster region, acute lymphocytic leukemia, exons 1a 1b, 210 kd protein, acute myelocytic leukemia,
Approximate Word count = 9434
Approximate Pages = 38 (250 words per page)
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