Xem 1-20 trên 106 kết quả Cancer progression
  • Harrison's Internal Medicine Chapter 79. Cancer Genetics Cancer Is a Genetic Disease Cancer arises through a series of somatic alterations in DNA that result in unrestrained cellular proliferation. Most of these alterations involve actual sequence changes in DNA (i.e., mutations). They may arise as a consequence of random replication errors, exposure to carcinogens (e.g., radiation), or faulty DNA repair processes. While most cancers arise sporadically, familial clustering of cancers occurs in certain families that carry a germline mutation in a cancer gene.

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  • According to the National Cancer Institute, cancer continues to take a devastating toll. Among women in the United States, cancer is the second-leading cause of death after heart disease. Medical researchers fighting against cancer have made significant progress, however. In recent years, cancer incidence rates have been stable, and—although the annual rate of decline in cancer death rates among men have been twice as large as the declines in women—mortality has decreased for ten of the top 15 cancers in women.

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  • Over the last three decades, knowledge on the molecular biology of human cancers has vastly expanded. A host of genes and proteins involved in cancer development and progression have been defined and many mechanisms at the molecular, cellular and even tissue level have been, at least partly, elucidated. Insights have also been gained into the molecular mechanisms underlying carcinogenesis by chemical, physical, and biological agents and into inherited susceptibility to cancer. Accordingly, Part I of the book presents many of the molecules and mechanisms generally important in human cancers.

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  • Over the past 20 years, technological advances in molecular biology have proven invaluable to the understanding of the pathogenesis of human cancer. The application of molecular technology to the study of cancer has not only led to advances in tumor diagnosis, but has also provided markers for the assessment of prognosis and disease progression. The aim of Molecular Analysis of Cancer is to provide a comprehensive collection of the most up-to-date techniques for the detection of molecular changes in human cancer.

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  • In spite of the massive efforts being made worldwide to understand molecular genetics and epigenetic factors responsible for the initiation and progression of cancer, the statistics on this malignancy have remained enormously negative; the following data testify to this unfortunate human condition. There are more than 100 types of cancers that can inflict any part of the body. In 2005, 7.6 million people died of cancer, which makes up 13% of the 58 million deaths worldwide. Approximately 1.

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  • Pain Pain occurs with variable frequency in the cancer patient: 25–50% of patients present with pain at diagnosis, 33% have pain associated with treatment, and 75% have pain with progressive disease. The pain may have several causes. In ~70% of cases, pain is caused by the tumor itself—by invasion of bone, nerves, blood vessels, or mucous membranes or obstruction of a hollow viscus or duct.

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  • Figure 80-6 Oncogene signaling pathways are activated during tumor progression and promote metastatic potential. This figure shows a cancer cell that has undergone epithelial to mesenchymal transition (EMT) under the influence of several environmental signals. Critical components include activated transforming growth factor beta (TGF-β) and the hepatocyte growth factor (HGF)/c-Met pathways, as well as changes in the expression of adhesion molecules that mediate cell-cell and cellextracellular matrix interactions.

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  • Cancer Chemoprevention Chemoprevention involves the use of specific natural or synthetic chemical agents to reverse, suppress, or prevent carcinogenesis before the development of invasive malignancy. Cancer develops through an accumulation of genetic and epigenetic changes that are potential points of intervention to prevent cancer. The initial changes are termed initiation. The alteration can be inherited or acquired through the action of physical, infectious, or chemical carcinogens.

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  • Signaling Pathways Downstream of Rtks: Ras and PI3K Several oncogene and tumor-suppressor gene products are components of signal transduction pathways that emanate from RTK activation (Fig. 80-2). The most extensively studied are the Ras/mitogen-activated protein (MAP) kinase pathway and the phosphatidylinositol-3-kinase (PI3K) pathway, both of which regulate multiple processes in cancer cells, including cell cycle progression, resistance to apoptotic signals, angiogenesis, and cell motility.

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  • Karnofsky was among the first to champion the evaluation of a chemotherapeutic agent's benefit by carefully quantitating its effect on tumor size and using these measurements to objectively decide the basis for further treatment of a particular patient or further clinical evaluation of a drug's potential.

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  • Clinical Features About 10% of esophageal cancers occur in the upper third of the esophagus (cervical esophagus), 35% in the middle third, and 55% in the lower third. Squamous cell carcinomas and adenocarcinomas cannot be distinguished radiographically or endoscopically. Progressive dysphagia and weight loss of short duration are the initial symptoms in the vast majority of patients. Dysphagia initially occurs with solid foods and gradually progresses to include semisolids and liquids.

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  • Cancer arises through a series of somatic alterations in DNA that result in unrestrained cellular proliferation. Most of these alterations involve actual sequence changes in DNA (i.e., mutations). They may arise as a consequence of random replication errors, exposure to carcinogens (e.g., radiation), or faulty DNA repair processes. While most cancers arise sporadically, familial clustering of cancers occurs in certain families that carry a germline mutation in a cancer gene.

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  • It is becoming increasingly clear that signals generated in tumor microenvi-ronments are crucial to tumor cell behavior, such as survival, progression and metastasis. The establishment of these malignant behaviors requires that tumor cells acquire novel adhesion and migration properties to detach from their original sites and to localize to distant organs.

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  • Direct DNA-Interactive Agents DNA replication occurs during the synthesis or S-phase of the cell cycle, with chromosome segregation of the replicated DNA occurring in the M, or mitosis, phase. The G1 and G2 "gap phases" precede S and M, respectively. Historically, chemotherapeutic agents have been divided into "phase-nonspecific" agents, which can act in any phase of the cell cycle, and "phase-specific" agents, which require the cell to be at a particular cell cycle phase to cause greatest effect.

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  • Antibodies In general, antibodies are not very effective at killing cancer cells. Because the tumor seems to influence the host toward making antibodies rather than generating cellular immunity, it is inferred that antibodies are easier for the tumor to fend off. Many patients can be shown to have serum antibodies directed at their tumors, but these do not appear to influence disease progression. However, the ability to grow very large quantities of high-affinity antibody directed at a tumor by the hybridoma technique has led to the application of antibodies to the treatment of cancer.

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  • It is innately human to comfort and provide care to those suffering from cancer, particularly those close to death. Yet what seems self-evident at an individual, personal level has, by and large, not guided policy at the level of institutions in this country. There is no argument that palliative care should be integrated into cancer care from diagnosis to death.

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  • Matrix metalloproteinases (MMPs) consist of a multigene family of zinc-dependent extracellular matrix (ECM) remodeling endopeptidases implicated in pathological processes, such as carcinogenesis. In this regard, their activity plays a pivotal role in tumor growth and the multistep processes of invasion and metastasis, including proteolytic degradation of ECM

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  • Previously, we demonstrated apoptotic cell death in the chorion laeve trophoblast layer of human fetal membrane tissues during the late stages of pregnancy, the progression of apoptosis during incubation in vitro, and its suppression by a low concentration of glucocorticoid hormones.

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  • Standard treatment of anal cancer is a protocol of combined chemotherapy and radiotherapy. Typically, a diagnosis of LSIL results only in more frequent monitoring in case it progresses to HSIL. When HSIL is diagnosed, treatment may be called for to reduce the likelihood of progres- sion to cancer. This may include surgical removal of the lesions. Data on the efficacy of treatment are scarce. However, treatment of cervical lesions has been shown to be effective in substantially reducing the risk of progression to cancer....

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  • Vaccinating girls and women before sexual debut, and therefore before exposure to HPV infection, provides an excellent opportunity to decrease the incidence of cervical cancer over time. As these vaccines protect against HPV types responsible for about 70% of cervical cancers, there will be a continued need to screen women who have been vaccinated as well as those who have not been vaccinated.

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