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Papers by Naty Lopez Rodriguez

Cold Spring Harbor Symposia on Quantitative Biology, 2005

The molecular pathology of cancer and possible new therapies have been a major concern of molecul... more The molecular pathology of cancer and possible new therapies have been a major concern of molecular biology since the first gene cloning experiments opened the possibility to clone, sequence, and study mutations in tumor cells. The very early observations of chromosomal changes in tumor cells (Boveri 1914) reflected genomic instability and raised the possibility of mutant proteins on the cancer cell surface to which antibodies might bind and elicit specific cell killing. There are a few examples of this, and most mutant proteins are firmly ensconced inside the cells and not available for antibody-mediated cell killing. Thus, although many mutations have been discovered, few specific therapies have been developed based on the molecular observations. Nevertheless, the cancer-specific mutations remain tantalizing targets for new cancer therapies. Cancers have somatic mutations ranging from point mutations in genes like those of the RAS family (for review, see Hanahan and Weinberg 2000), which create constitutively active signal transduction molecules (Fig. 1), to genes activated after chromosomal translocations, such as the CMYC gene in Burkitt's lymphoma, and to fusion genes created uniquely in cancer cells by chromosomal translocations, such as the BCR-ABL gene fusion (for review, see Rabbitts 1994). As a range of genes involved in chromosomal translocations was identified, some common features began to emerge, especially in the acute cancers (hematopoietic and mesenchymal tumors) which invariably involve transcription factors whose normal role in cell fate decisions (Cleary 1991; Rabbitts 1991) is subverted (the master gene model; Rabbitts 1991). These transcription factors are often involved in protein-protein interactions. For instance, the T-cell leukemia genes LMO2 and TAL1/SCL are activated by distinct chromo

Cold Spring Harbor Symposia on Quantitative Biology, 2005

The molecular pathology of cancer and possible new therapies have been a major concern of molecul... more The molecular pathology of cancer and possible new therapies have been a major concern of molecular biology since the first gene cloning experiments opened the possibility to clone, sequence, and study mutations in tumor cells. The very early observations of chromosomal changes in tumor cells (Boveri 1914) reflected genomic instability and raised the possibility of mutant proteins on the cancer cell surface to which antibodies might bind and elicit specific cell killing. There are a few examples of this, and most mutant proteins are firmly ensconced inside the cells and not available for antibody-mediated cell killing. Thus, although many mutations have been discovered, few specific therapies have been developed based on the molecular observations. Nevertheless, the cancer-specific mutations remain tantalizing targets for new cancer therapies. Cancers have somatic mutations ranging from point mutations in genes like those of the RAS family (for review, see Hanahan and Weinberg 2000), which create constitutively active signal transduction molecules (Fig. 1), to genes activated after chromosomal translocations, such as the CMYC gene in Burkitt's lymphoma, and to fusion genes created uniquely in cancer cells by chromosomal translocations, such as the BCR-ABL gene fusion (for review, see Rabbitts 1994). As a range of genes involved in chromosomal translocations was identified, some common features began to emerge, especially in the acute cancers (hematopoietic and mesenchymal tumors) which invariably involve transcription factors whose normal role in cell fate decisions (Cleary 1991; Rabbitts 1991) is subverted (the master gene model; Rabbitts 1991). These transcription factors are often involved in protein-protein interactions. For instance, the T-cell leukemia genes LMO2 and TAL1/SCL are activated by distinct chromo