Identifying the pathways activated and critical for cancer initiation and subsequent spread (invasion and metastasis) are essential for improved cancer therapies. Over the past 35 years, many genes have been identified which can cause or contribute to cancer. These include two major classes of genes, oncogenes and tumor suppressor genes. In some cases the genetic culprit involved in a particular cancer may be known, however, in most cases there are multiple genetic and epigenetic events occurring simultaneously which can interact and result in cancer cell formation and metastasis. In addition, there are other important contributions by the tumor microenvironment which can lead to the progression of cancer as well as resistance to various therapeutic approaches.
Increased NGAL (Lnc2) expression after chemotherapeutic drug treatment / W.H. Chappell; S.L. Abrams; K.M. Stadelman; M.M. LaHair; R.A. Franklin; L. Cocco; C. Evangelisti; F. Chiarini; A.M. Martelli; L.S. Steelman; J.A. McCubrey.. - In: ADVANCES IN BIOLOGICAL REGULATION. - ISSN 2212-4926. - STAMPA. - 53:(2013), pp. 146-155. [10.1016/j.jbior.2012.09.004.]
Increased NGAL (Lnc2) expression after chemotherapeutic drug treatment.
COCCO, LUCIO ILDEBRANDO;C. Evangelisti;MARTELLI, ALBERTO MARIA;
2013
Abstract
Identifying the pathways activated and critical for cancer initiation and subsequent spread (invasion and metastasis) are essential for improved cancer therapies. Over the past 35 years, many genes have been identified which can cause or contribute to cancer. These include two major classes of genes, oncogenes and tumor suppressor genes. In some cases the genetic culprit involved in a particular cancer may be known, however, in most cases there are multiple genetic and epigenetic events occurring simultaneously which can interact and result in cancer cell formation and metastasis. In addition, there are other important contributions by the tumor microenvironment which can lead to the progression of cancer as well as resistance to various therapeutic approaches.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
