The Biological Basis of Cancer

Abstract

This is a revised and updated edition of a text used in undergraduate courses on cancer biology. It covers everything from the molecular basis of cancer to clinical aspects of the subject, and has a lengthy bibliography designed to assist newcomers with the cancer literature. An introduction acquaints students with the biological principles of cancer and the human dimensions of the disease by considering genuine cases of cancer in fictionalized letters. Other chapters discuss cancer pathology, metastasis, carcinogenesis, genetics, oncogenes and tumor suppressors, epidemiology, and the biological basis of cancer treatment. Also included are an appendix with descriptions of common forms of cancer, a glossary of cancer-related terms and colour plates to illustrate the pathology of many of the types of cancer discussed in the text. Upper-division undergraduates with a background in freshman biology and chemistry, as well as beginning graduate students will find this a valuable text.

Identification of a transcriptional profile associated with in vitro invasion in non-small cell lung cancer cell lines

“…These steps are disruption of the basement membrane, cell separation from the primary tumor, cell motility, invasion, penetration of the vascular system, circulation, arrest, extravasation and proliferation. 3 Work in NSCLC metastasis has identified some genes that appear important in metastasis. However, because metastasis is a multi-step process, it is likely that many genes important in this process are as yet unknown.…”

Handheld subcellular-resolution single-fiber confocal microscope using high-reflectivity two-axis vertical combdrive silicon microscanner

“…However, histopathologic examination by reflectance confocal microscopy has shown subcellular morphological changes (nuclear size, density, nuclear-cytoplasmic ratio) to be unambiguous identifiers of epithelial precancers (Carlson 2006;McKinnell et al 2006), from which 85% of cancers originate. Also, local early detection and treatment dramatically improves patient survival chances (American Cancer Society 2007).…”

Characterization of a novel endoribonuclease capable of degrading c-myc mRNA in vitro.

“…Other evidence can be seen in studies employing antisense c-myc mRNA, which causes a reduction in the number of cells capable of entering the S phase (McKinnell et al 1998). In contrast, cells expressing high levels of c-myc traverse to G, more rapidly and are more efficient in supporting replication of SV40 DNA (McKinnell et al 1998).…”

“…This cancer disease involves the reciprocal chromosomal translocation of c-myc and one of the immunoglobulin genes (McKinnell et al 1998;Dang 1999). The c-myc oncogene breakpoint is located in human chromosome 8q24 (DeVita et al 1993;McKinnell et al 1998), while the immunoglobulin genes are located at the breakpoints 14q23, 2 pl2, and 2 2 q ll (McKinnell et al 1998;Dang 1999).…”

“…This cancer disease involves the reciprocal chromosomal translocation of c-myc and one of the immunoglobulin genes (McKinnell et al 1998;Dang 1999). The c-myc oncogene breakpoint is located in human chromosome 8q24 (DeVita et al 1993;McKinnell et al 1998), while the immunoglobulin genes are located at the breakpoints 14q23, 2 pl2, and 2 2 q ll (McKinnell et al 1998;Dang 1999). Burkitt's lymphomas are believed to have abnormal expression of the c-myc oncogene after this translocation, and it is believed that this abnormal expression is a result of the proximity of the c-myc oncogene to the transcriptional control elements of immunoglobulin (Brugge et al 1991;DeVita et al 1993;Dang 1999).…”