Abstract
Optical characterization of biological tissue in field carcinogenesis offers a method with which to study the mechanisms behind early cancer development and the potential to perform clinical diagnosis. Previously, low-coherence enhanced backscattering spectroscopy (LEBS) has demonstrated the ability to discriminate between normal and diseased organs based on measurements of histologically normal-appearing tissue in the field of colorectal (CRC) and pancreatic (PC) cancers. Here, we implement the more comprehensive enhanced backscattering (EBS) spectroscopy to better understand the structural and optical changes which lead to the previous findings. EBS provides high-resolution measurement of the spatial reflectance profile P(rs) between 30 microns and 2.7 mm, where information about nanoscale mass density fluctuations in the mucosa can be quantified. A demonstration of the length-scales at which P(rs) is optimally altered in CRC and PC field carcinogenesis is given and subsequently these changes are related to the tissue's structural composition. Three main conclusions are made. First, the most significant changes in P(rs) occur at short length-scales corresponding to the superficial mucosal layer. Second, these changes are predominantly attributable to a reduction in the presence of subdiffractional structures. Third, similar trends are seen for both cancer types, suggesting a common progression of structural alterations in each.
Highlights
Cancer is a multistep process in which a number of smaller mutations accumulate in a stepwise fashion that eventually leads to carcinoma and metastasis
One way to conceptualize this process is through the notion of field carcinogenesis.[1]
For smaller values of rs, the effect increases in magnitude, consistent with the argument that the alterations associated with field carcinogenesis are most pronounced in the superficial mucosal layers.[4]
Summary
Cancer is a multistep process in which a number of smaller mutations accumulate in a stepwise fashion that eventually leads to carcinoma and metastasis. One way to conceptualize this process is through the notion of field carcinogenesis.[1] Under this approach to understanding carcinogenesis, several genetic/epigenetic mutations are expressed diffusely throughout a diseased organ as subtle ultrastructural transformations that constitute a “fertile field” from which further cancer progression can arise. From within this field, localized neoplasia with malignant potential emerge through stochastic mutations. The exact origin and carcinogenic advantage these transformations confer are not fully understood
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