Abstract Number: 5

Stone age surgeon versus modern medicine: Current cancer conundrums

L. Requena

Meeting: 2013 Dermcoll

Session Information

Date: -

Session Title: Keynote Session: Bench to Bedside

Session Time: -

How many cancer cells need to be killed in order to cure
patients? The premise of most surgical cures is that we are
removing or destroying all the ‘bad’ cells; we are worried
that all the cells that look atypical to the pathologist have
a similar potential to proliferate and propagate disease. Or
at least we can ’ t tell the difference. Therefore, we take
out our hatchets. For cohesive, locally invasive, slowly
growing tumors with contiguous growth patterns, the
hatchet approach has excellent cure rates. Some cancers
Dermatopathology covers a large variety of entities, some
having very similar histologic appearances. Immunohistochemistry
is an important helpful tool that is useful in diagnosis,
differential diagnosis as well as prognosis of a large
series of cutaneous neoplasms. Immunohistochemistry is also an invaluable tool for assessing the tissue of origin or direction of differentiation of neoplastic cells. In some cases, this can result in a more precise diagnosis of the skin diseases and in a more adequate treatment for the patient. This presentation will focus in the role of some recently described immunohistochemical markers in order to decide the best therapeutic option. Specifi are however not detected early or spread quickly or escape the confi nes of the bulk of the tumor and are diffi cult to cure with this approach. Most modern chemotherapy drugs kill rapidly dividing cells and many of the drugs can be somewhat targeted for the cell type of the cancer. But not all the ‘bad’ cells are rapidly dividing, and only some cancers and some patients are cured. The current exciting research endeavors are pushing to modulate biology and/or target specifi c genetic abnormalities in order to have very sharp, scalpel-like, indeed laser-like, targeted effect on the cells that have the potential to maintain and propagate the disease. review the following markers in the following situations: How close are we to that goal? For dermatologists, there are three malignant processes we can discuss: lentigo maligna, dermatofi brosarcoma protuberans, and basal cell carcinoma. For lentigo maligna, a recent study validates the success of staged excision; however there is some data that modulating immune function by using topical imiquimod to stimulate interferon may be successful. We will look at the reports available and decide the strength of the evidence. B-RAF mutations and possible future targeted therapies for malignant melanocytes is a sidebar discussion for this superficial disease but one that is very exciting. Using the hatchet for treatment of dermatofi brosarcoma protuberans is standard procedure and the technique, histologic considerations and efficacy will be reviewed. In addition, we now know the genetic defect of dermatofi brosarcoma protuberans; can our biologic scalpel be imatinib mesylate? How does it work and how likely is it to be effective? Finally, we also know the genetic defect for patients with basal cell nevus syndrome and there is now an available drug that has treated a few patients with an overwhelming burden of disease. Could that have implications for the current algorithm of treatment of sporadic basal cell carcinoma? Is it a brave new world? Are we there yet? Which will you grab: the hatchet or the biological scalpel?