LWBK1006-17 LWW-Govindan-Review December 7, 2011 21:14
Chapter 17•Cancer of the Head and Neck 199ANSWERS
Answer 17.1. The answer is D.
Dr. Sriranski has proposed a molecular progression model of the develop-
ment of SCCHN based on analysis of the 10 most common allelic changes
found in these malignancies. The earliest events appear to be the loss of
9p and 3p given that these are found in preinvasive lesions. This is to
be followed soon afterward by the loss of 17p. The loss of 11q, 13q,
14q, and p53 mutation is not typically found in preinvasive lesions and,
therefore, must be a later event.Answer 17.2. The answer is A.
EGFR plays a key role in the development of SCCHN. There is often
a moderate increase in the number of copies of this gene. EGFR over-
expression leads to activation of multiple signaling pathways that lead
to cell growth and resistance to apoptosis. Evidence suggests that EGFR
overexpression can lead to an increase in vascular endothelial growth
factor production, leading to angiogenesis. Analysis of EGFR expression
in archived tumor tissue from a prospective clinical trial suggests that
EGFR overexpression is associated with resistance to radiation therapy.
Even though erlotinib is a small molecule inhibitor of the EGFR tyro-
sine kinase domain, it has not been shown so far to be effective in the
treatment of SCCHN while cetuximab has shown a survival benefit when
given concurrently with radiation for locally advanced or used as a part
of treatment for distantly metastatic disease.Answer 17.3. The answer is D.
Several risk factors for the development of SCCHN have been identified.
The two most important are tobacco and alcohol use. They seem to be
synergistic. Other risk factors include occupational exposure to chemicals
and irritants, such as aromatic hydrocarbons and wood dust, and viruses,
such as HPV and EBV. In addition, patients with Fanconi’s anemia are at
increased risk.Answer 17.4. The answer is C.
It has been recognized recently that HPV is the primary cause of many
squamous cell cancers of the oropharynx. HPV DNA can be found in
approximately 50% of tonsil and base of tongue tumors. These tumors
are often described as having a basal cell-like appearance and are fre-
quently nonkeratinizing. These tumors are more commonly found in
never smokers. In general, these tumors carry a better prognosis than other
tumors of the head and neck. The overall survival and disease-free survival
are improved, and the risk of second primaries is lower compared with
non–HPV-associated tumors. Patients with HPV-associated SCCHN have
better response to chemotherapy than patient s with tobacco-smoking-
associated SCCHN.