Table of Contents
1
UI - 11914946
AU - Issing PR; Hemmanouil I; Wilkens L; Karstens H; Lenarz T
TI -
[Long term results in adenoidcystic carcinoma]
SO - Laryngorhinootologie 2002 Feb;81(2):98-105
AD - Klinik fur Hals-Nasen-Ohrenheilkunde, Medizinische Hochschule Hannover.
issing@hno.mh-hannover.de
BACKGROUND: Due to the discreet initial symptoms and the locally
aggressive infiltration with perineural spread the adenoidcystic
carcinoma (ACC) presents a special diagnostical and therapeutical
challenge. PATIENTS:: In a retrospective study the forms of 54 patients
were analysed, whose average age was 55.5 (24 - 77) years. RESULTS: The
sex ratio showed a slight female preponderance with 57 % to 43 %. The
major salivary glands were affected in 26 cases. The exact distribution
of the ACC was: parotid gland (n = 18), submandibular gland (n = 8),
oral cavity (n = 10), paranasal sinuses (n = 11), nasopharynx (n = 4)
and larynx (n = 3). The most common symptoms were a tumor-related
swelling and pain which persisted for a duration of several months after
final diagnosis could be established. Facial palsy was observed in 4
patients. Histological examination revealed a tubular subtype in 4
cases, in 28 cases a cribriforme and in 12 cases a solid subtype. No
definitive differentiation was possible in 10 specimens. The skull base
was infiltrated in 16 patients. Except one patient all 54 underwent
surgical therapy. Postoperative radiotherapy was additionally given in
25 cases which was combined with a chemotherapy in 6 patients.
Nevertheless ACC recurred in 60 % of our patients. Lymphnode metastases
were observed in 13 patients after a latency of 3.3 years in average,
but predominantly pulmonary metastases as distant spread developed in 18
patients after 5.8 years significantly later. The overall survival rate
was 84.38 % after 2 years, 75.90 % after 5 years, 50.49 % after 10 years
and 20.11 % after 20 years. Male sex, infiltration of the skull base and
histological evidence of perineural and perivascular spread proved to be
statistically significant factors for an unfavourable prognosis.
CONCLUSIONS: Due to the uncommon biological behaviour with a slow growth
on the one hand side and an aggressive local invasion on the other hand
side the ACC can be regarded as a challenging malignant disease for the
clinician whose adequate therapy does not allow any standardized regime.
The tendency for recurrence even after a period clinically free of
symptoms makes a life long follow-up mandatory.
2
UI - 11771019
AU - Kirkbride P; Liu FF; O'Sullivan B; Payne D; Warde P; Gullane P; Pintilie
TI -
M; Keane TJ; Cummings B
Outcome of curative management of malignant tumours of the parotid
gland.
SO - J Otolaryngol 2001 Oct;30(5):271-9
AD - Department of Radiation Oncology, Princess Margaret Hospital, University
Health Network, University of Toronto, Ontario.
PURPOSE: The optimal management of malignant parotid gland tumours
remains to be defined precisely. Specifically, a further understanding
of the tumour features that influence treatment outcome is needed.
MATERIALS AND METHODS: A retrospective review was conducted on 184
patients who were registered at the Princess Margaret Hospital with a
diagnosis of a primary malignant parotid gland tumour. RESULTS: All
patients were initially managed with a parotidectomy, and postoperative
x-ray radiation therapy (XRT) was administered to 159 patients. The
actuarial 5-year cause-specific survival and locoregional control rates
were 76% and 81%, respectively. The survival and locoregional control
rates for patients treated with surgery alone versus surgery plus
postoperative XRT were not statistically different. A multiple
regression analysis identified only age and tumour category to be
independently significant prognostic factors for both survival and
locoregional control. CONCLUSION: We would recommend that patients with
malignant parotid gland tumours be managed with parotidectomy, followed
by postoperative XRT for tumours with residual disease, aggressive
histology, and/or positive lymph nodes.
3
UI - 11771010
AU - Hay MA; Witterick IJ; Mock D
TI -
Recurrent pleomorphic adenoma of the parotid gland with cervical
metastasis.
SO - J Otolaryngol 2001 Dec;30(6):361-5
AD - Department of Orolaryngology, Mount Sinai Hospital, Toronto, Ontario.
4
UI - 11770018
AU - Triantafyllou A
TI -
Acinar phenotypes in salivary pleomorphic adenoma: unusual
differentiation or disordered functional activity?
SO - Pathol Res Pract 2001;197(11):743-51
AD - Oral Pathology Laboratory, Liverpool University Dental Hospital and
School of Dentistry, The University of Liverpool, United Kingdom.
A.Triantafyllou@liverpool.ac.uk
To explain the occurrence in salivary pleomorphic adenoma of structures
with an arrangement and appearance of tumour cells resembling acini, two
tumours showing such structures and, for comparison, a tumour showing
goblet cells were examined with the use of histochemistry and
immunocytochemistry for constituents of the salivary secretory process.
One tumour consisted mainly of slightly granular cells with an acinar
arrangement, which contained neutral and carboxylated glycoproteins, -SH
groups and cytoplasmic epithelial membrane antigen. The second tumour
showed a minor component of structures resembling mucous acini, which
contained neutral and carboxylated glycoproteins, -SS- groups and
fucoglycoconjugates. The goblet cells of the third tumour contained
sulphated glycoproteins and were associated with cystic lumina. Acinar
phenotypes in salivary pleomorphic adenoma could reflect either an
unusual line of differentiation or luminal cells with increased
synthesis and/or retention of variably mature glycoproteins different
from those of goblet cells. Disordered secretion and externalization of
glycoproteins are possible factors influencing phenotypes in this
tumour.
5
UI - 11829237
AU - Ohki K; Kumamoto H; Ichinohasama R; Suzuki M; Yamaguchi T; Echigo S;
TI -
Motegi K; Ooya K
Genetic analysis of DNA microsatellite loci in salivary gland tumours:
comparison with immunohistochemical detection of hMSH2 and p53 proteins.
SO - Int J Oral Maxillofac Surg 2001 Dec;30(6):538-44
AD - Department of Oro-Maxillofacial Surgical Science, Tohoku University
Graduate School of Dentistry, Sendai, Japan.
To investigate genetic alterations in salivary gland tumours,
microsatellite instability at eight representative loci and loss of
heterozygosity (LOH) on chromosome 17 were analysed by polymerase chain
reaction amplification. The results were compared with
immunohistochemical expression of the hMSH2 and p53 proteins.
Microsatellite instability and expression loss of hMSH2 protein were not
recognized in the salivary gland tumours, suggesting a low frequency of
abnormalities of the mismatch repair system. LOH associated with the p53
gene was detected in approximately one-half of pleomorphic adenomas and
salivary carcinomas, which often showed strong p53 immunoreactivity.
These features suggest that the p53 gene plays an important role in
malignant transformation of salivary gland tumours. The genetic
characteristics of pleomorphic adenomas might reflect a low-grade
potential for malignant progression.
6
UI - 11757975
AU - Kempf VA; Petzold H; Autenrieth IB
TI -
Cat scratch disease due to Bartonella henselae infection mimicking
parotid malignancy.
SO - Eur J Clin Microbiol Infect Dis 2001 Oct;20(10):732-3
AD - Institut fur Medizinische Mikrobiologie, Eberhard-Karls-Universitat,
Tubingen, Germany. volkhard.kempf@med.uni-tuebingen.de
An unusual Bartonella henselae infection presenting clinically as a
putative parotid cancer was diagnosed based on serological tests,
histomorphology and amplification of a 16S-rDNA sequence of Bartonella
henselae. The patient improved greatly upon antibiotic treatment and did
not require surgery. Although uncommon, infection with Bartonella spp.,
particularly Bartonella henselae, should be included in the differential
diagnosis of parotid tumors.
7
UI - 11893982
AU - Kosnik SD; Emmons WW; Pitman KT
TI -
Parotid abscess caused by Salmonella enteriditis in a patient with
parotid masses.
SO - Am J Otolaryngol 2002 Mar-Apr;23(2):119-21
AD - Naval Medical Center Portsmouth, Portsmouth, VA 23708-5000, USA.
8
UI - 11915613
AU - Hallacq P; Labrousse F; Roullet B; Orsel S; Bessede JP; Moreau JJ
TI -
[Adenoid cystic carcinomas invading the skull base. Apropos of 4 cases
and review of the literature]
SO - Neurochirurgie 2001 Dec;47(6):542-51
AD - Service de Neurochirurgie, CHU Dupuytren, 87042 Limoges.
paulhallacq@nomade.fr
Head and neck adenoid cystic carcinomas may invade the adjacent skull
base by bone lysis and/or by perinervous and perivascular spread within
the skull base foramina. Neurosurgical decision making is not well
defined regarding the extent of intracranial tumor component removal, as
neurosurgical expertise is limited for this peculiar type of tumors. The
issue is to decide whether a radical supposedly locally curative surgery
should be attempted, or if a large non disfigurating surgery is
mandatory, keeping in mind the frequency of local recurrences and of
distant metastases. Over a 13-year period, four adenoid cystic
carcinomas invading the skull base were operated on at our institution:
two tumors originated in the parotid gland, one in the sphenoid sinus,
and one in the ethmoid sinus. Surgical removal was total in one case,
subtotal in three cases. Post-operative irradiation was delivered in the
four patients (two neutron irradiation, two conventional). One patient
with advanced metastatic disease was submitted to chemotherapy. Three
patients died from local tumor progression and distant metastases within
three years after the intracranial tumor extension has been diagnosed.
The patient with an ethmoid tumor is still alive seven years after
surgery without any evidence of local tumor progression nor distant
metastases. Surgery remains the gold standard treatment for adenoid
cystic carcinomas invading the skull base. However, in our opinion a
large tumor removal, without or with bone osteotomies, but without
sacrifice of cranial nerves, cavernous sinus, internal carotid artery,
and of the orbit allows patient survival with an acceptable comfort and
absence of psychological distress due to disfigurating surgery nor
surgically induced neurological functional deficit. Post-operative
irradiation may sometimes stabilize locally the lesions. The place of
chemotherapy has, yet, to be determined.
9
UI - 11944908
AU - Hino S; Kawamata H; Omotehara F; Uchida D; Miwa Y; Begum NM; Yoshida H;
TI -
Sato M; Fujimori T
Cytoplasmic TSC-22 (transforming growth factor-beta-stimulated clone-22)
markedly enhances the radiation sensitivity of salivary gland cancer
cells.
SO - Biochem Biophys Res Commun 2002 Apr 12;292(4):957-63
AD - Second Department of Oral and Maxillofacial Surgery, Tokushima
University School of Dentistry, 3-18-15 Kuramoto, Tokushima, 770-8504,
Japan.
We transfected a salivary gland cancer cell line, TYS, with three
different forms of TSC-22 (transforming growth factor-beta-stimulated
clone-22) gene: full-length TSC-22 (TSC-22FL) containing nuclear export
signal, TSC-box and leucine zipper, truncated TSC-22 (TSC-22LZ)
containing only TSC-box and leucine zipper, and truncated TSC-22 with
nuclear localization signal (NLS-TSC-22LZ). High expression of TSC-22FL
in the cytoplasm markedly enhanced the radiation-sensitivity of TYS
cells, while, moderate expression of TSC-22FL marginally affected the
radiation-sensitivity. TSC-22LZ, which was expressed in the cytoplasm
and the nucleus, enhanced the radiation-sensitivity of TYS cells
irrespective to its expression level. NLS-TSC-22LZ, which was expressed
only in the nucleus, marginally affected the radiation-sensitivity of
the cells even at high expression level. Interestingly, cytoplasmic
TSC-22 translocates to nucleus concomitant with radiation-induced
apoptosis. These results suggest that cytoplasmic localization of TSC-22
and translocation of TSC-22 from cytoplasm to nucleus is important for
regulating the cell death signal after irradiation-induced DNA damage.
(c)2002 Elsevier Science (USA).
10
UI - 11987951
AU - Loreti A; Sturla M; Gentileschi S; Bracaglia R; Prat Y; Fadda G; Farallo
TI -
E
Diffuse hyperplastic oncocytosis of the parotid gland.
SO - Br J Plast Surg 2002 Mar;55(2):151-2
AD - Division of Plastic Surgery, 'A. Gemelli' Medical School, Universita
Cattolica del Sacro Cuore, Policlinico 'A. Gemelli', Rome, Italy.
Oncocytic tumours rarely affect the major salivary glands, accounting
for less than 1% of all salivary-gland tumours. The World Health
Organisation classification groups these tumours into three principal
types: diffuse oncocytosis, focal adenomatous oncocytic hyperplasia and
oncocytoma. Diffuse hyperplastic oncocytosis is the rarest lesion: only
six cases have been previously reported in the literature. This
condition of putative hyperplastic pathogenesis follows a benign course,
whereas oncocytomas may recur after excision. No metastatic
dissemination or recurrence of diffuse hyperplastic oncocytosis has been
reported. We present and discuss a new case of diffuse hyperplastic
oncocytosis of the parotid gland. Copyright 2002 The British Association
of Plastic Surgeons.
11
UI - 11836609
AU - Asaumi J; Higuchi Y; Matsuzaki H; Murakami J; Kawasaki S; Kuroda M;
TI -
Shibuya K; Konouchi H; Hisatomi M; Wakasa T; Kishi K; Hiraki Y
Thermochemotherapy of a human salivary adenocarcinoma cell line.
SO - Oncol Rep 2002 Mar-Apr;9(2):365-9
AD - Department of Oral and Maxillofacial Radiology, Field of Tumor Biology,
Graduate School of Medicine and Dentistry, Okayama University Graduate
Schools, Okayama 700-8525, Japan. asaumi@md.okayama-u.ac.jp
We report on thermochemotherapy in a human salivary gland adenocarcinoma
cell line. Hyperthermia reduced the survival rate to 50 and 20% by
heating at 43 degrees C for 40 and 60 min, respectively, and is by
itself useful in human salivary gland carcinoma treatment. Adriamycin,
cisplatin, and mitomycin C can possible be used clinically, while
bleomycin and 5-fluorouracil cannot, to treat this carcinoma. The
optimal temperature was considered to be 41 degrees C in adriamycin, 42
degrees C in cisplatin, 37 degrees C in mitomycin C, and 42 degrees C in
bleomycin in the thermochemotherapy. Thermochemotherapy is a useful tool
in the treatment of human salivary gland carcinoma cells, but it is
necessary to select the best anticancer drugs and the optimal
temperature for optimal success using this treatment.
12
UI - 11836610
AU - Hino S; Kawamata H; Omotehara F; Uchida D; Begum NM; Yoshida H; Sato M;
TI -
Fujimori T
Leucine zipper structure of TSC-22 (TGF-beta stimulated clone-22)
markedly inhibits the anchorage-independent growth of salivary gland
cancer cells.
SO - Oncol Rep 2002 Mar-Apr;9(2):371-4
AD - Second Department of Oral and Maxillofacial Surgery, Tokushima
University School of Dentistry, Tokushima 770-8504, Japan.
Several investigators have demonstrated that TGF-beta stimulated
clone-22 (TSC-22) regulates cell growth and differentiation, and cell
death. TSC-22 is a putative transcriptional regulator containing a
leucine zipper-like structure and a nuclear export signal. We previously
showed the cytoplasmic localization of TSC-22 and the nuclear
translocation of TSC-22 concomitant with induction of apoptosis in
salivary gland cancer cells. In the present study, we attempted to
identify the active domain of TSC-22 protein that regulated the
biological functions of TSC-22. We constructed three mammalian
expression vectors, which could produce full length TSC-22 only in
cytoplasm, the leucine zipper structure of TSC-22 in both cytoplasm and
nucleus, and the leucine zipper structure only in nucleus. Then, we
transfected a salivary gland cancer cell line, HSG with these expression
vectors, and investigated the growth profile of the transfectants. None
of the TSC-22 constructs inhibited the monolayer growth and the
anchorage-dependent colony formation of HSG cells. However, the leucine
zipper structure of TSC-22 markedly inhibited the anchorage-independent
colony formation of HSG cells (p<0.001; one way ANOVA). Full length
TSC-22 also suppressed the anchorage-independent colony formation of HSG
cells, although the effect of full length TSC-22 was much lower than
those of the leucine zipper constructs. These observations suggest that
the leucine zipper structure in TSC-22 protein is an active domain that
negatively regulates the growth of salivary gland cancer cells.
13
UI - 11879932
AU - Claros P; Dominte G; Claros A; Castillo M; Cardesa A; Claros A
TI -
Parotid gland mucoepidermoid carcinoma in a 4-year-old child.
SO - Int J Pediatr Otorhinolaryngol 2002 Mar 15;63(1):67-72
AD - Clinica Claros, Los Vergos, 31, 08017 Barcelona, Spain.
clinica@clinicaclaros.com
Salivary gland tumors account for less than 5% of the head and neck
neoplasms. Among them, mucoepidermoid carcinoma is the most common
malignant salivary gland tumor. About 45% of mucoepidermoid carcinomas
occur in the parotid gland, and appear around the fifth decade of life,
being unusual in children under 10 years. We report a case of a parotid
mass arising in a 4-year-old female, who had no lateral adenopathy.
After histological examination, the diagnosis was of a low-grade
mucoepidermoid carcinoma of the parotid gland. Three years after surgery
no recurrence was observed. As a conclusion, although rare, the presence
of a parotid mass with progressive growth in children could correspond
to a neoplasm.
14
UI - 11991586
AU - Yencha MW
TI -
Primary parotid gland Hodgkin's lymphoma.
SO - Ann Otol Rhinol Laryngol 2002 Apr;111(4):338-42
AD - Department of Otolaryngology-Head and Neck Surgery, Naval Hospital,
Pensacola, Florida, USA.
Hodgkin's lymphoma with its primary manifestation in the parotid gland
is an exceedingly rare entity and is not usually suspected in the
initial evaluation of a parotid mass. Because it is not suspected, the
results of fine-needle aspiration cytology are often misleading, and
parotidectomy is needed for a definitive diagnosis. The most common
subtype encountered is lymphocyte-predominant. The prognosis is
favorable; the 5-year survival rate exceeds 90%. Treatment consists of
chemotherapy, radiotherapy, or both. A case of primary parotid gland
Hodgkin's lymphoma is presented along with a review of the literature
and a discussion of the evaluation and management of this rare entity.
15
UI - 11988942
AU - To EW; Tsang WM; Leung CY; Lee KL
TI -
Warthin's tumor with multiple sarcoid-like granulomas: a case report.
SO - J Oral Maxillofac Surg 2002 May;60(5):585-8
AD - Division of Head & Neck, Plastic and Reconstructive Surgery, Department
of Surgery, Prince of Wales Hospital, The Chinese University of Hong
Kong, Hong Kong. edwardtowh@yahoo.com
16
UI - 11964939
AU - Auvinen A; Hietanen M; Luukkonen R; Koskela RS
TI -
Brain tumors and salivary gland cancers among cellular telephone users.
SO - Epidemiology 2002 May;13(3):356-9
AD - Finnish Cancer Registry and STUK-Radiation and Nuclear Safety Authority,
Helsinki.
BACKGROUND: Possible risk of cancer associated with use of cellular
telephones has lately been a subject of public debate. METHODS: We
conducted a register-based, case-control study on cellular phone use and
cancer. The study subjects were all cases of brain tumor (N = 398) and
salivary gland cancer (N = 34) diagnosed in Finland in 1996, with five
controls per case. RESULTS: Cellular phone use was not associated with
brain tumors or salivary gland cancers overall, but there was a weak
association between gliomas and analog cellular phones. CONCLUSIONS: A
register-based approach has limited value in risk assessment of cellular
phone use owing to lack of information on exposure.
17
UI - 11836575
AU - Begum NM; Nakashiro K; Kawamata H; Uchida D; Shintani S; Ikawa Y; Sato
TI -
M; Hamakawa H
Expression of peroxisome proliferator-activated receptor gamma and the
growth inhibitory effect of its synthetic ligands in human salivary
gland cancer cell lines.
SO - Int J Oncol 2002 Mar;20(3):599-605
AD - Second Department of Oral and Maxillofacial Surgery, Tokushima
University School of Dentistry, Tokushima 770-8504, Japan.
Peroxisome proliferator-activated receptor gamma (PPARgamma) is a member
of the nuclear receptor superfamily of ligand-activated transcription
factors. It is expressed in several tissue types, including adipose
tissue in which it stimulates adipogenesis. Recent studies have
demonstrated that PPARgamma ligands induce cellular differentiation and
inhibit cell growth in carcinomas of various organs including the
breast, prostate, lung, colon, stomach, bladder, and pancreas. However,
whether PPARgamma is expressed in human salivary gland tumors and its
function in this tissue is unknown. In the present study, we examined
PPARgamma gene expression in human salivary gland cancer cells and
tested its ligands for any antitumor effect. PPARgamma mRNA was detected
by RT-PCR in both benign and malignant salivary gland tumor tissues. The
effect of PPARgamma on cell growth was investigated using four human
salivary gland cancer cell lines; HSG, AZA3, HSY and TYS, which were
confirmed to express PPARgamma1 mRNA and protein. Retinoid X receptor
alpha protein, which forms heterodimers with PPARgamma, was also
detected in all the cells tested. Data obtained by luciferase assay
indicated that the intrinsic PPARgamma protein was activated by the
synthetic ligands, troglitazone and pioglitazone, but not by the natural
ligand, 15-deoxy-delta12, 14-prostaglandin J2. The synthetic PPARgamma
ligands, particularly troglitazone, caused significant dose-dependent
inhibition of cancer cell growth. Furthermore, the overexpression of
PPARgamma1 or PPARgamma2 in cancer cells also reduced significantly
their growth rate. These results suggest that PPARgamma and its
synthetic ligands suppress the growth of human salivary gland cancer
cells and it may be a useful molecular target for cancer treatment.
18
UI - 11876610
AU - Patil S; Suvarna P; Dayal PK
TI -
Central mucoepidermoid carcinoma--a case report.
SO - Indian J Cancer 2000 Jun-Sep;37(2-3):123-6
AD - Department of Oral Medicine and Radiology, College of Dental Surery,
Mangalore, Karnataka, India.
The mucoepidermoid carcinoma (MEC) account for approximately 6-8 Percent
of all salivary gland tumors. Central mucoepidermoid carcinoma of the
jaws is rare. Following is a case report of central mucoepidermoid
carcinoma which involves the ramus of the mandible. Origin of the
central mucoepidermoid carcinoma is discussed.
19
UI - 11996451
AU - Satyanarayana S; Barthwal MS
TI -
Bronchial epithelial-myoepithelial carcinoma.
SO - J Assoc Physicians India 2001 Dec;49():1210
AD - Department of Pathology, AFMC, Pune.
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