Does adjuvant radiotherapy for primary adenoid cystic carcinoma of the parotid gland reduce the risk for loco-regional recurrence and associated morbidity?

Adenoid cystic carcinoma is an uncommon malignant neoplasm of the salivary gland. Liver metastasis from salivary gland cancer is a rare situation. In this article, we report the case of a 29-year-old woman treated 5 years previously for adenoid cystic carcinoma of the parotid gland by surgery and radiotherapy, who presented for a large hypervascularized hepatic metastasis of 20 cm. After 3-cycle chemotherapy stability, hepatic surgery was successfully performed. The patient maintained disease-free period of 12 months after the surgical treatment. This rare case represents a therapeutic challenge for oncologists and surgeons. Through this case and a review of the literature, we try to better detail the management of this uncommon entity.

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Adenoid cystic carcinoma of the skull base: results with an aggressive multidisciplinary approach

Journal of Neurosurgery ◽

10.3171/2015.1.jns142462 ◽

2016 ◽

Vol 124 (1) ◽

pp. 115-121 ◽

Cited By ~ 22

Author(s):

Rohan Ramakrishna ◽

Shaan M. Raza ◽

Michael Kupferman ◽

Ehab Hanna ◽

Franco DeMonte

Keyword(s):

Adenoid Cystic Carcinoma ◽

Skull Base ◽

Adjuvant Radiotherapy ◽

Multidisciplinary Approach ◽

Residual Disease ◽

Univariate Analysis ◽

Progression Free Survival ◽

Cancer Center ◽

Adenoid Cystic ◽

Md Anderson

OBJECT Adenoid cystic carcinoma (ACC) is a locally aggressive tumor of salivary gland origin. Little data exist to guide treatment when this tumor extends to involve the structures of the skull base. METHODS Fifty-one patients with a diagnosis of ACC affecting the skull base were identified from a prospective database at MD Anderson Cancer Center (from 1992 to 2010). RESULTS Median follow-up for study patients was 6.75 years. The 5- and 10-year overall survival (OS) rates were 78% and 50%, respectively. Sixty-six percent of patients had progression of their disease. The 5- and 10-year progression-free survival (PFS) rates were 46.7% and 21.0%, respectively. Gross-total resection was achieved in 75% of patients, with 49% having microscopically negative margins at the time of first operation. On univariate analysis, resections with microscopically negative margins were associated with a significant OS advantage (20.1 ± 3.3 years) compared with resections that left residual disease, even if microscopic (10.3 ± 1.6 years, p = 0.035). In patients who underwent reoperation, the effect persisted, with improved OS in those with negative margins (21.4 ± 0.0 vs 16.7 ± 4.0 years, p = 0.06). The use of adjuvant radiotherapy was associated with an OS advantage (16.2 ± 2.5 vs 5.5 ± 2.2 years, p = 0.03) at initial diagnosis and improved PFS (7.8 ± 1.0 vs 2.1 ± 0.62 years, p = 0.005), whereas repeat irradiation provided no benefit. The use of adjuvant chemotherapy at diagnosis or at recurrence was not associated with any significant advantage. Multivariate analysis revealed margin-negative resection at initial operation and at recurrence retained OS significance, even after controlling for age, radiation therapy, and T stage. CONCLUSIONS ACC of the skull base is best treated with a multidisciplinary approach aimed at maximal, safe resection. Adjuvant radiotherapy should be offered, whereas chemotherapy does not confer benefit.

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Two malignant salivary gland tumours of different type in one patient

The Journal of Laryngology & Otology ◽

10.1017/s0022215100128166 ◽

1994 ◽

Vol 108 (9) ◽

pp. 798-800 ◽

Cited By ~ 4

Author(s):

A. Hosni ◽

C. Fisher ◽

P. Rhŷ-Evans

Keyword(s):

Salivary Gland ◽

Parotid Gland ◽

Adenoid Cystic Carcinoma ◽

Salivary Glands ◽

Submandibular Gland ◽

Histological Type ◽

Salivary Gland Tumours ◽

Adenoid Cystic ◽

The Right ◽

Left Parotid Gland

AbstractThe synchronous or metachronous occurrence of two tumours of the salivary glands in one patient is rare. These are mainly benign and of the same histological type. Here we report a 56-year-old man who developed a mucoepidermoid tumour of the left parotid gland four years after diagnosis of adenoid cystic carcinoma of the right submandibular gland. This combination of neoplasms has not to our knowledge been reported before.

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Cell-Surface Galactosyltransferase Acts as a Modulator of Rat and Human Acinar Cell Proliferation

Advances in Dental Research ◽

10.1177/08959374900040010801 ◽

1990 ◽

Vol 4 (1) ◽

pp. 45-60 ◽

Cited By ~ 4

Author(s):

M.G. Humphreys-Beher ◽

T. Zelles ◽

N. Maeda ◽

K.R. Purushotham ◽

N. Cassisi ◽

...

Keyword(s):

Cell Proliferation ◽

Growth Factor ◽

Cell Surface ◽

Parotid Gland ◽

Adenoid Cystic Carcinoma ◽

Acinar Cell ◽

Egf Receptor ◽

Neoplastic Tissue ◽

Direct Role ◽

Adenoid Cystic

Several physiological parameters were examined for inducing acinar cell proliferation and corresponding increased expression of β1-4 galactosyltransferase. In this study, dietary changes causing acinar cell proliferation included the following: the introduction of animals to a liquid diet (causing gland atrophy) followed by re-introduction of solid chow, gustatory stimulation provided by the introduction of 0.5% citric acid to animal drinking water, and removal of the submandibular gland with subsequent reliance on the parotid gland for saliva protein and fluid. Alterations in growth factor levels were produced by injecting animals with a chronic (three-day) regimen of either nerve growth factor (NGF) or epidermal growth factor (EGF). In all cases of acinar cell proliferation in vivo, generated by the above treatments, cell-surface galactosyltransferase was detected along with the unique expression of a 4.5-kb proliferation-associated mRNA. Parotid gland proliferation could be blocked in all cases by the injection of the galactosyltransferase specific modifier protein, a-lactalbumin. Propranolol, a β-adrenergic receptor antagonist, blocked proliferation in all cases except EGF treatment. EGFinduced proliferation could, however, be prevented if the animals were treated with monoclonal antibody to EGF receptor or with the galactosyltransferase modifier a-lactalbumin. As a comparison, human parotid tissue samples obtained from neoplastic pleomorphic adenomas, mucoepidermoid carcinoma, adenoid cystic carcinoma, and a bulimia patient were analyzed for galactosyltransferase expression by Northern blot of mRNA and plasma membrane isolation. Elevated levels of galactosyltransferase were found in all neoplastic tissue preparations as well as in the bulimia sample. Amylase synthesis was reduced in samples compared with surrounding normal tissue from the same patient. In vitro cell culturing of pleomorphic adenoma cells in the presence of galactosyltransferase modifier a-lactalbumin and substrate UDP-galactose inhibited proliferation in a dose-dependent fashion. Southern blot analysis of DNA from neoplastic parotid cells showed an alteration in chromosomal gene structure for the galactosyltransferase activator cDNA from the adenoid cystic carcinoma. These results for induced acinar cell proliferation as well as human neoplastic pathologies suggest a direct role for cell surface β1-4 galactosyltransferase in signaling growth. Furthermore, the proliferation-associated activity of galactosyltransferase suggests that it may be considered as a new type of cell growth regulator.

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