Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.Adenoid Cystic Carcinoma Malignant salivary gland tumors are represent less than 1% of all malignancies. Adenoid cystic carcinoma represents less than 10% of all salivary gland neoplasms, including benign and malignant lesions, but is about 40% of all malignancies of major and minor salivary glands. This tumor is characterized by a prolonged natural history with slow growth, multiple recurrences, long clinical course, and late metastasis. Bilroth is generally credited with coining the term cylindroma, which was a precursor to the term adenoid cystic carcinoma. In 1856, Billroth described a 22-year-old male who had an orbital cylindroma who underwent seven operations over two years. "Whether or not this is a carcinoma is not known," Billroth wrote, "but this tumor certainly has a marked tendency to recur." Three years later, he published his article detailing the histology and described the cylindrical appearance. In 1930, Spies was the first to use the term adenoid cystic carcinoma. Thirteen years later in 1943, Dockery and Mayo stressed that this tumor was malignant and reaffirmed its peculiar property to spread along nerve sheaths. Finally, ten years later, Foote and Frezell published their famous treatise on tumors of the major salivary glands. They documented the variations and histology and stressed perineural spread in these tumors. Adenoid cystic carcinoma occurs most frequently in the 5 th decade of life. There is no sex predilection. It is seen in both the minor and major salivary glands but is more common in the minor salivary glands. It is the most common malignancy in the submandibular gland and the minor salivary glands, and it can be seen in other glandular tissue. It can be seen in the lacrimal glands, the ceruminous glands of the external auditory canal, the esophagus, the breast, Bartholin's glands of the vulva, the uterine cervix, and the prostate. Stell in 1986, reviewed 800 patients in the literature. The oral cavity was most common site, parotid was the second most common, then the submandibular gland, and finally the paranasal sinuses. Adenoid cystic carcinoma represented about one-third of all minor salivary gland tumors, 15% of submandibular gland tumors, and about 5% of parotid tumors. Adenoid cystic carcinoma (ACC) can be seen in other sites. Donovan and Conley published an article on adenoid cystic carcinoma in the subglottic region in 1983. In general, ACC represents about less than 0.25% of all laryngeal cancers. It arises in these instances from the submucosal mucous glands which are not truly submucosal but invaginations from the surface. These glands are most numerous in the false vocal cords and below the anterior commissure. Laryngeal ACC has a higher propensity for lymph node involvement. Distant metastases from laryngeal ACC are most commonly seen from the supraglottic and glottic sites versus the subglottic region. Although tracheal tumors are not very common either, adenoid cystic carcinoma is the second most common malignancy of the trachea, most commonly involving the proximal trachea. As mentioned earlier, ACC can be found in the external auditory canal, arising from the ceruminous glands from the skin and cartilaginous portion of the external auditory canal or extending from the parotid gland. Regarding presentation, there really are not any specific signs or symptoms with this disease. Most classic presentations are an asymptomatic mass. Then, as the tumor grows and has a propensity for invading nerves, pain and numbness are usually the symptoms that follow, which are seen in about one-third of patients. There really are not any other symptoms until this tumor becomes large enough to interfere with physiologic functions around the orbit, the nose or the oral cavity. Conley in 1974, wrote that "any non-ulcerating tumor in a major or minor salivary gland recognized for months or years, causing mild discomfort or pain and associated with paresthesias, is highly suggestive of adenoid carcinoma until proven otherwise." Physical examination focuses on the tumor itself, the presence of any regional metastases as well as a careful neurologic exam. As we all know, this tumor can exhibit malignant growth and can circumvent a nerve branch without actually causing any signs or symptoms. The histology of this tumor is very interesting, and it has a very classic characteristic histologic appearance. What we usually see are these uniform, small, round cells around the central cylinders and lumina containing hyalin and mucoid material. This is what is the classic Swiss cheese appearance. Perzin et al in 1978 described the three current subtypes; the cribiform and solid subtypes had been documented prior but he was the first to describe the tubular subtype, which he saw in 30% of patients. This is the most differentiated form. He found a 59% recurrence rate and overall nine-year survival. With this tubular form, you see small tubular units, less stratification of cells, and a single lumen. He described the three histologic subtypes as reflecting various degrees of progression of cellular differentiation as well as aggressiveness biologic behavior. The cribiform is the more classic presentation that is seen in about half of cases. This is characterized by an epithelial mass penetrated by cylindrical spaces. He found an 89% recurrence with cribiform tumors and an eight-year survival. Finally, the solid, seen in 10%, was clearly the most aggressive. This is the least differentiated, and he found a five year survival. Local control he found was not as important with the solid subtype because of the significant problem of death from distant metastases. Cribiform tumors tended to be more locally aggressive but overall survival for the tubular and cribriform variants was the same. The problem with creating strictly by histologic subtypes is that polymorphism is very common. You can see all three subtypes in a single specimen. So this pathologic grading system has been revised somewhat to three pathologic grades. This was first done at M.D. Anderson from Szanto et al in 1984. The first grade would be tubular and cribriform only without any solid component. Grade two would be mostly cribriform but less than 30% solid component. Grade three would be predominantly solid. Grade one tumors had the best survival and grade three tumors did the worst. Grade three tumors were larger, recurred frequently, and were lethal within about a four year time period. Another way to examine pathology is the amount of glandular spaces per unit area. This statistic was looked at by Santucci and Bondi in 1989. As the number of glands increased (in the tubular and cribiform variants), so did survival. More solid variants with less glandular spaces had worse outcomes. Another very important factor with adenoid cystic carcinoma is the tendency for perineural invasion. This tumor has a marked tendency to invade nerves. Perineural invasion is seen in about 80% of all specimens. In general, tumors greater than one square centimeter will manifest extension into the perineural spaces. Although this does not always have an adverse effect on survival, and studies have shown there is really no great correlation with survival based on perineural invasion alone. Several studies have shown that invasion of the larger named nerve is a poor prognosticator. Lymph node metastasis is not very common with this disease, seen in about 15% of cases. It is more common with solid tumors, and the site and stage are not very often reliable predictors of regional metastasis. FNA can be very useful with this tumor, and studies have shown one can make the correct diagnosis with FNA in 77% to 90% of cases. ACC has very specific cytologic features. There are magenta stained globules partially surrounded by basaloid tumor cells, often appearing in a rosette or cribriform arrangement. It is easier to see this with a cribriform subtype. It is more difficult to make this diagnosis with the tubular and solid subtypes due to the lack of the specific globules. One of the most frustrating things in dealing with ACC is the impact of distant metastasis, which can be frustratingly frequent and seen in 25% to 50% of cases. Because this tumor invades nerves, it also has propensity for intravascular and perivascular growth, which presumably leads to hematogenous spread. This occurs in an unpredictable manner. Distant mets can develop despite local regional control and can occur more than ten years after the initial therapy. Not surprisingly, these patients do not do as well but the mean survival after onset can be greater than five years. The lungs are the most common site, but distant mets can also be seen in the brain, liver and bone. Distant metastasis is more common with solid tumors. The most important study that focused just on distant metastasis was from Spiro from Sloan-Kettering. This looked at 196 patients treated there over 40 years. They found that 62% had some form of treatment failure and one-third had distant metastasis (DM). Of those 74 patients with DM, 51 were associated with locoregional recurrence but in 23, DM was the only kind of treatment failure. The lungs were the most common site. Half of these patients survived 3 years but 10% survived as long as 10 years. He found that survival was influenced by the tumor size and the presence of locoregional recurrence. This study highlights some important points. The most important one is these patients need to be followed for decades. The classic five year survival period is really not adequate with adenoid cystic carcinoma. He also found that the pulmonary mets were rarely solitary. Over time the normal lung parenchyma is replaced by confluent metastatic disease. These patients can do fairly well and are usually asymptomatic until late in their clinical course. Once symptoms develop, survival is usually less than two years. Another important thing to consider when reviewing studies that encompass patients treated over four decades is that treatment in the 1940's differed from treatment in the 1980's. Clearly, patients in the latter half of their study had a more liberal use of postoperative radiation but they found there was no change in the rate of DM with the use of post-operative XRT. Not surprising, larger tumors had a greater chance of distant metastases, but it was unclear why patients developed DM without any other signs of treatment failure. High tumor grade was suggestive but not statistically significant. They recommended chemotherapy really only to palliate symptoms. A follow up study from Sloan-Kettering stressed that stage was more important than histologic grade. They reviewed 184, previously untreated patients, with ten-year follow-up. They found that neither survival, regional metastases or distant metastases were predictable based on tumor grade alone. Early stage disease did very well with 75% ten-year survival, decreasing to 42% for stage two disease, and 15% ten-year survival for stage three and four disease. They felt that grading was subjective, but the size of the lesion was more important. Treatment of this tumor is frustrating due to its deceptive biologic behavior, characterized by multiple and late recurrences, but there is a long survival with recurrent and metastatic disease. Clearly, the best survival results are with combined surgery and radiation therapy. Surgical resection is the mainstay of therapy. Obviously, the surgical goals include obtaining disease-free margins, and at the same time preserving maximal physiological function. Even despite radical surgery, there is a frustratingly high recurrence rate. Clearly, surgery alone is not curative in advanced disease. When analyzing the role of radiation therapy, small case numbers preclude any true randomized studies to determine which groups are subgroups and more likely to benefit. The majority of studies are retrospective and document patients over a wide range of years and treatment protocols. The most important thing to remember about radiation therapy with this disease is that adenoid cystic carcinoma is radiosensitive, it is not radiocurative. These patients usually get a good response initially but most of these tumors will recur. This was nicely demonstrated in a study from Sloan-Kettering by Vikram et al in 1984. They looked at patients just treated with radiation therapy. 96% of them had tumor regression but 93% relapsed, and the majority of these or half of them relapsed in 18 months. They also looked at 25 patients that received adjunctive XRT after surgery. Of course, treatment protocols differed but there were 9 patients who received "adequate" radiation therapy, which they defined as a larger field and a higher dose, and 8 of those 9 were disease free at 5 years. Radiation for advanced tumors was rarely curative but postoperative radiation therapy improved local control rates if the field size and the dose are adequate. In a follow-up study from M.D. Anderson, Garden et al in 1994, reviewed 198 patients treated with surgery and radiation therapy. These patients were all treated with the same protocol. All of their patients received post-op XRT except those that were small and low grade with clear margins and no perineural invasions. At ten years, they had 70% survival with 50% to 60% freedom from relapse rate. Those tumors that had clear margins had an 85% local control rate at 10 years, which dropped to 70% with named nerve involvement. They concluded that radiation therapy is efficacious in reducing local failures. Radiation therapy was less effective with positive margins or named nerve involvement. They also found a significant problem with distant metastases. The curative potential of radiation therapy is most likely related to tumor burden. Radiation is probably most beneficial when there is minimal microscopic disease. The problem is that this tumor tends to occur in difficult anatomic areas where it is difficult to obtain clear margins. There can be perineural tracking back to the base of the skull and often times surgery cannot reduce the tumor burden to an acceptable level in which conventional radiation therapy can sterilize all the tumor cells. Clearly, surgery needs to be balanced though between obtaining clear margins, and the morbidity of removing all gross disease. Again, the small case numbers really preclude any true randomized trials. Neutron radiotherapy has been studied with this disease. Neutrons are more densely ionizing than protons. They induce greater damage in double stranded DNA, which results in less repair of DNA and less variation of tumor sensitivity across cell cycles. Neutrons are also less dependent on oxygen to achieve their therapeutic effects. A study from the University of Washington from 1993, examined at the role of neutron therapy with these tumors. Of 21 patients who were treated just with neutron radiotherapy, 17 achieved local control at 5 years. They recommended neutron radiotherapy for those tumors that were unresectable, tumors associated with high surgical morbidity, or and post-operative with a high tumor burden after surgery. In those patients with paranasal sinus tumors treated only with neutron radiotherapy, they were able to achieve 100% local control at 5 years. Chemotherapy has a limited, poorly defined role with ACC. There have been studies that have shown cisplatin, 5-fluoruracil, doxorubicin, and cyclophosphamide, have some activity, either as single agents or in combination. There are reports of some successes and remissions. Chemotherapy treatment protocols really offer no statistically significant differences in disease free survival when compared to well matched historic controls. When analyzing survival with this disease, it is important that the patients are treated with similar treatment protocols, and survival is best not determined with the classic five year survival rate. One of the larger more recent studies that have dealt with this topic was Fordice et al. They reviewed 160 patients treated from 1977 to 1996. Disease-specific survival at 5 years is 89%, dropping to 67% at 10 years and to 40% at 15 years. Distant metastases were the most common type of failure, occurring in 22% of patients. This was most commonly seen in the lungs. They noted of those with bone mets, the clinical course tended to be particularly lethal. Solid tumor type and named nerve invasions were the most statistically significant predictive factors of treatment failure. Patients with palate and parotid tumors did better than other sites. They suggested that maybe their were two treatment populations: one subgroup that would be doomed to a more rapid course of death from an aggressive tumor with survival measured in months to years while group two would have more of an indolent disease with sporadic recurrence and a survival measured in decades. Adenoid cystic carcinoma commonly affects the minor salivary glands. 50% of all oral cavity ACC occurs on the palate. The traditional school of thought is that minor salivary gland tumors have a worse prognosis. That is because it is easier for the tumor to infiltrate outside the gland and then invade surrounding tissue. Kuhel et al in 1992, 41 patients with palatal ACC dividing them into three categories. Category one was disease just confined to the palate. Category two and category three were progressive spread to adjacent sites. All patients were treated with the same modality. They all received postop radiation unless they were small tumors with clear margins and no perineural invasion. There was really no statistically significant difference in cumulative survival based on category alone although more advanced tumors tended to recur faster. Another controversial area to look at is parotid adenoid cystic carcinoma. When this tumor occurs here, obviously the facial nerve is at risk from the disease but also from the treatment. This brings up the controversy of facial nerve sacrifice without any evidence of facial nerve weakness. Casler and Conley looked at this in 1992, and they reviewed 108 patients. They were stratified into four categories based on the surgical type of resection. Group one patients all received superficial parotidectomy. Group two patients underwent a total parotidectomy. Groups three and four both underwent radical parotidectomy but Group three had no preoperative weakness, and group four had some preoperatively facial nerve deficits. They felt that a radical parotidectomy offered a clear survival advantage in T2 and T3 tumors. They looked at those who underwent a total parotidectomy versus radical parotidectomy and both had functional facial nerves. The 15-year survival was better for those who underwent a radical parotidectomy (60%) versus 37% for those in group two. This difference which was suggestive but not statistically significant. The radical parotidectomy offered some advantages over total because it was performed on block with a decreased chance of tumor spillage. Another important thing to keep in mind here is that tumor adjacent to a nerve may have already invaded it on a microscopic level. For smaller tumors that are T1 or early T2, those can be managed with a nerve sparing procedure. One of the more frustrating locations to deal with adenoid cystic carcinoma is the sinonasal tract. These most commonly arises in the maxillary antrum. Study after study shows that these patients do particularly poorly. This is not really surprising as tumors in this site can reach very large dimensions, growing in hollow sinus cavities before they become symptomatic. Some feel they should all be considered advanced stage due to their high risk of local recurrence. In fact, they have a 60% to 70% local recurrence rate. This is mostly due to invasion of cranial nerves, specifically, V2 and V3. You can also see vidian nerve involvement, and it is very difficult here to secure negative margins. Better than 50% have positive margins despite radical surgery. Aggressive surgical approaches are needed here, and the best chances for cure are with surgery and radiation therapy. These patients can survive up to five years with advanced disease. This brings up the role of skull based surgery with adenoid cystic carcinoma in the sinonasal tract. As skull based surgery has advanced, it clearly facilitates gross total resection of advanced lesions. Some will say that survival here can approximate tumors with lower stages at more favorable sites. Pittman et al looked at 35 patients that underwent skull base surgery for ACC of the sinonasal tract. They found that 46% were disease free at 40 months. Of 17 patients that recurred and then underwent surgical salvage, only one was disease free at 24 months. Surgery appeared to be palliative in these incidences. There are some that feel that invasion of the internal carotid, the orbit, and the cavernous sinus are only relative contraindications to surgery in these patients. Perhaps palliative surgery should be considered even when the extent of disease precludes a surgical cure. Since ACC is a very slow growing tumor, maybe there are different indications for resection. These patients can survive longer with local recurrences and distant metastases. Gormley et al looked at 16 patients with intracranial extension that all underwent surgery. Six of them were NED with a mean survival of 72 months but 9 patients were dead of disease. As the clinical course of this tumor is very difficult to predict, there is a search to find more objective markers to select those patients who might have a more ominous prognosis. E-cadherin is a cell-cell adhesion molecule and studies have shown that lower or absent E-cadherin expression is associated with larger tumors and a more frequent rate of distant metastases. Many institutions have looked at flow cytometry and have found that aneuploidy carcinomas correlate with a higher incidence of solid architecture and advanced clinical stage. PCNA is a nuclear protein related to DNA synthesis and cell proliferation. Several studies have shown shorter survival times and increased distant metastases in patients with a high PCNA index. So, in conclusion, adenoid cystic carcinoma is a frustrating tumor. It requires an aggressive combination of complete and adequate surgical excision with radiation therapy to yield optimal local regional control rates. The one important thing to remember that is particularly frustrating is that distant metastases can develop in up to 50% of patients. Survival is about 75% at five years but drops to as low as 25% at 15-20 years. It is almost like a systemic disease with an unpredictable clinical course. Clearly, we need better understanding of its biologic behavior to develop other forms of adjuvant therapy. Case Presentation: ST is a 45-year-old female involved in an MVA on 11/13/00. Evaluation at an outside hospital included a CT of the face, which revealed a large maxillary sinus mass. Further questioning revealed a one-year history of progressive right-sided facial swelling with proptosis over the last few months accompanied by occasional blurred vision and upper lip and cheek numbness. She has no past medical or surgical history. She takes Tylenol #3 for pain and has no known drug allergies. She has a 15-pack year tobacco history and drinks alcohol occasionally. Her family history is non-contributory. On physical examination, she is in no acute distress and appears her stated age. She has an obvious fullness of the right maxilla with proptosis. Her ears and nasal cavity are clear. Examination of the oral cavity reveals fullness of the right maxillary alveolus, decreased sensation of the right soft palate, and loose first and second maxillary molars. Her larynx is clear. There is no lymphadenopathy or masses in the neck. Neurologic exam reveals extra-ocular muscles are intact, with decreased sensation over the entire right face. CXR is clear. CT and MRI revealed tumor arising from the right maxillary sinus with extensive spread into the orbits, adjacent soft tissue, and oral cavity. There is extension into the pterygopalatine fossa with subsequent extension into the foramen rotundum and vidian canal. 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J Otolaryngol 1996;25:399-403. Grand Rounds Archive | Department Home page BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map | ©2001-2005 Baylor College of Medicine
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