Lesion catalogue

Browse Atlas

Lesion / Salivary gland lesions

Adenoid cystic carcinoma

Updated 2026-07-27 Suggest an edit

Overview and definition

Adenoid cystic carcinoma (ACC) is a malignant epithelial neoplasm of salivary gland origin with biphasic ductal-myoepithelial differentiation.[1][2] It is one of the most common malignant tumors of the minor salivary glands and the most common malignant salivary neoplasm of the maxillary sinus.[1][3] The tumor is characterized by slow but relentless growth, a hallmark propensity for perineural invasion, and a paradoxical combination of indolent clinical tempo with aggressive long-term behavior including late local recurrence and distant metastasis.[4][5] In the maxilla, ACC arises most frequently from the palatal minor salivary glands or the maxillary sinus mucosa, producing a soft-tissue mass that secondarily invades the underlying palatal bone, alveolar process, and adjacent structures.[6][7] The defining molecular alteration is a chromosomal rearrangement involving MYB or MYBL1, most commonly resulting in a MYB::NFIB fusion.[8][9] On dental radiographs, the tumor typically manifests as ill-defined bone destruction of the hard palate and alveolar process; cross-sectional imaging is essential for staging. Management centers on surgical resection with postoperative radiotherapy.[10]

Terminology and classification

The WHO Classification of Head and Neck Tumours (5th edition, 2022/2024) classifies ACC as a malignant epithelial salivary gland tumor.[11][12] The historically used term "cylindroma" is obsolete and should be avoided, as it causes confusion with the unrelated dermal cylindroma.[2][13] The abbreviation ACC (or AdCC) is standard. When the tumor arises as a primary intraosseous lesion within the jawbone, the designation "primary intraosseous adenoid cystic carcinoma" (PIACC) is used.[14][15] A recently described morphologic variant with squamous differentiation and trabecular/macrocystic growth has been termed "metatypical adenoid cystic carcinoma".[11][16]

Epidemiology

  • ACC accounts for approximately 1% of all head and neck malignancies and up to 10% of salivary gland neoplasms.[1][17]
  • Among minor salivary gland tumors, ACC is one of the most frequent malignant histotypes; the palate is the single most common minor salivary gland site, followed by the maxillary sinus.[6][18]
  • Peak incidence occurs in the fifth to sixth decades (mean age ~50–55 years), with a slight female predominance.[4][18]
  • In the maxillary sinus specifically, ACC is the most common malignant salivary gland tumor; the maxillary sinus accounts for approximately 47% of sinonasal ACC.[7]
  • Primary intraosseous ACC of the jaws is exceedingly rare, with fewer than 50 mandibular cases reported and even fewer in the maxilla; the mandible is affected 3–4 times more often than the maxilla in intraosseous cases.[14][19]

Clinical presentation

Presentation and symptoms

Most maxillary ACC presents as a firm, submucosal, non-ulcerated palatal swelling or a mass within the maxillary sinus.[3][6] The clinical course is insidious; symptom duration before diagnosis is often months to over a year.[20]

  • Palatal tumors: painless or painful swelling of the hard palate, sometimes with overlying mucosal discoloration; the mucosa may remain intact until late stages.[6][21]
  • Maxillary sinus tumors: nasal obstruction (25%), epistaxis (21%), facial pain or pressure (50%), and a palpable mass (88%) are common presenting complaints; most patients present with advanced (T3–T4) disease because the sinus cavity allows occult growth.[3][7]

Pain and neurologic findings

Pain is a prominent feature, reported in approximately 50% of cases, and should raise suspicion for perineural invasion.[3][22] Numbness or paresthesia of the palate, upper lip, or cheek (infraorbital nerve distribution) indicates involvement of branches of the maxillary division of the trigeminal nerve (V2).[23][24] Cranial nerve deficits—including diplopia, facial weakness, or trigeminal sensory loss—suggest skull base extension and are late findings.[24][25]

Tempo and complications

ACC follows a protracted clinical course with a high cumulative risk of local recurrence and distant metastasis (most commonly to the lungs) that may manifest years to decades after initial treatment.[5][26] Lymph node metastasis is uncommon, occurring in fewer than 5% of cases at presentation.[7]

Radiographic findings

Location and distribution

Maxillary ACC most commonly involves the hard palate and posterior alveolar ridge, reflecting the density of minor salivary glands in these regions.[6][20] Maxillary sinus tumors center within the antrum and extend into the palate, nasal cavity, or orbit.[3][7] Primary intraosseous ACC of the maxilla is exceptionally rare; when it occurs, it may present as a periapical radiolucency mimicking inflammatory disease.[27][28]

Periphery and shape

  • Palatal and alveolar lesions typically produce ill-defined, irregular radiolucencies of the hard palate and alveolar bone on panoramic and periapical radiographs, without a corticated border.[29][30]
  • Intraosseous cases may occasionally show well-defined or multilocular radiolucencies that simulate odontogenic cysts or ameloblastoma, though this presentation is rare.[14]
  • Maxillary sinus tumors may appear as opacification of the antrum with destruction of the sinus walls; the bony margins are typically ragged and non-corticated.[31][32]

Internal architecture

  • The lesion is predominantly radiolucent without internal mineralization on conventional radiographs.[29]
  • Internal calcification is uncommon, reported in approximately 13% of palatal ACC on CT.[33]
  • Tubular-subtype tumors may produce small cystic internal patterns, whereas solid-subtype tumors tend to appear homogeneously dense on cross-sectional imaging.[31][32]

Effects on teeth and adjacent structures

  • Root resorption of adjacent teeth is not a prominent feature but may occur when the tumor directly abuts the dental roots.[29]
  • Tooth displacement and widening of the periodontal ligament space can be seen when the tumor infiltrates the alveolar process.[27][28]
  • Periapical radiolucencies mimicking endodontic pathology have been reported in intraosseous cases, leading to misdiagnosis as periapical cysts or granulomas.[14][27]

Extent and cortical involvement

Bone invasion is a hallmark of maxillary ACC and is present in the majority of cases at diagnosis.[22][30] Three radiographic patterns of bone involvement have been described:[30]

  • Erosive type: smooth, pressure-remodeled cortical destruction without marrow infiltration
  • Diffuse invasive type: irregular, moth-eaten or permeative bone destruction with tumor infiltrating marrow spaces; associated with the solid histologic subtype
  • Minimal change type: subtle cortical defects with histologically confirmed tumor extension through small bony perforations; may be radiographically occult on conventional films

Palatal bone erosion is present in approximately 76% of palatal ACC.[33] CBCT and thin-section CT improve detection of cortical thinning, cortical perforation, and early bone destruction compared with panoramic radiography, particularly in the maxilla where superimposition limits conventional film interpretation.[34][35]

Osseous changes related to perineural spread

A distinctive feature of maxillary ACC is erosion and enlargement of neural foramina, canals, and fossae along the path of perineural tumor spread. In palatal ACC, the most frequently affected sites are:[33]

  • Greater palatine foramen/canal (76%)
  • Pterygopalatine fossa (45%)
  • Foramen rotundum (34%)
  • Vidian canal (32%)

Affected foramina and canals are enlarged to a mean of 187% of the contralateral normal size.[33] Surrounding bone sclerosis adjacent to the tumor is occasionally seen and, among salivary gland carcinomas, is significantly more frequent in ACC than in other histotypes.[36] Erosion or enlargement of foramina on bone-algorithm CT has 96% sensitivity and 100% specificity for MRI-confirmed perineural spread.[33]

Variants

  • Primary intraosseous ACC: presents as a central jaw radiolucency—unilocular or multilocular—that may simulate an odontogenic cyst, ameloblastoma, or periapical pathology; the mandible is far more commonly affected than the maxilla.[14][15]
  • Maxillary sinus ACC: appears as antral opacification with aggressive bony destruction of the sinus walls; the tubular subtype may show a cribriform (sieve-like) pattern of bone destruction with relatively well-defined margins, whereas the solid subtype produces more aggressive lytic destruction.[31][32]

Other imaging findings

CT findings

Contrast-enhanced CT demonstrates a soft-tissue-density mass with mild to moderate enhancement.[22][31] Bone-window CT is valuable for detecting cortical erosion, foraminal enlargement along neural pathways, and the pattern of bone destruction (erosive vs. permeative).[33][37] In maxillary sinus ACC, CT can differentiate histologic subtypes: tubular tumors tend to be smaller with well-defined margins and cribriform bone destruction, whereas solid tumors are larger with irregular margins and aggressive lytic destruction.[31][32]

MRI findings

MRI is the preferred modality for evaluating perineural tumor spread, skull base invasion, orbital extension, and bone marrow involvement.[10][38] ACC typically shows iso- to hypointense signal on T1-weighted images and hyperintense signal on T2-weighted images, with marked heterogeneous enhancement after gadolinium administration.[31][39] On T2-weighted images, low signal intensity correlates with the highly cellular solid subtype and a worse prognosis, whereas high signal intensity corresponds to the less cellular cribriform or tubular subtypes.[39] MRI sensitivity for detecting perineural spread ranges from 73% to 100%.[38][40] Key findings include nerve enlargement, abnormal nerve enhancement, and replacement of normal perineural fat planes along the trigeminal nerve pathway from the palate through the pterygopalatine fossa to the foramen rotundum, Meckel cave, and cavernous sinus.[23][24]

PET/CT

FDG-PET/CT may be considered for staging, particularly to evaluate distant metastases and to confirm metabolically active perineural disease along neural segments.[10][23]

Differential diagnosis

Maxillary ACC must be distinguished from other malignant and benign processes that produce bone destruction or soft-tissue masses in the palate and maxillary sinus. The differential depends on whether the lesion presents as a palatal/alveolar mass with bone destruction or as a primary intraosseous radiolucency.

EntityWhy it is consideredBest discriminator
Mucoepidermoid carcinomaMinor salivary gland tumor of the palate with bone destructionACC lacks mucin-producing cells and squamous differentiation; MEC harbors CRTC1::MAML2 fusion rather than MYB::NFIB[9][19]
Polymorphous adenocarcinomaLow-grade palatal salivary gland malignancy with infiltrative growthPolymorphous adenocarcinoma shows diverse architectural patterns with bland cytology and PRKD1 mutations; it lacks the biphasic cribriform pattern and MYB rearrangement of ACC[9]
Squamous cell carcinoma of the maxillary sinusAggressive maxillary sinus mass with bone destruction and soft-tissue extensionSCC shows keratinization and dysplastic squamous epithelium; it lacks the biphasic basaloid morphology and perineural predilection characteristic of ACC[10][41]
Pleomorphic adenomaPalatal submucosal mass, most common salivary gland tumor at this sitePleomorphic adenoma is well-circumscribed without bone destruction; its mesenchymal (chondromyxoid) matrix differs from the basement-membrane-type matrix of ACC[1][26]

The highest-risk diagnostic pitfall is misidentifying a palatal ACC as a benign pleomorphic adenoma or, in intraosseous cases, as an odontogenic cyst or periapical inflammatory lesion, which delays definitive diagnosis.[14][27] Incisional biopsy is essential for any persistent palatal mass or atypical maxillary radiolucency, and histopathologic examination with immunohistochemistry and molecular testing (MYB FISH or sequencing) should be pursued when the diagnosis is uncertain.[9][15]

Histopathology

Microscopic features

ACC is a biphasic tumor composed of ductal (luminal) epithelial cells and abluminal myoepithelial/basal cells.[1][2] Three recognized growth patterns occur in variable combinations:[1][2]

  • Cribriform: the most common and classic pattern; islands of basaloid cells with sharply demarcated, punched-out pseudocystic spaces ("Swiss cheese" pattern) filled with basophilic basement-membrane-type material
  • Tubular: bilayered tubular structures with inner cuboidal luminal cells and outer myoepithelial cells, surrounded by hyalinized stroma
  • Solid: sheets of basaloid cells without pseudocystic or tubular formations; associated with higher grade and worse prognosis

Most tumors contain a mixture of patterns; grading is based on the predominant component, with the solid pattern conferring the worst prognosis.[20][26]

Immunohistochemistry

  • Myoepithelial cells stain positively for smooth muscle actin, S-100, p63, and calponin.[2]
  • Luminal cells express CK7 and EMA.[2]
  • c-KIT (CD117) is strongly and diffusely positive in ACC regardless of grade.[2]
  • MYB nuclear expression is characteristic and supports the diagnosis.[15]

Molecular findings

The hallmark molecular alteration is the t(6;9)(q22-23;p23-24) translocation producing a MYB::NFIB fusion, present in approximately 50–80% of cases.[8][9][42] A smaller subset harbors MYBL1::NFIB fusions.[8][42] Rare noncanonical fusions (EWSR1::MYB, FUS::MYB) have been identified, predominantly in non-major-salivary-gland sites.[43][44] Transcriptomic profiling has identified two molecular subtypes: AdCC-I (MYC-upregulated, NOTCH-mutated, more aggressive) and AdCC-II (TP63-upregulated, more indolent).[45] Copy number losses at 6q and 14q have been associated with poor prognosis independent of histologic pattern.[46]

Radiologic-pathologic correlation

The solid histologic subtype correlates with diffuse invasive bone destruction on imaging, lower ADC values on diffusion-weighted MRI, and low T2 signal intensity.[30][31][39] Tubular and cribriform subtypes tend to produce erosive or cribriform patterns of bone destruction with relatively better-defined margins.[30][31]

Management and prognosis

Workup and referral

The NCCN Guidelines for Head and Neck Cancers recommend complete head and neck CT with contrast and/or MRI with and without contrast for all maxillary tumors, with chest CT to evaluate for pulmonary metastases.[10] FDG-PET/CT may be considered.[10] Biopsy is required; for maxillary sinus lesions, the preferred route is transnasal.[10] Multidisciplinary consultation is recommended, and referral to a specialized center should be considered given the rarity and histopathologic diversity of these tumors.[10]

Definitive treatment

Surgical resection with clear margins is the primary treatment.[5][10] For palatal and alveolar ACC, this typically requires partial or total maxillectomy with resection of the greater palatine neurovascular bundle to address perineural invasion.[6][47] The NCCN algorithm provides stage-specific guidance:[10]

  • T1–2, N0 adenoid cystic: resection followed by adjuvant radiotherapy (preferred), or observation may be considered if margins are negative and no perineural spread is present
  • T3–4a, N0 or any T with N+: complete resection (with neck dissection if N+) followed by adjuvant radiotherapy to the primary site and neck
  • T4b or unresectable: definitive radiotherapy ± systemic therapy

Adjuvant radiotherapy is recommended for all resected ACC, particularly when adverse features are present (perineural invasion, positive or close margins, lymphovascular invasion).[10][48] Radiation doses ≥60 Gy are associated with improved local control.[48][49] Elective neck dissection is generally not required given the low rate of nodal metastasis but should be performed when clinical or radiographic nodal disease is present.[7][50]

Recurrence and prognosis

  • Five-year overall survival rates range from 62% to 75%; 10-year rates decline to 35–62%, reflecting the characteristic pattern of late recurrence.[3][18][26]
  • Local recurrence occurs in 16–30% of patients; distant metastasis (predominantly pulmonary) develops in 20–38%.[3][7][26]
  • Median time to distant metastasis is approximately 46 months, but very late recurrences (>15 years) are well documented.[5][51]
  • Adverse prognostic factors include solid histologic pattern, advanced T stage, positive surgical margins, perineural invasion of named nerves, and skull base involvement.[20][26][48]
  • Sinonasal primary site confers worse outcomes compared with major salivary gland ACC.[52][53]

Surveillance

Given the propensity for very late recurrence, clinical follow-up should extend at least 15 years and ideally lifelong, with periodic cross-sectional imaging and chest imaging.[5]

Special considerations

Molecular subtypes and emerging targets

Transcriptomic classification into AdCC-I (NOTCH-mutated, MYC-driven) and AdCC-II (TP63-driven) subtypes has prognostic implications and may guide future targeted therapy.[45] Copy number variation–based molecular classification using 6q-loss and 14q-loss markers has been shown to improve prognostic accuracy beyond histologic grading alone.[46] For recurrent or metastatic disease, the NCCN recommends biomarker testing including androgen receptor, HER2, NTRK1/2/3, FGFR, BRAF, RET, MSI/dMMR, TMB, and PD-L1 prior to systemic therapy.[10] No FDA-approved targeted therapies currently exist specifically for ACC, but NTRK inhibitors (e.g., larotrectinib, entrectinib) are approved for NTRK fusion–positive tumors regardless of histology, and clinical trials investigating NOTCH pathway inhibitors and other agents are ongoing.[17]

ORAD reference data

Radiographic characteristics

18 characteristics

Banded distributions from the ORAD reference database.

Clinical Features

What is the sex of your patient? Female · commonly
What is the sex of your patient?
FindingFrequency
Male commonly
Female commonly
Unknown rarely
What is the race of your patient? Nonblack · usually
What is the race of your patient?
FindingFrequency
Black occasionally
Nonblack usually
Unknown rarely
What is the age of your patient? 50 + · commonly
What is the age of your patient?
FindingFrequency
0 - 10 rarely
11 - 25 rarely
26 - 50 sometimes
50 + commonly
Unknown rarely
Does your patient have pain or paresthesia? No pain · commonly
Does your patient have pain or paresthesia?
FindingFrequency
Pain commonly
No pain commonly
Unknown rarely

Radiographic Features

Which jaw contains the lesion? Maxilla only · usually
Which jaw contains the lesion?
FindingFrequency
Maxilla only usually
Mandible only not reported
Both jaws not reported
The lesion center is in what region ? Molar region · commonly
The lesion center is in what region ?
FindingFrequency
Incisor region occasionally
Canine/Premolar Region sometimes
Molar region commonly
Ramus region not reported
TMJ region not reported
Sinus region sometimes
The relationship of the lesion to teeth is: Not tooth associated · commonly
The relationship of the lesion to teeth is:
FindingFrequency
Crown associated occasionally
Root associated sometimes
Apex associated occasionally
Missing tooth associated sometimes
Not tooth associated commonly
Is the tooth associated with the lesion vital? Vital · usually
Is the tooth associated with the lesion vital?
FindingFrequency
Vital usually
Not vital rarely
Unknown rarely
Please estimate the number of lesions: One · usually
Please estimate the number of lesions:
FindingFrequency
One usually
Two not reported
Three or more not reported
Generalized not reported
What is the maximum size of the lesion? Less than 2 cm · commonly
What is the maximum size of the lesion?
FindingFrequency
Less than 2 cm commonly
2 to 3 cm sometimes
Greater than 3 cm sometimes
Where is the origin of the lesion? Central · commonly
Where is the origin of the lesion?
FindingFrequency
Central commonly
Peripheral commonly
The borders of the lesion are: Diffuse · usually
The borders of the lesion are:
FindingFrequency
Corticated not reported
Defined but not corticated sometimes
Diffuse usually
The loculation of the lesion is: Not loculated · usually
The loculation of the lesion is:
FindingFrequency
Unilocular not reported
Multilocular not reported
Not loculated usually
The contents of the lesions are: Radiolucent · usually
The contents of the lesions are:
FindingFrequency
Radiolucent usually
Radiopaque not reported
Mixed occasionally
Radiolucent with flecks not reported
Does the lesion contain one or more teeth ? No · usually
Does the lesion contain one or more teeth ?
FindingFrequency
Yes occasionally
No usually
Unknown occasionally
Does the lesion expand the bony cortex? No · usually
Does the lesion expand the bony cortex?
FindingFrequency
Yes not reported
No usually
Does the lesion cause root resorption ? No · usually
Does the lesion cause root resorption ?
FindingFrequency
Yes sometimes
No usually
Does the lesion cause tooth displacement or impaction? No · usually
Does the lesion cause tooth displacement or impaction?
FindingFrequency
Yes sometimes
No usually
Atlas sources

References

59 sources
  1. 1
    The cytology of salivary gland neoplasms with globules of extracellular matrix: Case‐based review of adenoid cystic carcinoma and its potential mimics. Saeed OA, Whaley RD, Segura S, Wu HH, Cramer H. Diagnostic Cytopathology. 2021;49(6):E195-E202. doi:10.1002/dc.24672.
  2. 2
    Adenoid cystic carcinoma: A review of recent advances, molecular targets, and clinical trials. Dillon PM, Chakraborty S, Moskaluk CA, Joshi PJ, Thomas CY. Head & Neck. 2016;38(4):620-7. doi:10.1002/hed.23925.
  3. 3
    Adenoid Cystic Carcinoma of the Maxillary Sinus: A Clinical-Pathological Report of 10 Years of Experience From a Single Institution. Andrade MF, de Faria PR, Cardoso SV, et al. International Journal of Oral and Maxillofacial Surgery. 2014;43(11):1313-8. doi:10.1016/j.ijom.2014.06.016.
  4. 4
    Adenoid Cystic Carcinoma, Clinical Presentation, Current Treatment and Approaches Towards Novel Therapies. Zupancic M, Näsman A, Friesland S, Dalianis T. Anticancer Research. 2024;44(4):1325-1334. doi:10.21873/anticanres.16929.
  5. 5
    Adenoid Cystic Carcinoma of the Head and Neck--an Update. Coca-Pelaz A, Rodrigo JP, Bradley PJ, et al. Oral Oncology. 2015;51(7):652-61. doi:10.1016/j.oraloncology.2015.04.005.
  6. 6
    Adenoid Cystic Carcinoma of the Minor Salivary Glands: A Retrospective Series of 29 Cases and Review of the Literature. Shum JW, Chatzistefanou I, Qaisi M, Lubek JE, Ord RA. Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology. 2016;121(3):210-4. doi:10.1016/j.oooo.2015.10.003.
  7. 7
    Sinonasal Adenoid Cystic Carcinoma: The M. D. Anderson Cancer Center Experience. Lupinetti AD, Roberts DB, Williams MD, et al. Cancer. 2007;110(12):2726-31. doi:10.1002/cncr.23096.
  8. 8
    Molecular Pathology of Adenoid Cystic Carcinoma. Wei S, Pei J, Zhang PJL. Histology and Histopathology. 2025:18915. doi:10.14670/HH-18-915.
  9. 9
    The Role of Molecular Testing in the Differential Diagnosis of Salivary Gland Carcinomas. Skálová A, Stenman G, Simpson RHW, et al. The American Journal of Surgical Pathology. 2018;42(2):e11-e27. doi:10.1097/PAS.0000000000000980.
  10. 10
    Head and Neck Cancers. National Comprehensive Cancer Network. Updated 2026-05-12.
  11. 11
    Recent Developments in Salivary Gland Pathology After the WHO 2024 Classification: New Developments in Existing Entities and Evolving New Entities. Skálová A, Laco J, Thompson LDR, et al. Virchows Archiv : An International Journal of Pathology. 2026;488(5):1005-1020. doi:10.1007/s00428-026-04532-z.
  12. 12
    Histopathological Aspects of the Prognostic Factors for Salivary Gland Cancers. Nishida H, Kusaba T, Kawamura K, Oyama Y, Daa T. Cancers. 2023;15(4):1236. doi:10.3390/cancers15041236.
  13. 13
    Primary Intraosseous Adenoid Cystic Carcinoma of the Jaw: Clinical and Histopathologic Analysis. Deng RX, Xu X, Zhang CP, Zhang ZY, He Y. Journal of Oral and Maxillofacial Surgery : Official Journal of the American Association of Oral and Maxillofacial Surgeons. 2014;72(4):835.e1-10. doi:10.1016/j.joms.2013.11.032.
  14. 14
    Central adenoid cystic carcinoma of the mandible with odontogenic features: Report of a case. Mahomed F, Altini M, Meer S, Rikhotso E, Pearl C. Head & Neck. 2009;31(7):975-80. doi:10.1002/hed.20983.
  15. 15
    Primary Intraosseous Adenoid Cystic Carcinoma of the Mandible: A Comprehensive Review and Analysis of Four New Cases With Emphasis on Morphologic, Immunophenotypic, and Molecular Characteristics. Han J, Gu T, Yang X, et al. Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology. 2017;123(3):365-373. doi:10.1016/j.oooo.2016.11.002.
  16. 16
    Metatypical Adenoid Cystic Carcinoma: A Variant Showing Prominent Squamous Differentiation With a Predilection for the Sinonasal Tract and Skull Base. Mathew EP, Todorovic E, Truong T, et al. The American Journal of Surgical Pathology. 2022;46(6):816-822. doi:10.1097/PAS.0000000000001850.
  17. 17
    HIF‐1/2α: The Silent Architects of Adenoid Cystic Carcinoma—A Systematic Review and Meta‐Analysis. Maheswari R, Chandra A, Agrawal R. Oral Diseases. 2026;32(1):37-47. doi:10.1111/odi.70048.
  18. 18
    Survival Outcomes in Adenoid Cystic Carcinoma of the Head and Neck: A Systematic Review of 17 497 Cases and Meta‐Analysis. Lavareze L, Kimura TC, Cacita N, et al. Head & Neck. 2025;47(5):1541-1553. doi:10.1002/hed.28132.
  19. 19
    Intraosseous carcinoma of the jaws—A clinicopathologic review. Part I: Metastatic and salivary‐type carcinomas. Woolgar JA, Triantafyllou A, Ferlito A, et al. Head & Neck. 2013;35(6):895-901. doi:10.1002/hed.22917.
  20. 20
    Adenoid Cystic Carcinoma of Salivary Glands. A Study of 61 Cases With Clinicopathologic Correlation. Nascimento AG, Amaral AL, Prado LA, Kligerman J, Silveira TR. Cancer. 1986;57(2):312-9. doi:10.1002/1097-0142(19860115)57:23.0.co;2-a.
  21. 21
    Adenoid Cystic Carcinoma: A Rare Clinical Entity and Literature Review. Gondivkar SM, Gadbail AR, Chole R, Parikh RV. Oral Oncology. 2011;47(4):231-6. doi:10.1016/j.oraloncology.2011.01.009.
  22. 22
    Adenoid Cystic Carcinoma of Head and Neck: Summary and Review of Imaging Findings. Wang Y, Guo X, Yu K, et al. Heliyon. 2023;9(11):e21901. doi:10.1016/j.heliyon.2023.e21901.
  23. 23
    Bidirectional Trigeminal Perineural Spread of Adenoid Cystic Carcinoma via the Pterygopalatine Fossa. Xie Y, Zhu Y, Zhang Y. Oral Oncology. 2026;177:107948. doi:10.1016/j.oraloncology.2026.107948.
  24. 24
    Imaging Features and Clinical Significance of Perineural Spread or Extension of Head and Neck Tumors. Caldemeyer KS, Mathews VP, Righi PD, Smith RR. Radiographics : A Review Publication of the Radiological Society of North America, Inc. 1998 Jan-Feb;18(1):97-110; quiz 147. doi:10.1148/radiographics.18.1.9460111.
  25. 25
    Case Report: Transcavernous Sinus Resection of Parotid Carcinoma With Perineural Invasion to Meckel's Cave and Cavernous Sinus. Cai L, Dammers R, Rushing EG, et al. Frontiers in Oncology. 2026;16:1741177. doi:10.3389/fonc.2026.1741177.
  26. 26
    Adenoid cystic carcinoma cytology: Salivary gland and nonsalivary gland. Chowsilpa S, An D, Maleki Z. Diagnostic Cytopathology. 2020;48(12):1282-1289. doi:10.1002/dc.24573.
  27. 27
    Central Adenoid Cystic Carcinoma of the Mandible Manifesting as an Endodontic Lesion. Chen YK, Chen CH, Lin CC, et al. International Endodontic Journal. 2004;37(10):711-6. doi:10.1111/j.1365-2591.2004.00862.x.
  28. 28
    Central (Intraosseous) Adenoid Cystic Carcinoma of the Mandible: Report of a Case With Periapical Involvement. Favia G, Maiorano E, Orsini G, Piattelli A. Journal of Endodontics. 2000;26(12):760-3. doi:10.1097/00004770-200012000-00026.
  29. 29
    Bilateral intraosseous adenoid cystic carcinoma of the mandible: report of a case with lung metastases at first clinical presentation. Capodiferro S, Scully C, Macaita MG, et al. Oral Diseases. 2005;11(2):109-12. doi:10.1111/j.1601-0825.2004.01060.x.
  30. 30
    Radiographic Evaluation of Bone Invasion of Adenoid Cystic Carcinoma in the Oral and Maxillofacial Region. Suei Y, Tanimoto K, Taguchi A, Wada T. Journal of Oral and Maxillofacial Surgery : Official Journal of the American Association of Oral and Maxillofacial Surgeons. 1994;52(8):821-6. doi:10.1016/0278-2391(94)90227-5.
  31. 31
    Computed Tomography and Magnetic Resonance Imaging of Adenoid Cystic Carcinoma in the Maxillary Sinus: A Retrospective Study With Radiologic-Histopathologic Correlations. Li Y, Hao D, Song X, Zhang C. Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology. 2021;131(1):111-121. doi:10.1016/j.oooo.2020.06.019.
  32. 32
    Computed Tomography and Magnetic Resonance Imaging Findings Contribute to Differentiating Solid- And Nonsolid-Type Adenoid Cystic Carcinoma in Maxillary Sinus. Wang Y, Ji Y, Guo L, Wang Y, Sha Y. Journal of Computer Assisted Tomography. 2023 Nov-Dec 01;47(6):989-995. doi:10.1097/RCT.0000000000001505.
  33. 33
    Osseous Changes on Bone-Window MDCT as Indicator of Perineural Spread in Palatal Adenoid Cystic Carcinoma. Guess GC, Dalley RW, Schumacher AE, Lee PP. Oral Oncology. 2026;177:107975. doi:10.1016/j.oraloncology.2026.107975.
  34. 34
    Comparison of Imaging Features of Intraosseous Jaw Lesions on Panoramic Radiographs and Cone Beam Computed Tomography. Sumer T, Sumer AP, Zengin AZ, Muğlali M, Abaci SH. The Journal of Craniofacial Surgery. 2026:00001665-990000000-03740. doi:10.1097/SCS.0000000000012531.
  35. 35
    Comparison of Radiographical Characteristics and Diagnostic Accuracy of Intraosseous Jaw Lesions on Panoramic Radiographs and CBCT. Mao WY, Lei J, Lim LZ, et al. Dento Maxillo Facial Radiology. 2021;50(2):20200165. doi:10.1259/dmfr.20200165.
  36. 36
    Frequency and Imaging Features of the Adjacent Osseous Changes of Salivary Gland Carcinomas in the Head and Neck Region. Horiuchi D, Shimono T, Tatekawa H, et al. Neuroradiology. 2022;64(9):1869-1877. doi:10.1007/s00234-022-02972-3.
  37. 37
    ACR Appropriateness Criteria® Staging and Post-Therapy Assessment of Head and Neck Cancer. Gule-Monroe MK, Calle S, Policeni B, et al. Journal of the American College of Radiology : JACR. 2023;20(11S):S521-S564. doi:10.1016/j.jacr.2023.08.008.
  38. 38
    ACR Appropriateness Criteria® Cranial Neuropathy: 2022 Update. Expert Panel on Neurological Imaging, Rath TJ, Policeni B, et al. Journal of the American College of Radiology : JACR. 2022;19(11S):S266-S303. doi:10.1016/j.jacr.2022.09.021.
  39. 39
    Adenoid Cystic Carcinoma of the Head and Neck: Evaluation With MR Imaging and Clinical-Pathologic Correlation in 27 Patients. Sigal R, Monnet O, de Baere T, et al. Radiology. 1992;184(1):95-101. doi:10.1148/radiology.184.1.1319079.
  40. 40
    The Sensitivity and Specificity of High-Resolution Imaging in Evaluating Perineural Spread of Adenoid Cystic Carcinoma to the Skull Base. Hanna E, Vural E, Prokopakis E, et al. Archives of Otolaryngology--Head & Neck Surgery. 2007;133(6):541-5. doi:10.1001/archotol.133.6.541.
  41. 41
    Malignant Lesions in the Anterior Maxilla. MacDonald D, Martin M, Nguyen C. Clinical Radiology. 2020;75(7):497-506. doi:10.1016/j.crad.2019.09.133.
  42. 42
    Molecular Pathology of Salivary Gland Neoplasms: Diagnostic, Prognostic, and Predictive Perspective. Toper MH, Sarioglu S. Advances in Anatomic Pathology. 2021;28(2):81-93. doi:10.1097/PAP.0000000000000291.
  43. 43
    Adenoid Cystic Carcinoma With Striking Tubular Hypereosinophilia: A Unique Pattern Associated With Nonparotid Location and Both Canonical and Novel EWSR1::MYB and FUS::MYB Fusions. Weinreb I, Rooper LM, Dickson BC, et al. The American Journal of Surgical Pathology. 2023;47(4):497-503. doi:10.1097/PAS.0000000000002023.
  44. 44
    Discovery of Novel TULP4/ACTN4/EWSR1/ACTB::MYB and ESRRG::DNM3 Fusions Expands Molecular Landscape of Adenoid Cystic Carcinoma Beyond Fusions Between MYB/MYBL1 and NFIB Genes. Skálová A, Klubíčková N, Bradová M, et al. The American Journal of Surgical Pathology. 2024;48(12):1503-1511. doi:10.1097/PAS.0000000000002304.
  45. 45
    Prognostic Impact of Tumor Stage and Growth Pattern in Sinonasal Adenoid Cystic Carcinoma: A 15‐Year Population‐Based Study. van de Velde LJ, Breimer GE, Devriese LA, et al. Head & Neck. 2026;48(7):1830-1840. doi:10.1002/hed.70203.
  46. 46
    Genomic and Transcriptomic Analysis of Salivary Adenoid Cystic Carcinomas Defines Molecular Subtypes. Liu L, Zhang Y, Hao M, et al. Journal of Dental Research. 2026:220345261416398. doi:10.1177/00220345261416398.
  47. 47
    Tumors of the Minor Salivary Glands. Eric R. Carlson, Robert A. Ord. Chapter 12.
  48. 48
    Adenoid Cystic Carcinoma of the Head and Neck Treated by Surgery With or Without Postoperative Radiation Therapy: Prognostic Features of Recurrence. Chen AM, Bucci MK, Weinberg V, et al. International Journal of Radiation Oncology, Biology, Physics. 2006;66(1):152-9. doi:10.1016/j.ijrobp.2006.04.014.
  49. 49
    Surgery Alone Provides Long-Term Survival Rates Comparable to Those of Surgery Plus Postoperative Radiotherapy for Patients With Adenoid Cystic Carcinoma of the Palate. Li Q, Xu T, Gao JM, et al. Oral Oncology. 2011;47(3):170-3. doi:10.1016/j.oraloncology.2010.12.005.
  50. 50
    Analysis of the Clinicopathological Characteristics and Prognosis of Adenoid Cystic Carcinoma of the Intraoral Minor Salivary Glands: A Retrospective Study of 40 Cases. He JF, Lin Y, Wang B, et al. International Journal of Oral and Maxillofacial Surgery. 2021;50(4):444-450. doi:10.1016/j.ijom.2020.07.031.
  51. 51
    Clinical outcomes in salivary adenoid cystic carcinoma. Dalal P, Dermody S, Brummel C, et al. Journal of Clinical Oncology. 2024;42(Suppl 16):6102. doi:10.1200/JCO.2024.42.16_suppl.6102.
  52. 52
    Clinicopathologic characteristics and treatment outcomes of adenoid cystic carcinoma (ACC) by different primary sites. Passarini L, Neto F, Cavalheiro V, et al. Journal of Clinical Oncology. 2026;44(Suppl 16):6121. doi:10.1200/JCO.2026.44.16_suppl.6121.
  53. 53
    Clinical and genomic characterisation of adenoid cystic carcinoma of the head and neck, lung, and breast. Heathcote E, Patel K, Rack S, et al. Journal of Clinical Oncology. 2023;41(Suppl 16):6094. doi:10.1200/JCO.2023.41.16_suppl.6094.
  54. 54
    Tumors of the Submandibular and Sublingual Glands. Eric R. Carlson, Robert A. Ord. Chapter 11.
  55. 55
    Diseases of the Head and Neck. Florian Dammann, Jan Wartenberg. Chapter 7.
  56. 56
    Salivary gland tumors: Molecular characterization and therapeutic advances for metastatic disease. Schvartsman G, Pinto NA, Bell D, Ferrarotto R. Head & Neck. 2019;41(1):239-247. doi:10.1002/hed.25468.
  57. 57
    The Molecular Landscape of Recurrent and Metastatic Head and Neck Cancers: Insights From a Precision Oncology Sequencing Platform. Morris LGT, Chandramohan R, West L, et al. JAMA Oncology. 2017;3(2):244-255. doi:10.1001/jamaoncol.2016.1790.
  58. 58
    Adenoid cystic carcinoma of the head and neck: Patterns of recurrence and implications for intensity‐modulated radiotherapy. Gao RW, Routman DM, Harmsen WS, et al. Head & Neck. 2023;45(1):187-196. doi:10.1002/hed.27223.
  59. 59
    Clinical characteristics and prognostic factors of malignant tumors involving pterygopalatine fossa. Woo HJ, Hwang PH, Kaplan MJ, Choby G. Head & Neck. 2020;42(2):281-288. doi:10.1002/hed.26000.

Build an interactive differential →

Nearest neighbours

Expand to full map ↗

This lesion (ringed) among its most radiographically similar entries. Region and origin must overlap, so every neighbour is a genuine differential.

Drag to explore · Ctrl/⌘ + scroll to zoom · click a neighbour to recentre

← All lesions