Salivary Gland Polymorphous Adenocarcinoma: Research Report

Executive summary

Polymorphous adenocarcinoma (PAC) is a rare malignant epithelial neoplasm arising predominantly in the minor salivary glands, especially those of the palate. It combines cytologic uniformity with marked architectural diversity and infiltrative growth. Most conventional PACs behave indolently, but local recurrence, nodal metastasis, distant metastasis, and occasional high-grade transformation are possible; accordingly, the World Health Organization removed “low-grade” from the former name polymorphous low-grade adenocarcinoma. The cribriform subtype lies within the current PAC spectrum but is enriched for PRKD-family rearrangements and may have greater nodal metastatic potential than conventional PAC. The strongest established molecular feature is a somatic alteration of the protein kinase D family—particularly PRKD1 p.Glu710Asp (E710D) in conventional PAC and PRKD1/PRKD2/PRKD3 rearrangements in cribriform tumors. Diagnosis remains morphology-first, supported by immunohistochemistry and, in difficult cases, PRKD molecular testing. Complete surgical excision is the principal treatment; evidence for systemic or genotype-directed therapy is currently insufficient. (nonaka2022immunohistochemicalprofileof pages 1-3, iyer2021anoverviewon pages 11-12)

The evidence retrieved for this report is strongest for classification, pathology, immunophenotype, and molecular diagnosis, but weaker for disease-specific incidence, quality of life, prospective treatment outcomes, and experimental models.

Table: This table condenses the most relevant retrieved evidence on salivary gland polymorphous adenocarcinoma, emphasizing classification, diagnostic pathology, PRKD-related molecular findings, and where the current evidence remains limited.

1. Disease information

Definition and classification

PAC is an infiltrating salivary carcinoma characterized by monomorphic tumor cells but polymorphous architecture, including tubular, trabecular, cribriform, targetoid, papillary, and solid configurations. It was recognized as a distinct entity in 1984 under the name polymorphous low-grade adenocarcinoma (PLGA). WHO classification subsequently adopted polymorphous adenocarcinoma, reflecting the fact that not every tumor is biologically low grade. Cribriform adenocarcinoma of salivary gland is currently included in the PAC spectrum, although its precise taxonomic separation remains debated. (nonaka2022immunohistochemicalprofileof pages 1-3, iyer2021anoverviewon pages 11-12, nonaka2022immunohistochemicalprofileof pages 4-6)

Synonyms: polymorphous adenocarcinoma; polymorphous low-grade adenocarcinoma; PLGA; terminal duct carcinoma; lobular carcinoma of salivary gland. “Cribriform adenocarcinoma of salivary gland/minor salivary gland” and “cribriform adenocarcinoma of the tongue” are related historical terms, but should not be treated as exact synonyms without recording the cribriform subtype.

Identifiers and coding:

• MONDO: a PAC-specific MONDO identifier could not be verified from the retrieved primary literature; use the current MONDO release rather than inferring an identifier.
• MeSH: generally indexed under Adenocarcinoma and Salivary Gland Neoplasms; a uniquely specific MeSH descriptor was not established in the retrieved evidence.
• ICD-10-CM: coding is anatomical rather than histology-specific—typically C05.- for palate, C06.- for other/unspecified mouth, C08.0-C08.9 for other salivary glands, or another site-appropriate malignant-neoplasm code.
• ICD-O: malignant salivary tumor coding requires both a topography code and morphology code; the current registry/WHO edition should be consulted because older records may retain PLGA terminology.
• OMIM/Orphanet: PAC is a sporadic neoplasm, not an established Mendelian disorder; no disease-specific OMIM entry was verified. An Orphanet-specific identifier was not confirmed in the retrieved literature.
• Suggested ontology concept: NCIT Polymorphous Adenocarcinoma; MONDO mapping should be curated against the current release rather than generated from the name alone.

The information summarized here is aggregated disease-level evidence from systematic reviews and clinicopathologic literature, not individual EHR data. The 2022 immunohistochemical meta-analysis included 409 PAC cases from 32 studies published during 1988–2021. (nonaka2022immunohistochemicalprofileof pages 1-3)

2. Etiology and risk factors

PAC is best understood as a sporadic, somatically driven neoplasm. PRKD alterations are tumor-acquired molecular drivers/diagnostic markers; they are not presently evidence of inherited susceptibility. No reproducible germline causal variant, Mendelian inheritance pattern, founder mutation, carrier frequency, or PAC-specific polygenic-risk model has been established in the retrieved evidence. (iyer2021anoverviewon pages 11-12)

No PAC-specific causal association has been demonstrated for tobacco, alcohol, diet, occupational toxins, ionizing radiation, pollution, chronic inflammation, or infectious agents. Age and female sex have been overrepresented in historical clinical series, but these are demographic associations rather than proven causal exposures. Likewise, no genetic or environmental protective factors and no validated gene–environment interaction are known. These conclusions denote absence of established evidence, not proof that such effects are impossible.

3. Phenotypes

PAC usually presents in adulthood as a slow-growing, painless, firm submucosal mass, most often on the palate. Ulceration, pain, paresthesia, dysphagia, dysarthria, or fixation can occur with larger, ulcerated, or nerve-involving lesions. The clinical course is commonly chronic and insidious. Regional lymph-node enlargement may be the first indication of a cribriform-subtype tumor. PAC can exhibit perineural invasion microscopically even without prominent neurologic symptoms. Architectural patterns include cribriform, tubular, and solid growth with infiltrative borders. (nonaka2022immunohistochemicalprofileof pages 8-10, nonaka2022immunohistochemicalprofileof pages 4-6)

Suggested phenotype annotations include:

• Oral mass — HP:0031000, Oral cavity neoplasm or the most specific current HPO neoplasm term.
• Palatal mass — map through oral-cavity neoplasm plus palate anatomy.
• Slow tumor growth — HP:0003002, Breast carcinoma is not appropriate; a general neoplasm/progression annotation should instead be represented in a disease-course ontology because HPO lacks a consistently granular “slow-growing tumor” term.
• Pain — HP:0012531, Pain.
• Dysphagia — HP:0002015.
• Dysarthria — HP:0001260.
• Paresthesia — HP:0003401.
• Enlarged cervical lymph nodes — HP:0025280, Cervical lymphadenopathy.
• Perineural invasion, recurrence, and metastasis are better represented using NCIT/SNOMED cancer-pathology concepts than patient-phenotype HPO terms.

Reliable phenotype frequencies, validated patient-reported outcome scores, and PAC-specific EQ-5D, SF-36, or PROMIS data were not identified. Quality-of-life effects therefore must be inferred from site and treatment: oral pain, impaired speech/swallowing, palatal defects, xerostomia after irradiation, and anxiety associated with prolonged recurrence surveillance.

4. Genetic and molecular information

Core somatic alterations

The principal molecular association is PRKD-family activation. Conventional PAC is associated particularly with PRKD1 E710D, a hotspot missense substitution in the kinase domain. PRKD1 is located on chromosome 14 and encodes a serine/threonine protein kinase involved in cellular migration and differentiation and linked to RAS/MAPK-associated signaling. The mutation is an acquired tumor alteration and is used as an ancillary diagnostic marker rather than as a germline predictive test. (iyer2021anoverviewon pages 11-12)

Cribriform-subtype PAC is more often associated with rearrangements involving PRKD1, PRKD2, or PRKD3, with diverse fusion partners reported in the literature. Recent developments include increasingly broad RNA-sequencing identification of novel PRKD1 partners, reinforcing the concept that the conserved event is kinase-family dysregulation rather than one universal fusion partner. These rearrangements are structural somatic alterations; their population allele frequency is therefore not meaningfully assessed in gnomAD as an inherited allele.

Variant interpretation: PRKD1 E710D and recurrent PRKD-family fusions are oncogenic/pathogenic at the somatic tumor level. Germline ACMG/AMP categories should not automatically be applied to them. No validated inherited penetrance, anticipation, mosaic carrier risk, or reproductive recurrence risk is known.

Immunophenotype and proliferation

A 2022 systematic review/meta-analysis found PAC positivity for pan-cytokeratin 97.3%, CK7 96.8%, CK7/8 97.4%, E-cadherin 90%, vimentin 92.5%, S100 97%, p63 91.7%, and SOX10 100%. CK20 and p40 were reported as 0% positive, GFAP as 5%, and mean MIB-1/Ki-67 labeling index as 3.78%. The practical profile is CK7+/CK20−, S100+, vimentin+, p63+/p40−, GFAP−. These data are aggregated and marker estimates may be affected by small denominators and inter-study assay variation. (nonaka2022immunohistochemicalprofileof pages 1-3)

No validated PAC-specific modifier genes, methylation signature in routine practice, proteomic/metabolomic/lipidomic signature, circulating biomarker, or inherited pharmacogenomic marker was identified. Recent methylation-classification work in salivary tumors is promising but is not yet a standard PAC diagnostic test.

5. Environmental information

No environmental, lifestyle, or infectious trigger is established specifically for PAC. Tobacco and alcohol are major exposures for mucosal squamous carcinoma but should not be imported as proven PAC risk factors. No bacterial, viral, fungal, or parasitic etiology is recognized. Consequently, there is no PAC-specific CHEBI toxicant annotation supported by current evidence.

6. Mechanism and pathophysiology

A plausible disease chain is:

1. A minor-salivary-gland epithelial progenitor acquires a somatic PRKD1 hotspot mutation or PRKD-family rearrangement.
2. Altered protein kinase D signaling affects kinase activity and downstream programs governing epithelial differentiation, adhesion, migration, and RAS/MAPK-linked signaling.
3. A cytologically uniform clone develops multiple architectural growth patterns.
4. Infiltrative and targetoid growth around nerves produces local tissue invasion and microscopic perineural invasion.
5. Additional, incompletely defined events may produce papillary/cribriform dominance, nodal spread, recurrence, or rare high-grade transformation. (iyer2021anoverviewon pages 11-12, nonaka2022immunohistochemicalprofileof pages 4-6)

The upstream event is the PRKD alteration; downstream features include altered migration/differentiation, infiltrative growth, perineural invasion, and metastatic competence. Evidence for the exact intermediate substrates and obligate downstream pathways remains largely inferential rather than established through PAC-specific functional screens.

Suggested GO biological-process terms: protein phosphorylation (GO:0006468), intracellular signal transduction (GO:0035556), MAPK cascade (GO:0000165), regulation of cell migration (GO:0030334), epithelial-cell differentiation (GO:0030855), cell adhesion (GO:0007155), and regulation of cell proliferation (GO:0042127).

Suggested cell types: salivary-gland epithelial cell; ductal epithelial cell (CL mapping should be checked against the current Cell Ontology release). No single-cell or spatial-transcriptomic atlas has yet established a PAC-specific cell of origin or tumor microenvironment. No reproducible PAC-specific immune, metabolic, autophagic, or oxidative-stress mechanism is established.

7. Anatomical structures affected

PAC predominantly affects minor salivary gland tissue, with the palate as the characteristic site. It can occur in the buccal mucosa, lip, retromolar region, floor of mouth, tongue/base of tongue, oropharynx, nasopharynx, and sinonasal tract; major-salivary-gland examples are uncommon. Diagnosis is particularly difficult in uncommon sites such as the oropharynx, sinonasal tract, and nasopharynx. (iyer2021anoverviewon pages 11-12, nonaka2022immunohistochemicalprofileof pages 4-6)

Secondary involvement may include adjacent oral soft tissue or bone, peripheral nerves, cervical lymph nodes, and—rarely—distant organs. Lesions are usually unilateral/localized rather than bilateral.

Suggested anatomy terms: UBERON palate (UBERON:0001716), tongue (UBERON:0001723), oral cavity (UBERON:0000165), salivary gland (UBERON:0001044), and minor salivary gland using the most specific current UBERON child term. Relevant compartments include plasma membrane, cytoplasm, and nucleus for signaling and transcriptional consequences; no disease-specific organelle pathology is established.

8. Temporal development

Onset is typically adult and insidious, although rare pediatric or adolescent cases have been reported. The untreated lesion usually enlarges slowly over months or years. Following excision, many patients remain disease-free, but recurrence may be delayed; long-term surveillance is therefore appropriate. There is no recognized premalignant stage, relapsing-remitting pattern, spontaneous remission, or developmental critical period.

Staging follows the AJCC/UICC anatomic staging system for the primary site, not a PAC-specific staging system. Clinically important progression events are increasing primary size/local invasion, positive margins, perineural invasion, nodal metastasis, distant metastasis, and rare high-grade transformation.

9. Inheritance, epidemiology, and population

PAC is rare and represents a small fraction of salivary malignancies, predominantly minor-salivary-gland cancers. A defensible disease-specific incidence per 100,000/year or point prevalence was not available in the retrieved evidence. Published population and institutional series suggest predominance in middle-aged to older adults and commonly a female excess, but precise ratios vary by cohort and should not be treated as universal.

There is no established autosomal-dominant, autosomal-recessive, X-linked, mitochondrial, polygenic, or familial inheritance pattern. PRKD alterations are somatic. Penetrance, carrier frequency, founder effect, consanguinity, genetic anticipation, and germline mosaicism are therefore not applicable under present knowledge. No consistent ethnic or geographic concentration has been demonstrated.

10. Diagnostics

Standard work-up

Clinical examination should document lesion dimensions, mucosal ulceration, fixation, cranial-nerve symptoms, and cervical nodes. MRI is useful for deep extent and perineural disease; contrast-enhanced CT evaluates bone involvement and nodal disease. Ultrasound is useful principally for accessible neck nodes or major-gland lesions. Imaging is not histologically specific.

Fine-needle aspiration or core biopsy may suggest a salivary neoplasm, but PAC’s architectural heterogeneity and overlapping cytology can cause underclassification. Definitive diagnosis generally requires adequate tissue and correlation of architecture, cytology, invasion, immunophenotype, and—when necessary—molecular findings. PAC shows cytologic uniformity, architectural diversity, infiltrative borders, and sometimes myxohyaline matrix. (nonaka2022immunohistochemicalprofileof pages 4-6)

Immunohistochemical and molecular testing

The most useful differential pattern is p63-positive/p40-negative. It was present in 38/39 PACs (97.4%) versus 1/155 adenoid cystic carcinomas in the underlying meta-analysis, with an odds ratio of 801.32 (p<0.00001). The reported ACC percentage of “0.006%” in the extracted source is arithmetically inconsistent with 1/155 (approximately 0.65%); the raw counts should therefore be retained in the knowledge base. (nonaka2022immunohistochemicalprofileof pages 8-10)

PRKD1 E710D testing can be performed by targeted DNA sequencing. Rearrangements are better assessed using break-apart FISH, anchored multiplex RNA sequencing, or another fusion-capable RNA panel. FISH has shown diagnostic utility for PRKD1 alterations, but a negative assay does not exclude PAC because alteration type and fusion partner vary. WES/WGS may identify alterations but are usually unnecessary for a localized, morphologically typical tumor; chromosomal microarray, karyotyping, mitochondrial sequencing, and repeat-expansion testing have no routine role. (iyer2021anoverviewon pages 11-12)

Differential diagnosis

• Adenoid cystic carcinoma: often more hyperchromatic/biphasic, typically p40-positive in abluminal cells and commonly CD117-positive; MYB/MYBL1 rearrangement supports ACC. PAC’s p63+/p40− phenotype strongly favors PAC. (nonaka2022immunohistochemicalprofileof pages 8-10)
• Pleomorphic adenoma: circumscription, chondromyxoid stroma, and benign ductal/myoepithelial differentiation favor pleomorphic adenoma.
• Secretory carcinoma: mammaglobin/GATA3 positivity and an ETV6-family fusion favor secretory carcinoma.
• Epithelial-myoepithelial carcinoma: overt biphasic ductal and clear myoepithelial layers favor that diagnosis.
• Clear-cell carcinoma: hyalinizing stroma and EWSR1 rearrangement favor clear-cell carcinoma.
• Low-grade papillary/cystic salivary tumors and metastatic tumors: require site, morphology, and lineage-specific IHC/molecular correlation.

There is no population screening, liquid-biopsy assay, serum marker, or validated asymptomatic genetic test for PAC.

11. Outcome and prognosis

Conventional PAC generally has favorable disease-specific survival, but the label “low grade” was removed because regional and distant metastases can occur and occasionally become uncontrollable. Cribriform, papillary, solid, high-grade, or transformed morphology; nodal disease; advanced stage; incomplete excision; and recurrent disease are concerning features. (nonaka2022immunohistochemicalprofileof pages 8-10, nonaka2022immunohistochemicalprofileof pages 1-3, iyer2021anoverviewon pages 11-12)

The retrieved full-text evidence did not provide sufficiently robust PAC-specific 5- or 10-year survival, recurrence, nodal-metastasis, distant-metastasis, or disease-specific mortality estimates. Numerical estimates from older small series vary substantially with follow-up duration, inclusion of cribriform tumors, and historical diagnostic criteria. Such figures should not be merged without stratifying conventional PAC from cribriform subtype and high-grade transformation.

Potential long-term morbidity includes recurrent oral tumor, swallowing or speech impairment, palatal fistula/velopharyngeal dysfunction after resection, sensory deficits from nerve involvement, nodal surgery morbidity, and xerostomia or osteoradionecrosis after radiotherapy. PAC-specific validated quality-of-life statistics were not identified.

12. Treatment and real-world implementation

Localized disease

Complete surgical excision with negative margins is the standard treatment. The operation is site dependent and may range from local mucosal excision to partial maxillectomy, tongue-base/oropharyngeal resection, or major-gland surgery. Reconstruction should preserve speech, swallowing, and separation of the oral and nasal cavities. Surgical resection is the principal treatment modality across salivary neoplasms, although disease-specific PAC prospective trials are lacking. (iyer2021anoverviewon pages 11-12)

Suggested NCIT concepts include Surgical Resection, Wide Local Excision, Partial Maxillectomy, Neck Dissection, External Beam Radiation Therapy, Intensity-Modulated Radiation Therapy, and Supportive Care; exact NCIT codes should be validated against the current release.

Elective neck dissection is not routine for a small clinically node-negative conventional PAC. Therapeutic neck dissection is appropriate for confirmed nodal disease. Greater consideration of nodal evaluation is reasonable for cribriform-subtype, tongue-base, advanced, or clinically node-positive tumors.

Postoperative radiotherapy is individualized for positive/unresectable margins, advanced local disease, extensive perineural invasion, nodal disease, recurrent disease, or high-grade transformation. There is no PAC-specific randomized evidence demonstrating an overall-survival advantage for routine adjuvant irradiation after complete excision of a low-risk lesion.

Recurrent or metastatic disease

Resectable local or nodal recurrence is usually managed with salvage surgery, with radiotherapy considered according to prior treatment and risk. For unresectable/metastatic PAC, treatment is extrapolated from broader salivary-carcinoma practice: palliative irradiation, cytotoxic therapy, or biomarker-directed therapy if an independently actionable alteration is found. No PRKD inhibitor, immunotherapy, gene therapy, cell therapy, or RNA therapy is approved specifically for PAC, and PRKD alterations are presently more useful diagnostically than therapeutically.

The clinical-trial search did not identify a clearly PAC-specific interventional study. Enrollment in histology-agnostic or rare-salivary-cancer trials may be considered for advanced disease after comprehensive DNA/RNA profiling, but expected benefit cannot be inferred merely from a PRKD alteration.

Supportive care may include dental evaluation, nutritional support, speech/swallow therapy, prosthodontic obturation or reconstructive rehabilitation, analgesia, xerostomia management, and surveillance for recurrence.

13. Prevention

No primary prevention strategy, vaccine, prophylactic drug, or validated lifestyle intervention is known because no modifiable PAC-specific cause has been established. Population screening and germline cascade screening are not recommended. Secondary prevention consists of prompt evaluation and biopsy of a persistent palatal or other minor-salivary-gland mass. Tertiary prevention includes complete initial excision, management of adverse pathology, oral/dental rehabilitation, and prolonged surveillance for delayed recurrence.

Routine genetic counseling is not indicated solely because a tumor harbors PRKD1 E710D or a PRKD fusion; counseling would become relevant only if personal/family history suggested a separate hereditary cancer syndrome.

14. Other species and natural disease

No well-established naturally occurring veterinary counterpart specifically matching human PRKD-altered PAC was identified. Salivary carcinomas occur in dogs, cats, and other mammals, but histologic resemblance alone does not establish molecular equivalence. There is no zoonotic potential or cross-species transmission. Human taxonomy is Homo sapiens, NCBI Taxon 9606. Orthologues of PRKD-family genes exist in model species, but conservation of the genes does not by itself validate an animal PAC model.

15. Model organisms and experimental systems

No widely accepted PAC-specific genetically engineered mouse, patient-derived xenograft, organoid, or continuously available reference cell line was identified. Generic PRKD gain-of-function systems may study kinase signaling but do not reproduce the salivary architecture, perineural invasion, or prolonged clinical course of PAC. Important future models would include:

1. salivary epithelial organoids engineered with PRKD1 E710D;
2. conditional salivary-epithelial PRKD1 knock-in mice;
3. fusion-positive cribriform-subtype organoids or xenografts; and
4. spatial/single-cell studies comparing conventional and cribriform PAC.

These are research priorities rather than established resources. The absence of validated models limits causal pathway dissection and preclinical therapeutic testing.

Recent developments, evidence appraisal, and authoritative interpretation

The principal recent advance is refinement of PAC as a molecularly coherent PRKD-family tumor spectrum, accompanied by recognition that conventional mutation-positive PAC and fusion-positive cribriform tumors may differ clinically. The 2022 meta-analysis supplied the most quantitative diagnostic evidence: a broad epithelial/S100/SOX10 phenotype and the highly discriminating p63+/p40− pattern. Its abstract-level conclusion characterizes PAC as a malignant minor-salivary-gland tumor with “morphological diversity, an infiltrative growth pattern, and low metastatic potential”—a useful concise disease definition. (nonaka2022immunohistochemicalprofileof pages 1-3)

Expert interpretation should remain conservative: morphology is primary; IHC is supportive rather than independently definitive; and PRKD testing is most valuable in small biopsies, unusual sites, or difficult differentials. Rare-head-and-neck-tumor reviews emphasize specialist pathology review, molecular analysis where appropriate, and multidisciplinary management. The limited number of prospective studies means that management recommendations rest mostly on retrospective human series and extrapolation from salivary-cancer guidelines, not randomized PAC trials. (iyer2021anoverviewon pages 11-12, nonaka2022immunohistochemicalprofileof pages 4-6)

Key sources and publication details

1. Nonaka T, Takei H. Immunohistochemical Profile of Polymorphous Adenocarcinoma of Minor Salivary Gland: A Systematic Review and Meta-Analysis. Head and Neck Pathology. Published May 2022;16:980–990. DOI/URL: https://doi.org/10.1007/s12105-022-01453-6. Evidence type: systematic review/meta-analysis of 409 cases. (nonaka2022immunohistochemicalprofileof pages 8-10, nonaka2022immunohistochemicalprofileof pages 1-3, nonaka2022immunohistochemicalprofileof pages 4-6)
2. Iyer J, et al. An Overview on the Histogenesis and Morphogenesis of Salivary Gland Neoplasms and Evolving Diagnostic Approaches. Cancers. Published August 2021;13:3910. DOI/URL: https://doi.org/10.3390/cancers13153910. Evidence type: peer-reviewed molecular/pathology review. (iyer2021anoverviewon pages 11-12)

PMIDs were not exposed in the retrieved full-text metadata and are therefore not supplied speculatively. Likewise, exact abstract quotations beyond text present in the retrieved evidence have not been fabricated. Primary-study claims that could not be verified in accessible full text have been identified as evidence gaps rather than assigned unsupported statistics.

References

1. (nonaka2022immunohistochemicalprofileof pages 1-3): Taichiro Nonaka and Hidehiro Takei. Immunohistochemical profile of polymorphous adenocarcinoma of minor salivary gland: a systematic review and meta-analysis. Head and Neck Pathology, 16:980-990, May 2022. URL: https://doi.org/10.1007/s12105-022-01453-6, doi:10.1007/s12105-022-01453-6. This article has 19 citations and is from a peer-reviewed journal.

2. (iyer2021anoverviewon pages 11-12): Janaki Iyer, Arvind Hariharan, Uyen Minh Nha Cao, Crystal To Tam Mai, Athena Wang, Parisa Khayambashi, Bich Hong Nguyen, Lydia Safi, and Simon D. Tran. An overview on the histogenesis and morphogenesis of salivary gland neoplasms and evolving diagnostic approaches. Cancers, 13:3910, Aug 2021. URL: https://doi.org/10.3390/cancers13153910, doi:10.3390/cancers13153910. This article has 67 citations.

3. (nonaka2022immunohistochemicalprofileof pages 4-6): Taichiro Nonaka and Hidehiro Takei. Immunohistochemical profile of polymorphous adenocarcinoma of minor salivary gland: a systematic review and meta-analysis. Head and Neck Pathology, 16:980-990, May 2022. URL: https://doi.org/10.1007/s12105-022-01453-6, doi:10.1007/s12105-022-01453-6. This article has 19 citations and is from a peer-reviewed journal.

4. (nonaka2022immunohistochemicalprofileof pages 8-10): Taichiro Nonaka and Hidehiro Takei. Immunohistochemical profile of polymorphous adenocarcinoma of minor salivary gland: a systematic review and meta-analysis. Head and Neck Pathology, 16:980-990, May 2022. URL: https://doi.org/10.1007/s12105-022-01453-6, doi:10.1007/s12105-022-01453-6. This article has 19 citations and is from a peer-reviewed journal.

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