Abstract:The classification of poorly differentiated sinonasal carcinomas and their nonepithelial mimics has experienced tremendous developments during the last 2 decades. These recent developments paved the way for an increasingly adopted approach to a molecularbased or etiology-based refined classification of the many carcinoma variants that have been historically lumped into the sinonasal undifferentiated carcinoma category. Among these new achievements, recognition of carcinoma subtypes driven by defects in the Swi… Show more
Background
Poorly differentiated sinonasal small round cell tumors (SRCTs) are rare and heterogeneous, posing challenges in diagnosis and treatment.
Methods
Recent advances in molecular findings and diagnostic refinement have promoted better understanding and management of these tumors.
Results
The newly defined and emerging sinonasal entities demonstrate diverse morphologies, specific genomic signatures, and clinical behavior from conventional counterparts. In this review of SRCTs, emphasis is placed on the diagnostic approach with the employment of a pertinent panel of immunohistochemistry studies and/or molecular tests, fine-tuned to the latest WHO 5 classification of sinonasal/paranasal tumors and personalized treatment.
Conclusion
Specifically, this review focuses on tumors with epithelial and neuroectodermal derivation.
Background
Poorly differentiated sinonasal small round cell tumors (SRCTs) are rare and heterogeneous, posing challenges in diagnosis and treatment.
Methods
Recent advances in molecular findings and diagnostic refinement have promoted better understanding and management of these tumors.
Results
The newly defined and emerging sinonasal entities demonstrate diverse morphologies, specific genomic signatures, and clinical behavior from conventional counterparts. In this review of SRCTs, emphasis is placed on the diagnostic approach with the employment of a pertinent panel of immunohistochemistry studies and/or molecular tests, fine-tuned to the latest WHO 5 classification of sinonasal/paranasal tumors and personalized treatment.
Conclusion
Specifically, this review focuses on tumors with epithelial and neuroectodermal derivation.
“…6 A-C). SWI/SNF complex deficient malignancies can be preferentially identified by immunohistochemical antibodies to SMARCB1 (INI1) and SMARCA4 (BRG1) which are sensitive diagnostic tools [ 63 ].The therapeutic option rests in local control of the disease with polychemotherapy and radiotherapy [ 61 , 62 ]. Fig.…”
Section: Swi/snf Complex Deficient Sinonasal Carcinoma and Other Mali...mentioning
Classification of head and neck tumors has evolved in recent decades including a widespread application of molecular testing in tumors of the salivary glands, sinonasal tract, oropharynx, nasopharynx, and soft tissue. Availability of new molecular techniques allowed for the definition of multiple novel tumor types unique to head and neck sites. Moreover, the expanding spectrum of immunohistochemical markers facilitates a rapid identification of diagnostic molecular abnormalities. As such, it is currently possible for head and neck pathologists to benefit from a molecularly defined classifications, while making diagnoses that are still based largely on histopathology and immunohistochemistry. This review highlights some principal molecular alterations in head and neck neoplasms presently available to assist pathologists in the practice of diagnosis, prognostication and prediction of response to treatment.
“…Sinonasal tumors are often treated with surgical excision followed by adjuvant radiation or concurrent chemoradiation. The most common cause of death was locally advanced unresectable disease [20]; with required surgery without complete tumor resection for locally advanced cases increasing operation difficulties and morbidity. It's worth investigating if chemotherapy or radiotherapy could be used before surgery.…”
Section: Patient Characteristics the Clinicopathological Features Are...mentioning
Currently, less than 200 cases of SMARCB1-deficient sinus cancer (SDSC) have been documented. Little information is available about the best treatment options or prognosis for SDSC. From September 2016 to November 2022, the medical records of 22 people with SDSC were evaluated retrospectively. Patient demographics, staging, pathology findings, treatment details, recurrence, metastasis, and survival outcomes were all investigated by the researchers. The 1-, 2-, and 3-year overall survival (OS) rates for the entire cohort were 89.8%, 84.2%, and 45.1%, respectively, as were the 1-, 2-, and 3-year progression-free survival (PFS) rates of 81.8%, 63.8%, and 31.9%. After induction chemotherapy, 66.7% (10/15) of patients exhibited decreased tumor volume. Patients who accepted chemoradiotherapy had a better 2-year OS (100% vs. 72.7%, p=0.048) than those who accepted surgery as a preference. However, there is no difference in 2-year PFS between the two groups (53.0% vs. 75.8%, p=0.59). Patients with progressed or stable disease after induction chemotherapy had a higher risk of developing local recurrence (p=0.007); they also showed poor 2-year PFS (40.0% vs. 82.1%, p=0.019). SDSC had a poor 3-year OS, with a PFS of less than 50%. For locally advanced SDSC, chemoradiotherapy might be managed before surgery, especially in patients who benefit from induction chemotherapy.
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