Spontaneous Regression Of Intraoral Mucosa-associated Lymphoid Tissue Lymphoma: Molecular Study Of A Case
Sakuma, H., Okabe, M., Yokoi, M., Eimoto, T., & Inagaki, H. (2006). spontaneous regression of intraoral mucosa-associated lymphoid tissue lymphoma: molecular study of a case. Pathology international, 56(6), 331–335. https://doi.org/10.1111/j.1440-1827.2006.01967.x
View Original Source →Abstract
Mucosa‐associated lymphoid tissue (MALT) lymphoma presentation in the oral cavity is very rare. Reported herein is a case of intraoral MALT lymphoma of the minor salivary gland in a 70‐year‐old woman with Sjogren’s syndrome. Unexpectedly, a spontaneous clinically and histologically confirmed regression occurred 1 month after the tumor biopsy for diagnosis. Considering that salivary MALT lymphoma is associated with Sjogren’s syndrome and that the chronic inflammation caused by Sjogren’s syndrome persisted, it is hypothesized that the tumor clone might be present in the regressed lesion. Minimal residual tumor clone identical with the primary lesion was detected using the polymerase chain reaction (PCR) clonality assay for immunoglobulin heavy chain gene ( IgH ) rearrangement. No recurrence was clinically evident 38 months after the diagnosis. Spontaneous regression of MALT lymphoma should be examined at the molecular level in addition to clinical and histological evaluations. When minimal residual disease is detected, close follow up is necessary for early detection of the tumor relapse.
Case Details
Disease Location
Intraoral
Personal Characteristics
70 -year-old female, japanese 13 year history of sjogren's syndrome (sjs)
Clinical Characteristics
Presented with a 10- months history of painless ulcer of the hard palate in the oral cavity. She did not complain of fever, weight loss, or night sweats. She had mild symptoms of sjs and had not included any specific treatment oral cavity exam revealed an ulcerated induration (15x17mm) located in the center of the hard palate the liver, spleen, and superficial lymph nodes were not palpable lad data showed normal serum rheumatoid factor, anti-ss-a/ro antibody, and anti-ss-bilaterala antibody biopsy of the ulcerated lesion was performed and the diagnosis of malt lymphoma was made bone marrow aspirate showed no tumor involvement, CT and ga-67 scans showed no tumor dissemination other than that confined the palate the patient was diagnosed as having stage 1 disease. Pathological findings included a histological exam of the first biopsy that showed a diffuse and dense infiltrate f tumor cells with centrocyte-like or monocytoid appearance around the minor salivary glands and involvement of tumor cells in the glands forming lymphoepithelial lesions immunohistochemistry showed tumor cells were positive for CD20 and negative for CD3, 5, 10, 23, and cyclin d1 tumor cells were negative for immunoglobulin light chains the second biopsy from the regressed lesion showed fibrosis and mild infiltrate of small mature lymphoid cells with no centrocyte-like features or lymphoepithelial lesions, compatible with sjs polymerase chain reaction indicated monoclonal proliferation of b-cells in the initial lesion and the presence of residual tumor clone in the regressed lesion both pcr products were cloned into pgem t-easy vector and 12 clones from each lesion were cycle-sequenced with dye-labeled terminators and analyzed on the sequencer. Gene sequences of the 1st and 2nd biopsy specimens were identical and showed 91% homology to the closest matched germline sequence vh3-21. Ongoing mutation was absent both first and sceond biopsy specimens were negative for the ap12-malt1 fusion transcription
Remission Characteristics
One months after the biopsy, the lesions showed a complete regression after a gradual decrease in size without treatment biopsy specimen 3 months later showed no histological evidence of malt lymphoma. No follow-up treatment was given and the patient remains alive and well with no recurrence evident 38 months after diagnosis
Treatment & Mechanisms
Proposed Remission Mechanisms
Immune mediation, tumor inhibition by growth factors and/or cytokines, induction of differentiation, hormonal mediation, elimination of a carcinogen, tumor necrosis or angiogesis inhibition, psychological factors, apoptosis and epigenetic mechanisms for this case, traumatic effect and localized infection induced by the surgical intervention might have activated tumor immunity i.e. Post-biopsy procedure
Clinical Treatment
None reported
Non-Clinical Treatment
None reported