• Korean Journal of Head & Neck Oncology
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• v.31 no.1
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• pp.39-42
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• 2015

Basal cell adenocarcinoma is a extremely rare low grade malignancy of the salivary gland. It is composed of basaloid cells with dark cell, light cells and pale cytoplasm which shows infiltrative growth pattern into adjacent glandular parenchyme. The pathophysiology of basal cell adenocarcinoma is not well known. First hypothesis is a malignant transformation of the monomorphic adenoma and second one is a de novo origin. Metastasis to the regional lymph nodes is rare. Recently, we have experienced a case of basal cell adenocarcinoma with neck metastasis after previous superficial parotidectomy. For this reason we report this rare case discussed with references.

• Korean Journal of Head & Neck Oncology
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• v.36 no.1
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• pp.15-19
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• 2020

Basal cell adenocarcinoma is 1 ~ 2 % of salivary gland carcinoma. It was recently classified as low grade malignancy. It is low grade malignant counterpart of basal cell adenoma. It has similar morphologic attributes with basal cell adenoma, but it has distinctive malignant potential including infiltrative growth into surrounding tissues and distant metastasis. Recently, we have experienced a case of basal cell adenocarcinoma arising from the bilateral parotid gland in a 38-year old woman who was previously operated on superficial parotidectomy due to pleomorphic adenoma. We report this rare case with a review of literature.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.28 no.5
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• pp.390-394
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• 2002

Basal cell adenocarcinoma is an epithelial neoplasm which is cytologically and histomorphologically similar to basal cell adenoma but is different because of the infilitrative growth. This tumor, a rare salivary gland tumor newly classified as basal cell adenocarcinoma by the WHO in 1991, is infiltrative, locally destructive and tends to recur but metastasis is less common. The differential diagnosis includes basal cell adenoma, adenoid cystic carcinoma, and basaloid squamous carcinoma. Nearly 90 percent of these tumors occurr in the parotid gland and can be classified into low grade carcinomas with a relative good prognosis. Basal cell adenocarcinoma of minor salivary gland is very rare and has a less favorable clinical course compared with that of the major salivary glands. This is a case of basal cell adenocarcinoma occurring at the minor salivary gland of the soft palate. We treated this patient with block excision and adjunctive radiation therapy.

• Korean Journal of Head & Neck Oncology
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• v.13 no.1
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• pp.81-85
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• 1997

Basal cell adenocarcinoma is a rare, recently described neoplasm of the salivary gland. We have experienced three cases of basal cell adenocarcinoma of the parotid gland. The tumors from patient 1 and patient 2 showed intraparotid growth in superficial lobe without cervical lymphnode metastasis. So, patient 1 and patient 2 underwent only a superficial parotidectomy and subdigastric lymphnode dissection without any adjuvant therapy. They are alive without recurrence or distant metastasis. But that of patient 3 showed widely invasive growth with multiple cervical lymph node metastases. The CT scan showed a $8{\times}7cm$ sized huge mass replacing the parotid gland with irregular margin and multiple lymphnode enlargements along the internal jugular vein. Total parotidectomy with sacrifying the facial nerve and standard radical neck dissection were caried out. Microscopically, the tumor consisted of solid nest and sheet of uniform basaloid cells separated by a fibrous connective tissue stroma with the evidence of lymphovascular invasion. As a result of the lymphnode metastasis and invasiveness of the tumor, radiation therapy was given postoperatively. We thought that close follow-up would be mandatory in this patient because of high risk of possible local recurrence and distant metastasis.

• Journal of Digestive Cancer Reports
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• v.5 no.2
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• pp.97-104
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• 2017

Background: Cachexia is a multi-factorial syndrome presenting with chronic illness, decreases in body weight, and loss of adipose tissue and skeletal muscle, mostly in patients with advanced cancer and chronic wasting disease. Even after years of intensive researches, there remains no convincing therapy to prevent cancer cachexia. Methods: In this in vivo study, we have established C26 adenocarcinoma-induced cancer cachexia model in mice to explore the underlying core changes in cytokine, signal transduction, and muscle wasting. The ultimate aim of establishing animal model is to find optimal therapeutics to mitigate cancer cachexia. Results: We have administered C26 adenocarcinoma cells onto BALB/c mice and observed 4 weeks to assess the progression of cancer cachexia. Significant loss of weight accompanied with loss of appetite was noted. As C26 adenocarcinoma xenograft progressed, mortality was started from 3 weeks, accompanied with significant sarcopenia and decreased mice movement. Surges in TNF-α and IL-6 were noted with the commencement of cancer cachexia. Conclusion: Using C26 adenocarcinoma cancer cachexia model, we can screen the optimal therapeutics to mitigate cancer cachexia, in which agents to modulate IL-6, TNF-α, and NF-κB were essential.

• Journal of Digestive Cancer Research
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• v.5 no.2
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• pp.97-104
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• 2017

Background: Cachexia is a multi-factorial syndrome presenting with chronic illness, decreases in body weight, and loss of adipose tissue and skeletal muscle, mostly in patients with advanced cancer and chronic wasting disease. Even after years of intensive researches, there remains no convincing therapy to prevent cancer cachexia. Methods: In this in vivo study, we have established C26 adenocarcinoma-induced cancer cachexia model in mice to explore the underlying core changes in cytokine, signal transduction, and muscle wasting. The ultimate aim of establishing animal model is to find optimal therapeutics to mitigate cancer cachexia. Results: We have administered C26 adenocarcinoma cells onto BALB/c mice and observed 4 weeks to assess the progression of cancer cachexia. Significant loss of weight accompanied with loss of appetite was noted. As C26 adenocarcinoma xenograft progressed, mortality was started from 3 weeks, accompanied with significant sarcopenia and decreased mice movement. Surges in TNF-α and IL-6 were noted with the commencement of cancer cachexia. Conclusion: Using C26 adenocarcinoma cancer cachexia model, we can screen the optimal therapeutics to mitigate cancer cachexia, in which agents to modulate IL-6, TNF-α, and NF-κB were essential.