How does adenosquamous carcinoma arise in the small intestine?

Teramoto, Tadahisa; Kawamata, Hitoshi; Fujimori, Takahiro

doi:10.1007/s00535-003-1192-x

Cited by 2 publications

(2 citation statements)

References 6 publications

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“…This gene encodes a protein that is an EGFR ligand up-regulated in diverse pathological conditions, including cancer (46,47). Interestingly, HBEGF , together with two other genes, COX2 and ST6GALNAC5 , mediate breast cancer cell passage through the blood-brain barrier (46).…”

Section: Discussionmentioning

confidence: 99%

Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?

Cervigne

Machado²,

Goswami

et al. 2014

Human Molecular Genetics

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A significant proportion (up to 62%) of oral squamous cell carcinomas (OSCCs) may arise from oral potential malignant lesions (OPMLs), such as leukoplakia. Patient outcomes may thus be improved through detection of lesions at a risk for malignant transformation, by identifying and categorizing genetic changes in sequential, progressive OPMLs. We conducted array comparative genomic hybridization analysis of 25 sequential, progressive OPMLs and same-site OSCCs from five patients. Recurrent DNA copy number gains were identified on 1p in 20/25 cases (80%) with minimal, high-level amplification regions on 1p35 and 1p36. Other regions of gains were frequently observed: 11q13.4 (68%), 9q34.13 (64%), 21q22.3 (60%), 6p21 and 6q25 (56%) and 10q24, 19q13.2, 22q12, 5q31.2, 7p13, 10q24 and 14q22 (48%). DNA losses were observed in >20% of samples and mainly detected on 5q31.2 (35%), 16p13.2 (30%), 9q33.1 and 9q33.29 (25%) and 17q11.2, 3p26.2, 18q21.1, 4q34.1 and 8p23.2 (20%). Such copy number alterations (CNAs) were mapped in all grades of dysplasia that progressed, and their corresponding OSCCs, in 70% of patients, indicating that these CNAs may be associated with disease progression. Amplified genes mapping within recurrent CNAs (KHDRBS1, PARP1, RAB1A, HBEGF, PAIP2, BTBD7) were selected for validation, by quantitative real-time PCR, in an independent set of 32 progressive leukoplakia, 32 OSSCs and 21 non-progressive leukoplakia samples. Amplification of BTBD7, KHDRBS1, PARP1 and RAB1A was exclusively detected in progressive leukoplakia and corresponding OSCC. BTBD7, KHDRBS1, PARP1 and RAB1A may be associated with OSCC progression. Protein–protein interaction networks were created to identify possible pathways associated with OSCC progression.

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Section: Discussionmentioning

confidence: 99%

Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?

Cervigne

Machado²,

Goswami

et al. 2014

Human Molecular Genetics

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“…The scenario has become more complicated now as we face such newer, competing theories as cancer stem cell and transdifferentiation, succinctly summarized by Teramoto et al 28 . These theories center on the turning on and off of phenotype‐determining genes, and may promise a molecular answer to the ever mysterious cellular origin of squamous carcinoma, alone or in combination with indigenous glandular element.…”

Section: Discussionmentioning

confidence: 99%

Primary adenosquamous carcinoma of the jejunum

Wang

Gong

et al. 2005

Pathology International

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Adenosquamous carcinomas of the small intestine are extremely rare, with only three documented jejunal and three ileal cases being reported in the English-language medical literature. Presented herein is a case of primary jejunal adenosquamous carcinoma in an 80-year-old woman. The jejunal carcinoma consisted predominantly of a squamous component throughout the tumor but peritoneal nodules carrying metastases from the adenocarcinoma element were noted, making it the first case of jejunal adenosquamous carcinoma with metastases from the adenocarcinoma component. The finding that metastases could arise from the minor component of a jejunal adenosquamous carcinoma indicates that an accurate diagnosis must be based upon thorough examination of both the primary and the metastases, not just mesenteric nodule biopsy alone. Histological foci of closely intermingled squamous and glandular components with apparent morphological transition were noted, indicating the pathogenetic possibility that the squamous component might arise by transformation from the glandular element. The squamous component was strongly positive with immunostaining for p63 (nuclear staining) and for cytokeratin 10/13 (cytoplasmic staining), while the adenocarcinoma element was negative. The immunohistochemical results suggest that p63 and cytokeratin 10/13 might be useful in identifying squamous differentiation in jejunal carcinoma.

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How does adenosquamous carcinoma arise in the small intestine?

Cited by 2 publications

References 6 publications

Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?

Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?

Primary adenosquamous carcinoma of the jejunum

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