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Entity | MESENCHYMAL BENIGN TUMORS as follows: |
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Entity | Lipoma |
Disease | benign adipocyte tumor |
Prognosis | good |
Cytogenetics | various rearrangements involving 12q15 (translocations, inversions, deletions...); reciprocal translocations involve 12q15 with different partners such as chromosomes 1, 2, 3, 7, 10, 11, 13, 15, 17, 21, X; the most frequent anomaly is t(3;12)(q27-28;q15); cryptic rearrangements, such as paracentric inversions not detectable by conventional cytogenetics but detectable by FISH, have been described |
Hybrid/Mutated Gene | for t(3;12): HMGIC-LPP (LPP: lipoma preferred partner; 3q27-28); a gene located in 13q, LHFP (lipoma HMGIC fusion partner) was found to be fused with HMGIC in one case of lipoma; one lipoma displayed fusion of HMGA2 exon 4 with a sequence from intron 4, indicating abnormal splicing; HMGA2-CMKOR1 in three cases with aberrations involving 2q35-37 and 12q13-15; HMGA2-NFIB in one lipoma; |
Abnormal Protein | HMGIC-LPP; the three AT hook domains at the aminoterminal of HMGIC are fused to the LIM domain of LPP; another fusion protein due to the fusion of HMGIC with a putative gene located at 15q24 predicted to encode a protein with a serine/threonine-rich domain has also been described |
Oncogenesis | the relevance of the exact role LPP in the HMGA2-LPP fusion is not established yet, but the transactivation functions of the LPP LIM domains is retained in the fusion protein and the fusion protein can function as a transcription factor; the truncation of HMGA2 by itself may have a role in the tumorigenesis |
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Entity | Uterine leiomyoma (uterine fibroids) |
Disease | benign mesenchymal tumors |
Prognosis | good |
Cytogenetics | approximately 40% of uterine leiomyomas have structural chromosomal rearrangements, about 10% of which involve 12q15 (translocations, inversions, deletions...); the most frequent anomaly is t(12;14)(q15;q23-24) |
Hybrid/Mutated Gene | in a majority of cases, there is no fusion gene: the breakpoint is located 10 kb up to 100 kb 5' to HMGIC; the recombinational repair gene RAD51B is a candidate to be the partner gene of HMGIC in t(12;14). In two cases (out of 81 primary tumors) exon 7 of RAD51B was fused in frame to either exon 2 or 3 of the HMGA2 gene; in one case with paracentric inversion, HMGIC exon 3 was fused to ALDH2 exon 13 (12q24.1); in one case (no cytogenetic analysis) HMGIC exon 3 was fused to COX6C 3' UTR (8q22-23); in one case, with apparently normal karyotype, exon 3 of HMGIC was fused to retrotransposon-like sequences RTVLH 3' LTRs; three fusion transcripts contained 3' cryptic exonic sequences present in intron 3 of the HMGA2 gene (breakpoints downstream of exons 3 or 4), suggesting that they are due to alternative splicing; one case displayed fusion of the first two exons of HMGA2 to the 3' portion of the CCNB1IP1/C14orf18/HEI10 gene |
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Abnormal Protein | HMGIC-ALDH2: ALDH2 contribution was only 10 amino acids; |
Oncogenesis | HMGIC-ALDH2: it is suggested that the truncation of HMGIC, rather than fusion may be responsible for tumorigenesis; the 3' untranslated region may stabilize the HMGIC messenger RNA |
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Entity | Pleomorphic adenoma of the salivary gland (or mixed salivary gland tumor) |
Disease | benign tumors from the major or minor salivary glands |
Prognosis | good |
Cytogenetics | approximately 12% of pleomorphic adenomas of salivary glands show abnormalities involving HMGIC in 12q15; the most frequent aberration is t(9;12)(p24.1;q15) |
Hybrid/Mutated Gene | in t(9;12): HMGIC-NFIB fusion; another type of fusion HMGIC-FHIT (3p14.2) has also been described |
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Entity | Pulmonary chondroid hamartoma of the lung |
Disease | benign mesenchymal tumors of the lung |
Prognosis | good |
Cytogenetics | various rearrangements involving 12q15 leading to HMGIC dysregulation; cryptic rearrangements such as paracentric inversions not detectable by conventional cytogenetics but detectable by FISH have been described |
Hybrid/Mutated Gene | in two cases with apparently normal karyotypes, exon 3 of HMGIC was fused to retrotransposon-like sequences RTVLH 3' LTRs; in cases with t(3;12)(q27-28;q14-15) (see lipomas), a fusion of HMGA2-LPP was described; only 1/61 cases with normal karyotype displayed HMGA2-LPP fusion; three cases with rearrangements involving 12q14-15 and 13q12-14 lacked rearrangements of HMGA2-LHFP; |
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Entity | Endometrial polyps |
Disease | uterine benign tumors |
Prognosis | good |
Cytogenetics | various rearrangements involving 12q15 leading to HMGIC dysregulation; cryptic rearrangements such as paracentric inversions not detectable by conventional cytogenetics but detectable by FISH have been described; in one case, HMGIC was amplified and overexpressed |
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Entity | Myofibroblastic inflammatory tumor |
Disease | benign mesenchymal tumors |
Prognosis | good |
Cytogenetics | in one case, a complex rearrangement involving chromosomes 12 (in 12q15), 4 and 21 was described |
Hybrid/Mutated Gene | an aberrant transcript was produced by the fusion of HMGIC exon 3 to an ectopic sequence originating from the third intron of HMGIC |
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Entity | Chondrolipoangioma |
Disease | a rare benign type of mesenchyomas composed predominantly of cartilage and adipose tissue with vascular elements and myxoid elements |
Cytogenetics | One case demonstrated t(12;15)(q13;q26). FISH analysis revealed rearrangement of chromosomes 2, 12 and 15 and HMGA2. |
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Entity | Chondromas |
Disease | benign cartilage tumours |
Cytogenetics | HMGA2 was expressed in 4/6 soft tissue chondromas (all with 12q-rearrangements cytogenetically), three cases showed truncated (exons 1-3) transcripts, one case displayed a t(3;12)(q27;q15) and RT-PCR demonstrated a HMGA2-LPP fusion transcript composed of HMGA2 exons 1-3 and LPP exons 9-11. |
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Entity | Hyaline vascular Castleman's disease |
Cytogenetics | one case with der(6)t(6;12)(q23;q15)del(12)(q15) is described. |
Hybrid/Mutated Gene | a combined immunologic-cytogenetic approach demonstrated HMGA2 rearrangement in follicular dendritic cells |
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Entity | Prolactinoma |
Disease | prolactin-secreting pituary adenoma, non-metastasizing |
Cytogenetics | trisomy 12 nonrandom finding in pituary adenomas |
Hybrid/Mutated Gene | HMGA2 locus amplified in 7/8 prolactinomas |
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Entity | Aggressive angiomyxoma of the vulva |
Disease | myxoid mesenchymal neoplasm |
Prognosis | infiltrative neoplasm, locally destructive recurrences, no metastatic potential |
Cytogenetics | one case displayed t(8;12)(p12;q15) |
Hybrid/Mutated Gene | FISH demonstrated a breakpoint 3' of the gene, the tumour expressed HMGA2 |
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Entity | MALIGNANT TUMORS as follows: |
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Entity | Well-differentiated liposarcoma |
Disease | malignant adipocyte tumor; peripheral or retroperitoneal location |
Prognosis | rather good; borderline malignancy; locally aggressive, rarely metastasizes |
Cytogenetics | supernumerary ring or giant marker chromosomes containing 12q14-15 amplification (surrounding MDM2); HMGIC is frequently amplified together with MDM2; rearrangement of HMGA2, in addition to amplification has been described |
Hybrid/Mutated Gene | ectopic sequences from 12q14-15, 1q24, 11q14, and chromosome 2 was shown to be fused to HMGA2 exon 2 or 3 |
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Entity | Uterine leiomyosarcoma |
Disease | malignant counterpart of uterine leiomyoma |
Prognosis | poor |
Cytogenetics | 12q13-15 region is recurrently amplified |
Hybrid/Mutated Gene | HMGA2 amplified within this region |
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Entity | Osteosarcoma |
Disease | malignant tumor |
Hybrid/Mutated Gene | in one osteosarcoma cell line (OsA-Cl) the three DNA binding domains of HMGIC fused to the keratan sulfate protein glycan gene LUM (12q22-23); LUM was fused out of frame, and only 3 amino acids were fused to HMGIC; in addition, the rearranged gene was amplified |
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Entity | Myelofibrosis with myeloid metaplasia |
Disease | rare chronic myeloproliferative disorder |
Prognosis | variable |
Cytogenetics | one case with t(4;12)(q32;q15) and one case with t(5;12)(p14;q15) |
Hybrid/Mutated Gene | FISH analysis suggested breakpoint in HMGA2, RT-PCR revealed that HMGA2 is expressed in blood mononuclear cells from patients with this disease |
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Entity | Acute lymphoblastic leukaemia |
Disease | Heterogenous disease that arises in precursor B or T cells |
Cytogenetics | One case with a t(9;12)(p22;q14), frequent deletions at 12q14.3 |
Hybrid/Mutated Gene | t(9;12): FISH analysis indicated a breakpoint in the 5' region of the gene, RT-PCR showed overexpression of HMGA2 lacking the carboxyterminal tail; deletions covering the 5' end of HMGA2 |
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Entity | High-grade serous carcinoma of the fallopian tubes |
Disease | Serous carcinoma arising from fallopian tube secretory epithelia. |
Oncogenesis | Overexpression of HMGA2 regulated by several genetic mechanism, including CTNNB1 (β -Catenin), TGF- β, miRNAs. Currently well definied miRNAs including let-7 and MIR-182. MiR-182 promotes HMGA2 expression through negative regulation of BRCA1 (Moskwa et al. 2011, Liu et al. 2012). HMGA2 regulates several EMT genes including STC2 and LUM (Wu et al. 2011). Overexpression of HMGA2 is associated with early tumorigenesis, tumor cell proliferation, invasion and worse outcome through regulation of cell cycle, epithelial to mesenchymal transition (Wu et al. 2011). |
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Entity | Pancreatic carcinoma |
Disease | Pancreatic ductal carcinoma. |
Oncogenesis | Overexpression of HMGA2 promote EMT by regulation of SNAIL, SLUG, SIP1, TCF3 (E12/E47), and ZEB1 (Watanabe et al. 2009). HMGA2 nuclear immunoreactivity correlates positively with lymph node metastases and high tumor grade (Hristov et al. 2009). |
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Entity | Breast Cancer |
Disease | Serous carcinoma arising from fallopian tube secretory epithelia. |
Oncogenesis | HMGA2 gene and protein are highly expressed in metastatic breast cancer cells. HMGA2 as an important regulator of PAR1-mediated invasion. Inhibition of PAR1 signaling suppresses HMGA2-driven invasion in breast cancer cells (Yang et al. 2015). |
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Entity | Colon Cancer |
Disease | Colonic adenocarcinoma. |
Oncogenesis | HMGA2 delays the clearance of H2AFX(γ-H2AX) in colon cancer. Overexpression of HMGA2 is associated with metastasis and unequivocally occurred in parallel with reduced survival rates of patients with colorectal carcinoma (Wang et al. 2011). |
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Entity | Lung Cancer |
Disease | Non-small-cell lung cancer (NSCLC) |
Oncogenesis | HMGA2 can operate as competing endogenous RNA (ceRNA) for the let-7 microRNA (miRNA) family, suggesting that Hmga2 affects let-7 activity by altering miRNA targeting. HMGA2 promotes the transformation of lung cancer cells independent of protein-coding function. Tgfbr3 expression is regulated by the Hmga2 ceRNA through differential recruitment to Argonaute 2 (AGO2), and TGF-β signalling driven by Tgfbr3 is important for Hmga2 to promote lung cancer progression (Kumar et al. 2014). |
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