Disease relevance of INTS2

• Int-2/hst-1 coamplification was also significantly correlated with a high incidence of eventual metastasis in distant organs in these patients [1].
• In their analysis, Southern hybridization and DNA dot-blot analysis were used to screen 49 breast cancer DNAs for Myc, Neu, and Int-2 gene amplification [2].
• Int-2 allelic imbalance was significantly associated with carcinoid tumor formation (P < 0.01) [3].
• Forty-two endometrial carcinomas of various stages of progression were analyzed to search for loss of chromosomal regions and for point mutations of ras genes and amplification of Int-2 gene [4].
• The highest frequency of HPV infection was found in hypopharyngeal carcinomas, while amplification of Int-2 or Hst-1 was distributed more equally among the different localisations [5].

Psychiatry related information on INTS2

• Stimulated activity in a single Int-2 can entirely suppress the rhythmic motor activity of the feeding network evoked by electrical stimulation of the stomatogastric nerve [6].

High impact information on INTS2

• The International Prognostic Scoring System (IPSS) groups Low/Intermediate-1 (Low/Int-1) had longer response duration than Int-2/High (25 versus 7 months, P = .002) [7].
• Int-2/hst-1 coamplification greater than 3-fold was observed in the primary tumors of 30 of 107 cases (28%), and in the metastatic lymph nodes of 12 of 40 cases (30%) [1].
• Int-2 allelic imbalance was shown to be an early event in carcinoid tumor formation by virtue of the absence of allelic imbalance for other common cancer-related gene disturbances involving 11p13 (Wilms' tumor), 3p25 (von-Hippel-Lindau), and 17p13 (p53) [3].
• Of 21 cases of metastatic invasive cancer, 43% had Myc, 43% had Neu, and 40% had Int-2 gene amplification [2].
• The high incidence of Int-2 amplifications strongly suggests a role of this proto-oncogene in the pathogenesis of NPC [8].

Biological context of INTS2

• Of 25 cases of nonmetastatic invasive cancer, 28% had at least one extra Myc gene, whereas 24% had Neu, and 21% had Int-2 gene amplification [2].
• Among these aberrations, 7, 8, and 11 gains were further investigated on a series of NPC tissue samples, by interphase fluorescent in situ hybridization (FISH), for the incidence of alpha-satellites: 7, 8, and 11 c-myc and Int-2 [8].
• Further studies are underway looking for evidence of expression of Int-2 in fresh tissues and for amplification and expression of other oncogenes on this amplicon [9].
• Most recently, we have used in situ hybridization, which allows detection of gene expression in tissue sections to localize transcripts of a fibroblast-growth-factor related gene (Int-2 proto-oncogene) in developing teeth [10].
• More recently interest has focused on chromosome 11q13; oncogenes therein undergoing ongoing investigation include Bcl-1/Prad-1, Hst-1 and Int-2 [9].

Anatomical context of INTS2

• BACKGROUND: Int-2 (fibroblast growth factor-3) is a gene that belongs to the fibroblast growth factor gene family [11].

Associations of INTS2 with chemical compounds

• Int-2/FGF3 gene amplications were good indicators of prognosis, especially in premenopausal patients, and also in lymph-node-positive and steroid-receptor-negative patients [12].

Other interactions of INTS2

• Int-2/FGF3 amplification is a better independent predictor of relapse than c-myc and c-erbB-2/neu amplifications in primary human breast cancer [12].
• Frequent c-myc and Int-2 overrepresentations in nasopharyngeal carcinoma [8].

References