A 2.3-kb cDNA probe for the human bek fibroblast growth factor receptor was used to determine the chromosomal localization of the corresponding gene by in situ hybridization. The results show that this gene, a form of which is amplified in some poorly differentiated stomach cancers, is localized on chromosome region 10q26. The two previously identified fibroblast growth factor receptor genes are thus not on the same chromosome, as the related flg ("fms-like gene") fibroblast growth factor receptor gene has previously been mapped to human chromosome region 8p12.
We show here that tumor infiltrating lymphocytes (TIL) derived from three renal carcinoma (RC) tumors, which developed in the same patient over a 3-yr period, were systematically enriched in gamma delta + T cells (27-74%) after short term in vitro culture. Analysis of the repertoire of gamma delta + TIL and PBL from this patient, revealed the predominant expression of structurally diverse V delta 1 gamma delta TCR by TIL from the three tumors, contrasting with the classically dominant use of V delta 2 TCR by PBL. Functional analysis further showed that, independently of the V gamma genes expressed, all the V delta 1+ TIL clones exhibited a lytic activity apparently restricted to RC lines, while V gamma 9+V delta 2+ clones (either PBL- or TIL-derived) had a broad killing activity. Surprisingly most V delta 1+ CTL clones lysed several allogeneic, but not the autologous, RC lines. Only one V gamma 3+V delta 1+ TIL clone, identified by its specific variable TCR gene sequence, consistently killed autologous tumor cells, apparently via TCR-mediated MHC-unrestricted recognition. This clone also lysed two allogeneic RC lines out of four tested but did not kill 30 non-RC lines, except for one breast carcinoma line. Significantly, this clone was found in recurrent fashion in all three tumors analyzed, including a metastasis. The high frequency of V delta 1 expressing RC-reactive gamma delta cells among TIL from this patient suggests that this gamma delta subset was selectively trapped and/or preferentially induced to proliferate in the autologous tumors. The recurrence of a single V gamma 3+V delta 1+ gamma delta clone, reacting with autologous tumor cells, inside three tumors of different localizations additionally suggests that, for this clone, intratumor selection and/or proliferation was due to TCR-mediated recognition of a non-MHC-restricted RC-specific Ag.
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