Twenty‐one esophageal cancer cell lines (KYSE series) have been established from the resected specimens of patients with esophageal cancer. Three lines, KYSE‐30, KYSE‐50, and KYSE‐70, were derived from the implanted tumor of nude mice (initial passage); others were derived from resected specimens. Each cell line was morphologically distinct. Detailed cytogenetic analysis indicated that each cell line was karyotypically unique, and DNA fingerprint analysis showed no cross‐contamination among cells. Doubling time ranged from 13.7 to 75.5 hours, and modal chromosome numbers ranged from 46 to 120. Most cell lines grew in monolayer, but two cell lines (KYSE‐50 and KYSE‐360) grew as floating cell aggregates. No correlation was demonstrated between the establishment of cell lines and cell differentiation. These cell lines are the first reported to be homogeneous and individually unique and may provide a useful model for the study of human esophageal cancer.

Secretin was injected into a feeding or nonfeeding artery of a gastrinoma and blood samples were taken from the hepatic vein (HV) or a peripheral artery (PA) to measure the changes of serum immunoreactive gastrin concentration (IRG). The IRG in the HV rose within 40 seconds and in the PA rose within 60 seconds after the injection of secretin into a feeding artery, but not after secretin was injected into a nonfeeder. These results indicated that secretin directly stimulates a gastrinoma to release gastrin in vivo. The selective arterial secretin injection test (SASI test) was applied in three patients in whom gastrinomas could not be located by computed tomography, ultrasonography, or arteriography, and functioning gastrinomas were located in all three patients. In one patient, malignant gastrinomas in the head of the pancreas and in the duodenum could be resected radically with the help of this test.S INCE ISENBERG ET AL.' discovered the paradoxical rise of serum gastrin levels after the intravenous injection ofsecretin in patients with the ZollingerEllison syndrome (ZE syndrome), the differential diagnosis of the ZE syndrome has become easier.2 In vitro studies of this reaction have shown that secretin directly stimulates gastrinoma to release gastrin.3'4 To ascertain whether this is also true in vivo, secretin was injected into the feeding arteries of the tumors visualized by arteriography in two patients with the ZE syndrome, and serial changes in the serum immunoreactive gastrin concentration (IRG) in the hepatic vein (HV)

Recently a number of surgeons have recommended radical resection of gastrinomas in Zollinger-Ellison syndrome (ZES). We have developed a useful technique for preoperative localization of gastrinomas--the selective arterial secretin injection test (SASI)--and we recommend an intraoperative secretin test (IOS) for deciding the radicality of resection of gastrinomas. Here the results of SASI and IOS tests in 11 patients with ZES are examined and compared with the results of other techniques. The SASI test localized gastrinomas in all of the patients, while the sensitivity of ultrasonography, computed tomography, arteriography, or portal venous blood samplings was between 1/11 and 5/11. On the basis of the results of the SASI test, radical resection of gastrinoma was performed in four patients (three pancreatoduodenectomies and one extirpation). After pancreatoduodenectomy, immunohistologic study of the specimen revealed multiple microgastrinomas and lymph node metastases in two patients and the coexistence of a microgastrinoma and a gastinoma in one patient. The IOS test was useful in the estimation of the advisability of radicality, and in two patients total gastrectomy was not performed because of the results of the IOS test. These four patients are well and have returned to work, and their serum gastrin levels are below 35 pg/mL. Thus we believe SASI and IOS tests are helpful for planning curative resection of gastrinomas.

Nonsense mutations affecting the positive regulatory gene (htpR) of heat shock response have been obtained in a strain of Escherichia coli carrying no suppressor. The mutants can grow only at temperatures below 34°C-35°C. Heat, ethanol, and coumermycin induce major heat shock proteins in the wild-type but not in the htpR mutants. In contrast, the level of heat shock proteins synthesized at low temperature is unaffected. The htpR gene product is thus required for induction of heat shock proteins by heat or other stresses but not for their "basal-level" synthesis. Nucleotide sequence has been determined for the wild-type and the mutant alleles of htpR.The coding region appears to consist of 852 nucleotide pairs that correspond to 284 amino acids. Sequences commonly considered as signals for transcriptional initiation and termination were found flanking the coding region. Within this region, six amber, one opal, and two missense mutations were identified; the nonsense mutations are scattered along the gene, some being very close to the presumed amino terminus. These results indicate that the absence of htpR gene product is directly responsible for the failure to respond to heat shock or other stresses and for the inability to grow at high temperature. We propose that htpR represents a new class of genes that are essential for growth only at high temperatures (>35°C). Implications of the sequence homologies found among htpR, rpoD, and nusA proteins are discussed.A specific set of proteins called heat shock proteins (HSP) is induced when organisms or cells are exposed to high temperature or other environmental stresses. Such induction of HSP seems to represent part of homeostatic response, at the cellular level, to environmental changes in both eukaryotes and prokaryotes. Extensive structural homology between some of the HSP genes (1) and proteins (2) from a variety of distantly related organisms suggests that the response to heat shock or stress is universal and well conserved during evolution. In spite of the recent progress in this field, little is known about the mechanisms involved in regulating heatshock response.Induction of HSP in Escherichia coli occurs primarily at the transcriptional level (3, 4). Analysis of a mutant defective in heat shock induction led us to identify a gene (htpR or hin) whose product is apparently required for the enhanced transcription of heat shock operons upon exposure to high temperature (4, 5). Furthermore, heat shock induction controlled by the htpR gene appears to play a critical role in bacterial growth at high temperature and in acquired thermotolerance under certain conditions (4). The importance of htpR in heat shock induction and growth at high temperature was further substantiated by isolation and characterization of additional htpR mutants (6). The htpR gene has been cloned into multicopy plasmids, and its product has been identified as a protein with an apparent molecular weight of 33,000-36,000 (6, 7). The recombinant plasmids carrying htpR (or part thereof) hav...