Tumorigenicity of human HT1080 fibrosarcoma X normal fibroblast hybrids: chromosome dosage dependency

The tumorigenic capacity of hybrids formed by fusion of the highly tumorigenic HT1080 human fibrosarcoma cell line with nontumorigenic normal fibroblasts was examined. The HT1080 also contains an activated N-ras oncogene. Near-tetraploid hybrids which contained an approximately complete chromosomal complement from both parental cells were nontumorigenic when 1 X 10(7) cells were injected s.c. into athymic (nude) mice, whereas the parental HT1080 cells produced tumors in 100% of the animals with no latency period following injection of 2 X 10(6) cells. Tumorigenic variants were obtained from these hybrids which had lost only a few chromosomes compared to cells from the nontumorigenic mass cultures. In addition, several near-hexaploid hybrids were obtained which contained approximately a double chromosomal complement from the HT1080 parental line and a single chromosomal complement from the normal fibroblasts. All of these near-hexaploid hybrids produce tumors in 100% of nude mice with no latency period. Our results indicate that tumorigenicity of these particular human malignant cells of mesenchymal origin can be suppressed when fused with normal diploid fibroblasts. In addition, the results suggest that tumorigenicity in this system is chromosomal dosage dependent, since a diploid chromosomal complement from normal fibroblasts is capable of suppressing the tumorigenicity of a near-diploid but not a near-tetraploid chromosomal complement from the tumorigenic HT1080 parent. Finally, the loss of chromosome 1 (the chromosome to which the N-ras oncogene has been assigned) as well as chromosome 4 was correlated with the reappearance of tumorigenicity in the rare variant populations from otherwise nontumorigenic near-tetraploid hybrid cultures. Our results also suggest the possibility that tumorigenicity in these hybrids may be a gene dosage effect involving the number of activated N-ras genes in the hybrids compared to the gene(s) controlling the suppression of the activated N-ras genes.     

Bonding erythrocytes to plastic substrates by glow-discharge activation.

A procedure was developed for attaching erythrocytes to various plastics. Plastic disks were exposed to ammonia glow discharge (AGD) and found thereafter to form weak bonds with red cells settling from a dilute saline suspension poured over the disks. When the disks were used to produce a rotating shear flow, complete cell detachment was observed for stresses exceeding 34 dynes/cm2. Far stronger bonding was achieved by treating AGD-bonded cells with glutaraldehyde, and subsequent shearing failed to detach any cells (maximum stress 58 dynes/cm2). The proposed chemical mechanism involves attachment of -NH2 groups on the plastic during AGD, and formation also of carbonyl oxygen later, to provide sites for hydrogen bonding with the cell membrane. Subsequent glutaraldehyde exposure produces crosslinking between disk and cell, as well as fixing the cell in the normal way. Thus, the initial step succeeds in attaching erythrocytes in a deformable condition but rather weakly, while the second step produces rigid cells which are also bonded more strongly.     

Mirizzi syndrome secondary to an adenoma of the cystic duct

Bile duct adenomas are uncommon lesions that can cause obstructive jaundice. We report the unusual case of a 54-year-old man who developed Mirizzi syndrome secondary to a bile duct papillary adenoma located in the cystic duct remnant. A case report is presented, together with a review of extrahepatic bile duct adenomas published in the English-language literature, with special attention directed toward the clinical manifestations, locations, and prognosis of these tumors. Bile duct adenomas are very rare tumors. Although cholangiography can detect many of these lesions, few cases were correctly diagnosed preoperatively. Most lesions were located in the distal common bile duct or at the ampulla of Vater. Pathologic examination often revealed foci of carcinoma in situ, dysplasia, or atypia. Local resection was performed in most cases. There were no previous case reports of extrinsic common bile duct obstruction caused by tumors within the cystic duct. We describe here a very rare, acalculous variant of Mirizzi syndrome secondary to a solitary papillary adenoma of the cystic duct. In general, bile duct adenomas are uncommon lesions that are difficult to diagnoses preoperatively. These tumors usually present with jaundice secondary to intraluminal biliary obstruction. These lesions are premalignant and should be managed by complete surgical resection.     

Sublobar resection for the subcentimeter pulmonary nodule

Several studies have demonstrated an increased local recurrence rate with sublobar resection (SR) when compared with lobar resection for the treatment of non-small-cell lung cancer (NSCLC). Therefore, lobectomy has remained the gold standard therapy for NSCLC with lesser resection reserved as a compromise operation for high-risk patients. The increased identification of small NSCLC tumors by CT scan is leading many surgeons to question the appropriateness of lobectomy for these tumors. There has been increasing interest by many surgeons to use SR as intentional therapy for patients with small peripheral NSCLC. This article reviews the recent literature and evidence supporting intentional SR for NSCLC. Although lobectomy should continue to be regarded as the procedure of choice for NSCLC, we believe that a subset of patients with favorable characteristics may be appropriately treated with intentional SR as long as good assessment of nodal involvement is made. Future investigation is required to better define when SR is appropriate.