Transcript
Page 1: Neuron-specific enolase — A selective marker of the small-cell bronchial carcinoma

40

oxygenated conditions. It is concluded from

these studies that NSE immunoreactivity per

se is an unreliable marker for the SCLC

phenotype.

Neuron-Specific Enolase - A Selective Marker

of the Small-Cell Bronchial Carcinoma.

Lorenz, J., Mai, G.A., Schulz, V. Abteilung

fur Pneumologie, Universitatsklinikum Mainz,

D-6500 Mainz, Germany. Prax. Klin. Pneumol.

40: 100-102, 1986.

Neuron-specific enolase, the dimer of

an isoenzyme of the glycolysis enzyme

enolase, is a marker enzyme of the neuroen-

docrinal cells and is expressed by neuroen-

docrinel tumours and small-cell (or oat

cell) carcinomas. The authors report on ex-

periences with serum determinations of the

neuron-specific enolase using radioimmunoas-

say methods. Patients with small-cell bron-

chial carcinoma have enhanced neuron-

specific enolase (NSE) levels. Neuroen-

docrinal tumours are also associated to

about 50% with elevated NSE serum levels

compared with other solid tumours. It can be

shown that during the first chemotherapy

course the serum level increases markedly

with small-cell bronchial carcinomas fol-

lowed by a decline until the next treatment

cycle is initiated. Due to this dynamic

relationship we can expect that there is

some kind of link with the probable treat-

ment response.

Clinical Value of a Multiple Biomarker Assay

in Patients with Bronchogenic Carcinoma.

Buccheri, G.F., Violante, B., Sartoris, A.M.

et al. Medical Department, A. Carle Hospital

of Chest Diseases, 12100 Cuneo, Italy. Can-

cer 57: 2389-2396, 1986.

In 98 newly diagnosed patients with

histologically proven bronchogenic carcinoma

seen at Cuneo Hospital of Chest Diseases

from July 1983 to December 1984, multiple

biomarker assays were performed. Fifty-nine

cases had more than one carcinoembryonic an-

tigen (CEA) and/or tissue polypeptide an-

tigen (TPA) assay during the course of the

disease, at 3- to 12-weeks interval. A total

of 209 CEA (91 pretreatment), 170 TPA (80

pretreatment), 62 human chorionic

gonadotropin (HCG)-beta subunits and 60 lac-

tate dehydrogenase (LDH) was assayed. In ad-

dition, serum samples were taken from 141

blood donors and their TPA values were used

as a control. The percentages of elevated

values were, respectively, 37%, 52%, 18%,

and 25%. In 85% of the patients at least one

biomarker was found to be higher than nor-

mal. Neither significant differences between

mean biomarker levels in tumors of various

histologic types nor positive intermarker

correlations were found. The number of

patients with elevated CEA, TPA, and LDH

serum levels and their mean values increased

significantly according to the disease ex-

tent. Among evaluated markers TPA showed the

highest accordance to tumor burden. The

raising of two markers was never associated

with stage I-II disease, except in one

patient. Both CEA and TPA concentrations

changed significantly during the course of

the illness in relation to the clinical

status assessment. Abnormal pretreatment

levels of CEA, LDH, and particularly, TPA

were independently and significantly as-

sociated with a poor outcome. Patients with

abnormal levels of TPA and LDH and, to a

lesser degree, TPA and beta-HCG had shorter

survival as compared with patients with high

TPA values, irrespective of the LDH and

beta-HCG levels, although not significantly

so.

Serum Amyloid A in Carcinoma of the Lung.

Benson, M.D., Eyanson, S., Fineberg, N.S.

Department of Medicine, Rheumatology Divi-

sion, Richard L. Roudebush Veterans Ad-

ministration Medical Center, Indianapolis,

IN 46202, U.S.A. Cancer 57: 1783-1787, 1986.

Serum concentrations of serum amyloid A

protein (SAA), peripheral blood lymphocytes

(PBL) mitogenic response to phytohemag-

glutinin (PHA) and Concanavalin A (Con A),

numbers of circulating T- and B-lymphocytes

and length of survival after diagnosis were

measured in 50 patients with cancer of the

lung. SAA levels were significantly elevated

when compared to 50 control subjects

(P<O.O01), but did not correlate with state

of tumor spread at the time of diagnosis.

Mitogenic responses of PBL from the cancer

patients to PHA and Con A were significantly

depressed (P<O.001), but also did not pre-

dict state of metastatic spread. The per-

centage of circulating T-lymphocytes was

also significantly depressed in cancer

patients when compared to controls. In six

patients who survived tumor-free for greater

than 2.5 years, SAA serum concentrations

returned to normal. Statistical analysis

showed a significant correlation between SAA

serum concentrations and PBL mitogenic

response to Con A. In addition, both high

Top Related