PMID- 10436809
OWN - NLM
STAT- MEDLINE
DCOM- 19990909
LR  - 20161017
IS  - 0923-7534 (Print)
IS  - 0923-7534 (Linking)
VI  - 10 Suppl 4
DP  - 1999
TI  - Role of tumour markers, cytogenetics.
PG  - 145-9
AB  - A review is presented on the role of conventional and molecular tumour markers
      (TM) in diagnosis and monitoring of patients with biliopancreatic malignancies.
      For biliopancreatic malignancy, following CEA as more historical and basic TM of 
      gastrointestinal diseases, the mainstay marker is CA 19-9 as
      monosialo-ganglioside/glycolipid and sialyl derivative of lacto-N-fucopentaose II
      (sialyl-Lewis(a), hapten of human Lewis(a) bloodgroup determinant). It is
      detected in serum of healthy individuals at low concentration < 40 U/ml, with
      lower and often transitional elevation in benign hepatobiliary diseases and with 
      highest levels in excretory ductal pancreatic adenocarcinoma (s = 70%-95%, sp =
      72%-90%), biliary (s = 55%-79%), hepatocellular and cholangiocellular cancer (s =
      22%-51%) besides gastric, colorectal and ovarian cancer and occasionally in lung,
      breast and uterine cancer. Physiologically elevated concentrations in healthy
      individuals have to be considered in all sorts of secretions (e.g. sputum,
      saliva, bronchial/gastric secretions, bile juice) of individuals with
      Lewis(a)-positive secretor status in contrast with low or lacking serum levels of
      CA 19-9 in patients with Lewis(a-/b-) status (7%-10% of population). In
      biliopancreatic malignancies, especially pancreatic cancer, CA 19-9 correlates
      well with clinical course of disease following surgical, chemo- or radiotherapy
      by a quick normalisation within 2-4 weeks after complete surgery, a transient
      decrease with successful palliative therapy and an often anticipated increase
      (lead time up to 6 months) before clinical detection in case of relapse or
      progressive disease. From CA 19-9 related TM tests some are detecting in addition
      to sialyl-Lewis(a) (sialyllacto-N-fucopentaose II) also the non-fucosylated
      precursor sialyl-Lewis(c) (sialyllacto-N-tetraose: CA 50, CA 242, Span-1) solely 
      detected by the DUPAN-2 test and independent of the Lewis(a) secretor status.
      Some other markers comprise in addition to sialyl-Lewis(a) partially the
      non-sialylated Lewis(a) antigen (CA 195, CAM 43, CA 494) or are less related (CAM
      17.1). The initial phase of screening and early detection is hoped to be better
      assessed by using molecular markers detecting gene mutations (p53, K-ras), growth
      factors (EGF, TGF-alpha, TGF-beta, HB-EGF, a/bFGFs, KGF) and growth factor
      receptor alterations (EGFr, c-erbB2/3/4). From these, K-ras mutations detected in
      blood, stool and bile juice of patients at risk for pancreatic cancer seem to be 
      more promising than p53 alterations as a more later step in carcinogenesis,
      although they are neither yet well established nor standardised by reliable
      assays. In contrast growth factor and growth factor receptor alterations mainly
      concerning signal transducing systems seem to reflect increased tumour
      aggressiveness, thus shorter survival and poorer prognosis thereby contributing
      in the selection of patients for more aggressive therapy.
FAU - Lamerz, R
AU  - Lamerz R
AD  - Medical Department II, Klinikum Grosshadern, University of Munich, Germany.
      lamerz@med2.med.uni-muenchen.de
LA  - eng
PT  - Journal Article
PT  - Review
PL  - England
TA  - Ann Oncol
JT  - Annals of oncology : official journal of the European Society for Medical
      Oncology
JID - 9007735
RN  - 0 (Antigens, Tumor-Associated, Carbohydrate)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (CA 242 antigen)
RN  - 0 (CA-19-9 Antigen)
RN  - 0 (Carcinoembryonic Antigen)
SB  - IM
MH  - Antigens, Tumor-Associated, Carbohydrate/analysis
MH  - Biomarkers, Tumor/*analysis
MH  - CA-19-9 Antigen/analysis
MH  - Carcinoembryonic Antigen/analysis
MH  - *Chromosome Aberrations
MH  - DNA Repair/genetics
MH  - Genes, Tumor Suppressor
MH  - Humans
MH  - Pancreatic Neoplasms/*diagnosis/genetics
RF  - 53
EDAT- 1999/08/07 00:00
MHDA- 1999/08/07 00:01
CRDT- 1999/08/07 00:00
PHST- 1999/08/07 00:00 [pubmed]
PHST- 1999/08/07 00:01 [medline]
PHST- 1999/08/07 00:00 [entrez]
PST - ppublish
SO  - Ann Oncol. 1999;10 Suppl 4:145-9.