Lipid-bound sialic acid, prostaglandin e and histamine in head and neck cancer

Klapan, Ivica; Katić, Vladimir; Čulo, Filip; Sabolović, Domagoj; Ćuk, Viseslav; Fumić, Ksenija; Simović, Stjepan

doi:10.1016/s0959-8049(05)80420-4

Cited by 10 publications

(6 citation statements)

References 15 publications

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“…Breast cancer as well as head and neck tumors have been shown to produce PGE 2 (Watson and Chuah 1992;Klapan et al 1993). Production of prostaglandins (PGE 2 ) by colorectal cancers has also been reported (Rigas et al 1993).…”

Section: Discussionmentioning

confidence: 99%

Expression of Prostaglandin G/H Synthase Type 1, but not Type 2, in Human Ovarian Adenocarcinomas

Doré

Cóté

Mitchell

et al. 1998

J Histochem Cytochem.

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Prostaglandin endoperoxide synthase (PGHS) is a key rate-limiting enzyme in prostaglandin biosynthesis. PGHS has recently been shown to be expressed in human colorectal cancers and in experimental cutaneous papillomas and carcinomas. However, PGHS expression has not been investigated in ovarian cancers. The objectives of this study were to determine whether PGHS isoenzymes are expressed in human ovarian cancer and, if so, to identify which isoform is involved (PGHS-1 and/or PGHS-2) and to characterize its cellular localization. Sixteen human ovarian adenocarcinomas were studied by immunohistochemistry using specific antibodies recognizing PGHS-1 or PGHS-2. Results showed that all adenocarcinomas demonstrated the presence of tumor cells expressing PGHS-1 but not PGHS-2. Patterns of staining of tumor cells varied among different types of adenocarcinomas, with cells presenting either a mostly diffuse cytoplasmic immunoreactivity or, alternatively, a staining mainly concentrated around the nucleus. No correlation between the intensity of the immunostaining and the degree of malignancy of tumors could be established (r 5 20.03; p>0.05). Immunoblot analysis with PGHS-1-selective antibodies of cell extracts from adenocarcinomas revealed the presence of a characteristic 72,000 Mr immunoreactive band. Therefore, these results show for the first time that PGHS-1 is expressed in human ovarian adenocarcinomas. (J Histochem Cytochem 46:77-84, 1998)

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Section: Discussionmentioning

confidence: 99%

Expression of Prostaglandin G/H Synthase Type 1, but not Type 2, in Human Ovarian Adenocarcinomas

Doré

Cóté

Mitchell

et al. 1998

J Histochem Cytochem.

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“…Some findings also suggest that SA levels could be elevated in cancer patients before the occurrence of clinical symptoms [54]. In addition, several reports have described normalization of SA levels after the successful treatment of cancer, there being subsequent elevation of SA levels with residividism [56,59,60,69], thus tentatively suggesting that SA levels could be used, when combined with other markers [52], in the follow-up of treatment response. For example, in a recent study with patients suffering from colorectal cancer, TSA seemed to give useful information about the spreading and metastatic properties of the tumour [70].…”

Section: Sa Concentrations In Malignanciesmentioning

confidence: 91%

“…Increased levels of serum TSA and/or LSA have been observed in various patient groups suffering from advanced ovarian carcinoma [52], brain tumours [53][54][55], leukaemia [56], lung cancer [57], cervical cancer [58], carcinoma of the hypopharynx and larynx [59], rectal, large intestinal and bronchogenic cancers [60], malign pleural effusion [61], oral cancer [62], melanoma [63], stomach, breast [64], colorectal, gall bladder cancer [65], thyroid and Hodgkin's cancers [55], sarcoma [52], and endometrial cancer [66]. For levels of TSA, LSA, TSA/total protein and protein-bound SA in sera from cancer patients and their control subjects (see Table 4).…”

Section: Sa Concentrations In Malignanciesmentioning

confidence: 99%

Occurrence of sialic acids in healthy humans and different disorders

Sillanaukee

Pönniö

Jä̈askëlainen

1999

Eur J Clin Investigation

226

166

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Sialic acid (SA), N-acetylated derivatives of neuraminic acid, play a central role in the biomedical functioning of humans. The normal range of total sialic acid (TSA) level in serum/plasma is 1.58-2.22 mmol L-1, the free form of SA only constituting 0.5-3 mumol L-1 and the lipid-associated (LSA) forms 10-50 mumol L-1. Notably, considerably higher amounts of free SA are found in urine than in serum/plasma (approximately 50% of the total SA). In inherited SA storage diseases such as Salla's disease, SA levels are elevated many times over, and their determination during clinical investigation is well established. Furthermore, a number of reports describe elevated SA levels in various other diseases, tentatively suggesting broader clinical utility for SA markers. Increased SA concentrations have been reported during inflammatory processes, probably resulting from increased levels of richly sialylated acute-phase glycoproteins. A connection between increased SA levels and elevated stroke and cardiovascular mortality risk has also been reported. In addition, SA levels are slightly increased in cancer, positively correlating with the degree of metastasis, as well as in alcohol abuse, diabetes, chronic renal failure and chronic glomerulonephritis. Several different mechanisms are assumed to underlie the elevated SA concentrations in these disorders. The apparent non-specificity of SA to a given disease limits the potential clinical usefulness of SA determination. In addition, some non-pathological factors, such as aging, pregnancy and smoking, may cause changes in SA concentrations. The absolute increases in SA levels are also rather small (save those in inherited SA storage disorders); this further limits the clinical potential of SA as a marker. Tentatively, SA markers might serve as adjuncts, when combined with other markers, in disease screening, disease progression follow-up, and in the monitoring of treatment response. To become clinically useful, however, the existing SA determination assays need to be considerably refined to reduce interferences, to be specific for certain SA forms, and to be more easy to use.

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“…Reduced response to ␣CD3 stimulation may be caused by alterations in the CD3chain function or the presence of immunosuppressive factors such as prostaglandin E 2 or tumor growth factor ␤. 25,26 The exact cause of immune unresponsiveness has not been identified.…”

Section: Commentmentioning

confidence: 99%

Anti-CD3/Anti-CD28 Bead Stimulation Overcomes CD3 Unresponsiveness in Patients With Head and Neck Squamous Cell Carcinoma

Shibuya

Wei

Zormeier

et al. 2000

Arch Otolaryngol Head Neck Surg

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A subpopulation of patients with HNSCC who are nonresponders to alphaCD3 stimulation has been identified, showing reduced proliferation and IL-12 and IFN-gamma secretion. Nonresponders stimulated with alphaCD3/alphaCD28 beads reversed immune unresponsiveness and induced a type 1 cytokine response. Bead-generated ATCs from patient 11 in the responder group lysed autologous and allogeneic HNSCC in vitro, suggesting a possible effective immunotherapeutic modality in the treatment of HNSCC.

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Lipid-bound sialic acid, prostaglandin e and histamine in head and neck cancer

Cited by 10 publications

References 15 publications

Expression of Prostaglandin G/H Synthase Type 1, but not Type 2, in Human Ovarian Adenocarcinomas

Expression of Prostaglandin G/H Synthase Type 1, but not Type 2, in Human Ovarian Adenocarcinomas

Occurrence of sialic acids in healthy humans and different disorders

Anti-CD3/Anti-CD28 Bead Stimulation Overcomes CD3 Unresponsiveness in Patients With Head and Neck Squamous Cell Carcinoma

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