Spontaneous remission of cranial diabetes insipidus due to concomitant development of ADH-producing lung cancer – an autopsied case

1983 ◽  
Vol 104 (4) ◽  
pp. 417-422 ◽  
Author(s):  
R. Takeda ◽  
Y. Hiraiwa ◽  
T. Hayashi ◽  
S. Yasuhara ◽  
E. Yanase ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Diabetes Insipidus ◽  
Immunohistochemical Staining ◽  
Clinical Course ◽  
Spontaneous Remission ◽  
Staining Technique ◽  
Small Cell ◽  
Lung Tumour ◽  
Rare Occurrence ◽  
Cranial Diabetes Insipidus

Abstract. The very rare occurrence of an ADH-producing small cell carcinoma of the lung in a 52 year old male patient with cranial diabetes insipidus since childhood is described. In this case diabetes insipidus disappeared concomitantly with development of lung cancer and re-appeared with shrinkage of the lung tumour by radiation therapy. Further progressive expansion of the primary and metastatic tumours induced the syndrome of inappropriate ADH secretion once again (SIADH). This deterioration in the clinical course was reflected in the plasma levels of ADH and neurophysins. The existence of vasopressin in the tumour tissue was also demonstrated by means of an immunohistochemical staining technique combined with anti-vasopressin serum.

Plasma cell free PD-L1 RNA expression correlated with tissue PD-L1 immunohistochemical staining and tumor mutation burden in non-small cell lung cancer.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15049-e15049
Author(s):  
Paul R. Walker ◽  
Mark Bowling ◽  
Nitika Sharma ◽  
Praveen Namireddy ◽  
Teresa Parent ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Expression ◽  
Immune Checkpoint ◽  
Immunohistochemical Staining ◽  
Immune Checkpoint Inhibitor ◽  
Advanced Nsclc ◽  
Checkpoint Inhibitor ◽  
Small Cell ◽  
Small Cell Lung ◽  
L1 Protein

e15049 Background: Programmed death ligand-1 (PD-L1) protein expression by immunohistochemical staining (IHC) correlates with response to immune checkpoint inhibitor (ICI) therapies in non-small cell lung cancer (NSCLC). Tumor mutational burden (TMB) is another immune biomarker of ICI response in NSCLC. Clinical studies indicate tissue PD-L1 protein expression and TMB are independent yet complementary. Both are limited by tissue acquisition and potential heterogeneity. Plasma cell free PD-L1 RNA (cfRNA) levels and tissue protein PD-L1 expression and TMB was analyzed and correlated in patients with advanced NSCLC. Methods: Patients with advanced NSCLC underwent complementary plasma and tissue next generation sequencing (NGS) with immune biomarkers prior to treatment. Plasma PD-L1 cfRNA was assessed by the Circulogene proprietary direct-on-specimen enrichment technology NGS platform. Correlating tissue testing was performed by the Caris Molecular Intelligence platform with the anti-PD-L1 22C3 IHC antibody and TMB measuring the total number of non-synonymous somatic mutations per megabase. Results: 107 patients with advanced NSCLC were evaluated with simultaneous plasma and tissue NGS testing. 17% (95% confidence interval [CI] 10-24%) patients plasma PD-L1 positive. 48.5% (CI 38-57%) tissue IHC PD-L1 positive. 7 of 18 plasma PD-L1 positive patients were tissue PD-L1 negative. 48% (CI 39-58%) total patients TMB ≥ 10 mutations per megabase (TMB high). Correlating TMB high in 72% (CI 50-94%) of plasma PD-L1 positive and 56% (CI 42-69%) of tissue PD-L1 positive patients. TMB high in 49% (CI 37-59%) plasma PD-L1 negative and 50% (CI 35-65%) tissue PD-L1 negative patients. Conclusions: Although less frequent than tissue PD-L1 protein expression, plasma PD-L1 cfRNA expression correlated with a higher association of tissue TMB high findings than tissue PD-L1 positive patients. There was not any TMB high difference between plasma PD-L1 negative and tissue PD-L1 negative patients. Over one-third of plasma PD-L1 positive patients were tissue PD-L1 negative. Clinical correlation with immune checkpoint inhibitor therapies is ongoing.

scholarly journals Method for the validation of immunohistochemical staining using SCID mouse xenografts: Expression of CD40 and CD154 in human non-small cell lung cancer

2013 ◽  
Vol 29 (4) ◽  
pp. 1315-1321 ◽  
Author(s):  
KEIDAI ISHIKAWA ◽  
MASAKI MIYAMOTO ◽  
TATSUYA YOSHIOKA ◽  
MASATOSHI KADOYA ◽  
LI LI ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Immunohistochemical Staining ◽  
Scid Mouse ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals E-box motifs within the human vasopressin gene promoter contribute to a major enhancer in small-cell lung cancer

1999 ◽  
Vol 344 (3) ◽  
pp. 961-970 ◽  
Author(s):  
Judy M. COULSON ◽  
Carolyn E. FISKERSTRAND ◽  
Penella J. WOLL ◽  
John P. QUINN
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lines ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Proximal Promoter ◽  
Lung Tumour ◽  
Small Cell Lung ◽  
Cell Extracts ◽  
E Box

[Arginine]vasopressin (AVP) is a neuropeptide physiologically synthesized in the hypothalamus but pathologically expressed by small-cell lung cancer (SCLC). A minimal 65 bp AVP promoter can restrict basal activity to SCLC in vitro, but a 199 bp fragment directs 5-fold higher expression in SCLC [Coulson, Stanley and Woll (1999) Br. J. Cancer 80, 1935-1944]. Several predicted E-box motifs occur within the 199 bp fragment, and we now describe an enhancer which contributes to AVP promoter tumour-specificity in some cell lines. The deletion of two adjacent E-boxes (-157 to -131) resulted in an approx. 70% loss of reporter gene expression in a SCLC line (Lu-165) with high endogenous AVP production. Using a series of AVP promoter deletion constructs and site-directed mutagenesis, we show that both these E-box sites were required for enhancer function, whereas mutation of an adjacent AP-1 site had no effect on the promoter activity. Electrophoretic-mobility-shift analysis indicated that, although both the predicted E-box motifs bound specific complexes, only one appeared to function as a strong E-box which binds basic helix-loop-helix (bHLH) factors. This motif formed a complex in lung tumour-cell extracts, which was particularly strongly bound in Lu-165, and was competed for by a characterized E-box motif from the preprotachykinin A promoter. Antibody supershifts indicate that this complex is a heterodimer of upstream stimulatory factor (USF)-1 and USF-2. Non-bHLH complexes weakly bound the second potential E-box motif in a SCLC-specific manner. These complexes were not recognized by the bHLH antibodies and remain unidentified; however, they were detected in seven of eight SCLC cell lines and not in four control lines. We postulate that there is a co-operative and complex interaction between an E-box and an adjacent site constituting a SCLC-specific enhancer within the AVP proximal promoter.

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