scholarly journals Rate of Prolactin suppression can predict future prolactin normalisation, tumour shrinkage and time to remission in male macroprolactinomas

2015 ◽  
Author(s):  
Amit Tirosh ◽  
Carlos Benbassat ◽  
Ilan Shimon
Keyword(s):  
Tumour Shrinkage ◽  
Prolactin Suppression

Treatment of human hyperprolactinaemia with a new dopamine agonist: CU 32085 (mesulergin)

1985 ◽  
Vol 110 (4) ◽  
pp. 433-439 ◽  
Author(s):  
D. Dewailly ◽  
P. Thomas ◽  
J. Buvat ◽  
J. L. Wemeau ◽  
J. C. Fourlinnie ◽  
...  
Keyword(s):  
Side Effects ◽  
Oral Administration ◽  
Dopamine Agonist ◽  
Histological Examination ◽  
Suppressive Effect ◽  
Normal Range ◽  
Tumour Shrinkage ◽  
Dose Dependent

Abstract. CU 38085 (mesulergin) was given at doses ranging from 0.5 to 5 mg/day to 37 patients with pathological hyperprolactinaemia of varying aetiology. The effectiveness of this drug on the suppression of hyperprolactinaemia and on the recovery of gonadal functions was equivalent to that of bromocriptine previously given to a different group of 83 hyperprolactinaemic patients. Tumour shrinkage during treatment with CU 32085 was ascertained in two cases of macroprolactinoma. Histological examination after adenomectomy revealed extensive peri-vascular fibrosis in both cases. In most patients, the efficient doses of CU 32085 were 5-fold lower than those of bromocriptine. After acute oral administration in 10 previously untreated patients, 0.5 mg of CU 32085 had a more prolonged suppressive effect on Prl levels than 2.5 mg of bromocriptine (approximately 18 vs 12 h). According to this, 0.5 mg CU 32085 once a day was sufficient to maintain Prl levels within the normal range in 16 patients. Side-effects were similar in nature and frequency to those induced by bromocriptine and seemed to be dose-dependent. They can be avoided by slowly increases of dose at initiation of treatment.

scholarly journals Analysis of the anticancer effect of endostatin on oral squamous cell carcinoma based on results of experimental studies

2020 ◽  
pp. 134-139
Author(s):  
Г.М. Тугузбаева ◽  
В.Н. Павлов ◽  
Д.А. Еникеев
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cancer Progression ◽  
Squamous Cell ◽  
Experimental Studies ◽  
Antitumor Agent ◽  
Regional Lymph Nodes ◽  
Tumour Shrinkage ◽  
Oral Malignancy

При плоскоклеточном раке полости рта основной причиной летальных исходов является метастазирование в регионарные лимфатические узлы. Злокачественный рост и формирование метастазов напрямую зависят от степени кровоснабжения первичного очага новообразования. Известно, что по мере прогрессирования опухолевый процесс сопровождается нарушением сбалансированной в норме системы регуляции ангиогенеза с превалированием уровня ангиогенных стимуляторов над ингибиторами. В связи с этим, использование антиангиогенных средств является патофизиологически обоснованным методом борьбы со злокачественным ростом. В обзоре обсуждаются данные доклинических исследований участия эндостатина, природного ингибитора ангиогенеза, в процессах подавления прогрессии и метастазирования плоскоклеточного рака челюстно-лицевой области. Проанализированы патогенетические механизмы ингибирования эндостатином опухолевого роста в экспериментальных моделях рака полости рта. Эндостатин можно рассматривать в качестве потенциального противоопухолевого средства для лечения данной нозологии. The main reason for cancer-associated mortality in patients with oral squamous cell carcinoma is metastatic spread to regional lymph nodes. It is known that the processes of malignant growth and metastasis are highly dependent on blood supply to the primary cancerous focus. The development of malignancy is accompanied by failure of the normally well-balanced system of angiogenesis regulation with prevalence of proangiogenic factors over inhibitors. Therefore, the use of angiogenic inhibitors is a pathophysiologically justified method aimed at suppression of cancer progression. This review presents reports of experimental studies on the role of endostatin, a natural inhibitor of angiogenesis, in processes of tumour shrinkage in squamous cell carcinoma of the maxillofacial region. The authors analysed pathogenic mechanisms of the anticancer effects exhibited by endostatin in preclinical models of oral malignancy. Endostatin can be regarded as a potential antitumor agent for the treatment of oral squamous cell carcinoma.

First-line octreotide-LAR therapy induces tumour shrinkage and controls hormone excess in patients with acromegaly: results from an open, prospective, multicentre trial

2006 ◽  
Vol 64 (3) ◽  
pp. 342-351 ◽  
Author(s):  
Annamaria Colao ◽  
Rosario Pivonello ◽  
Francesca Rosato ◽  
Patrizia Tita ◽  
Ernesto Menis ◽  
...  
Keyword(s):  
Multicentre Trial ◽  
First Line ◽  
Octreotide Lar ◽  
Tumour Shrinkage

scholarly journals Overall Survival (OS) and Tumour Shrinkage Outcomes in Patients with Symptomatic/Asymptomatic Metastatic Colorectal Cancer (MCRC): Data From the Prime Study

2013 ◽  
Vol 24 ◽  
pp. iv32 ◽  
Author(s):  
Jean-Yves Douillard ◽  
Salvatore Siena ◽  
Josep Tabernero ◽  
Marc Peeters ◽  
Chris Davison ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Overall Survival ◽  
Metastatic Colorectal Cancer ◽  
Tumour Shrinkage

scholarly journals P066 Pharmacologic inhibition of integrin αvβ6 causes tumour shrinkage in colitis associated mouse colon tumours

2018 ◽  
Vol 12 (supplement_1) ◽  
pp. S126-S126
Author(s):  
P Busenhart ◽  
L Hering ◽  
K Atrott ◽  
E Patsenker ◽  
F Stickel ◽  
...  
Keyword(s):  
Mouse Colon ◽  
Integrin Αvβ6 ◽  
Tumour Shrinkage ◽  
Pharmacologic Inhibition

scholarly journals Prolactin Suppression of Gonadotropin-Releasing Hormone Initiation of Mammary Gland Involution in Female Rats

Endocrinology ◽  
2016 ◽  
Vol 157 (7) ◽  
pp. 2750-2758 ◽  
Author(s):  
Duangjai Rieanrakwong ◽  
Titaree Laoharatchatathanin ◽  
Ryota Terashima ◽  
Tomohiro Yonezawa ◽  
Shiro Kurusu ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Mast Cells ◽  
Epithelial Cells ◽  
Female Rats ◽  
Local Administration ◽  
Boyden Chamber ◽  
Plasma Prolactin ◽  
Mammary Gland Involution ◽  
Prolactin Suppression ◽  
Mammary Tissues

It has been demonstrated that mammary gland involution after lactation is initiated by accumulation of milk in alveoli after weaning. Here, we report that involution is also dependent on mammary GnRH expression that is suppressed by PRL during lactation. Reduction of plasma prolactin (PRL) by the withdrawal of suckling stimuli increased GnRH and annexin A5 (ANXA5) expression in the mammary tissues after lactation with augmentation of epithelial apoptosis. Intramammary injection of a GnRH antagonist suppressed ANXA5 expression and apoptosis of epithelial cells after forcible weaning at midlactation, whereas local administration of GnRH agonist (GnRHa) caused apoptosis of epithelial cells with ANXA5 augmentation in lactating rats. The latter treatment also decreased mammary weight, milk production, and casein accumulation. Mammary mast cells were strongly immunopositive for GnRH and the number increased in the mammary tissues after weaning. GnRHa was shown to be a chemoattractant for mast cells by mammary local administration of GnRHa and Boyden chamber assay. PRL suppressed the mammary expression of both ANXA5 and GnRH mRNA. It also decreased mast cell numbers in the gland after lactation. These results are the first to demonstrate that GnRH, synthesized locally in the mammary tissues, is required for mammary involution after lactation. GnRH is also suggested to introduce mast cells into the regressing mammary gland and would be in favor of tissue remodeling. The suppression of these processes by PRL is a novel physiological function of PRL.

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