Invasive pituitary adenoma

Invasive pituitary adenoma

Invasive pituitary adenomas are benign pituitary tumors that infiltrate the dura matercranial bone, or sphenoid sinus. Gross invasion at the time of operation is observed in up to 35 % of pituitary adenoma1) 2) 3).

Clinically nonfunctioning pituitary adenoma (NFPA) is a very common type of intracranial tumor, which can be locally invasive and can have a high recurrence rate.

Atypical or aggressive pituitary adenomas are tumors that rapidly increase in size and may invade into the suprasellar or parasellar regions. They are characterized by a Ki-67 nuclear labeling index greater than 10 %.

Invasive pituitary adenoma molecular markers.

They can be presented as Non-pulsatile exophthalmos.

Infrequently they produce cerebrospinal fluid rhinorrhea.

Invasive pituitary adenomas and pituitary carcinomas are clinically indistinguishable from pituitary adenoma until identification of metastases.

Invasive pituitary adenoma treatment.

Aggressive pituitary adenomas (APAs) are pituitary tumors that are refractory to standard treatments and carry a poor prognosis.

A 57-year-old man presented with visual deterioration and bitemporal hemianopsiaMRI of the brain demonstrated a sellamass suspected to be pituitary macroadenoma with a displacement of the stalk and optic nerve impingement. The patient underwent stereotactic endoscopic transsphenoidal resection of the mass. Postoperative MRI demonstrated gross total resectionPathology revealed a sparsely granulated corticotroph adenoma with malignant transformationImmunohistochemistry showed a loss of expression of MLH1 and PMS2 in the tumor cells. Proton therapy was recommended given an elevated Ki67 index and p53 positivity. Before radiotherapy, there was no radiographic evidence of residual tumor. Temozolomide therapy was initiated after surveillance MRI showed recurrence at 16 months postoperatively. However, MRI demonstrated marked progression after 3 cycles. Next-generation sequencing using the MSK-IMPACT platform identified somatic mutations in MLH1 Y548lfs*9 and TP53 R337C. Immunotherapy with ipilimumab/nivolumab was initiated, and MRI demonstrated no residual tumor burden 34 months postoperatively.

APA is a tumor with frequent recurrence and a short median expected length of survival. Shah et al. demonstrated the utility of immunotherapy in a single case report of APA, with complete resolution of recurrent APA and improved survival compared with a life expectancy 4).


Oruçkaptan HH, Senmevsim O, Ozcan OE, Ozgen T. Pituitary adenomas: results of 684 surgically treated patients and review of the literature. Surg Neurol. 2000;53:211–219.

Scheithauer BW, Kovacs KT, Laws ER, Jr, Randall RV. Pathology of invasive pituitary tumors with special reference to functional classification. J Neurosurg. 1986;65:733–744.

Selman WR, Laws ER, Scheithauer BW, et al. The occurrence of dural invasion in pituitary adenomas. J Neurosurg. 1986;64:402–407.

Shah S, Manzoor S, Rothman Y, Hagen M, Pater L, Golnik K, Mahammedi A, Lin AL, Bhabhra R, Forbes JA, Sengupta S. Complete Response of a Patient With a Mismatch Repair Deficient Aggressive Pituitary Adenoma to Immune Checkpoint Inhibitor Therapy: A Case Report. Neurosurgery. 2022 May 13. doi: 10.1227/neu.0000000000002024. Epub ahead of print. PMID: 35544035.

Somatotroph adenoma

Somatotroph adenoma

Somatotroph adenomas (GH producing adenomas, somatotropinomas) are typically recognized when they secrete GH excessively and cause the clinical syndrome of acromegaly. This recognition not only identifies a sellar mass as a somatotroph adenoma but also expands the therapeutic options. Occasional reports in the literature also describe ‘silent somatotroph adenomas,’ referring to adenomas that can be identified as somatotroph adenomas by positive immunohistochemical staining for GH, but are not associated with clinical evidence of GH excess. Some of these adenomas are totally silent, in that they are not associated with either clinical manifestations of GH excess or elevated serum concentrations of GH or IGF1.

75 % of Somatotroph adenomas are > 10 mm at time of diagnosis.

Somatotroph adenoma pathogenesis.

Somatotroph adenoma classification.

Somatotroph adenoma clinical features.

Somatotroph adenoma diagnosis.

see Somatotroph adenoma treatment.

see Somatotroph adenoma outcome

Somatotroph adenoma case series.

Somatotroph adenoma case reports.

Pituitary adenoma

Pituitary adenoma

Pituitary adenoma (PA) is a common pituitary tumor that arise from the adenohypophysis, in the pituitary gland.

Pituitary adenoma epidemiology.

see Pituitary adenoma classification.

The microenvironment of pituitary adenomas (PAs) includes a range of non-tumoral cells, such as immune and stromal cells, as well as cell signaling molecules such as cytokines, chemokines, and growth factors, which surround pituitary tumor cells and may modulate tumor initiation, progressioninvasionangiogenesis, and other tumorigenic processes. The microenvironment of PAs has been actively investigated over the last years, with several immune and stromal cell populations, as well as different cytokines, chemokines, and growth factors being recently characterized in PAs. Moreover, key microenvironment-related genes, as well as immune-related molecules and pathways, have been investigated, with immune checkpoint regulators emerging as promising targets for immunotherapy. Understanding the microenvironment of PAs will contribute to a deeper knowledge of the complex biology of PAs, as well as will provide developments in terms of diagnosis, clinical management, and ultimately treatment of patients with aggressive and/or refractory PAs 1)

see Pituitary adenoma Natural History.

see Pituitary adenoma clinical features.

Pituitary Adenoma Diagnosis.

see Pituitary adenoma treatment.

Pituitary Adenoma Outcome.

see Pituitary adenoma recurrence.

see Pituitary adenoma case series.


Marques P, Silva AL, López-Presa D, Faria C, Bugalho MJ. The microenvironment of pituitary adenomas: biological, clinical and therapeutical implications. Pituitary. 2022 Feb 22. doi: 10.1007/s11102-022-01211-5. Epub ahead of print. PMID: 35194709.
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