Ceskoslovenska patologie最新文献

The fifth edition of the WHO classification of prostate tumors provides new insight into prostate cancer pathogenesis supported by molecular data. It discards the terms low-grade PIN and high-grade PIN. The new entity „Treatment-related neuroendocrine prostatic carcinoma“ is introduced. The importance of the diagnosis of intraductal carcinoma is highlighted. The terminology of prostatic basocellular carcinoma is upgraded. Some cancer subtypes are being relocated to different chapters based on new findings. Also, the role of the prostate as an origin of hereditary cancer is stressed. Finally, the new therapeutic approaches are mentioned.

Compared to the WHO classification of the male genital tumors in 2016, minimal changes were introduced in the current WHO 2022. Classification of germ cell tumors remains the same as in the previous edition, dividing germ cell tumors into those derived from germ cell neoplasia in situ (GCNIS) and those independent of GCNIS. The group of GCNIS derived germ cell tumors is essentially unchanged. Most remarkable change was made to the chapter teratoma with somatic malignancy. Primitive neuroectodermal tumor (PNET), a particular type of somatic malignancy arising in the setting of teratoma, is currently termed embryonic-type neuroectodermal tumor (ENET). Diagnostic criteria for teratoma with somatic type malignancy have been mildly modified. Seminoma now belongs to the group of germinomas. There is one novel entity in the category of germ cell tumors independent of GCNIS, namely testicular neuroendocrine tumor, prepubertal type. Similar to other organ systems, the term carcinoid is no longer used. Two new entities were introduced in the category of sex cord stromal tumors: myoid gonadal stromal tumor and signet ring stromal tumor. Diagnostic criteria for malignant sex cord stromal tumors were moderately changed. Mitotic activity is now assessed according to mm2 instead of historical assessment according to the number of mitoses per high power fields. There is a new separate chapter named Genetic tumor syndromes. Intratubular large cell hyalinizing Sertoli cell neoplasia which arises exclusively in patients with Peutz-Jeghers syndrome, now belongs here. Large cell calcifying Sertoli cell tumor occurs as a hereditary tumor in patients with Carney complex as well as sporadically. Therefore, it is enlisted both in the chapter on sex cord tumors and as well as in genetic tumor syndromes. Well differentiated papillary mesothelial tumor was added as a new entity to the section of testicular adnexal tumors. Sertoliform cystadenoma, a tumor previously belonging to testicular adnexal tumors, is currently recognized as a subtype of Sertoli cell tumor.

The new WHO classification of CNS tumors is largely based on molecular diagnostic. Without molecular methods some entities can no longer be diagnosed. We are trying to show a rational approach to the CNS tumors diagnostics, which is based on conventional molecular methods such as RT-PCR, Sanger sequencing, MLPA, extended by the next generation sequencing (NGS) and methylation SNP array.

Tumors of the central nervous system (CNS) include primary tumors - itraaxial, growing from brain and spinal cord cells (neuroepithelial tumors) or extraaxial, growing from surrounding structures (brain and spinal cord, nerve sheaths, vascular structures, lymphatic tissue, germ cells, malformations, pituitary glands). Much more often they are located in the intracranial space a solitary or multiple metastatic spread of malignancy originating from another organ (eg lung, breast, malignant melanoma, Grawitzs tumor). The occurrence of metastases of solid tumors is then in the intraaxial or extraaxial region, leptomeningeal or dural. Even morphologically benign tumors with their occurrence in a closed CNS compartment can have malignant behaviour and cause severe slowly developing to acute neurological symptoms, including intracranial hypertension. Primary tumors of the central nervous system present 1-2% of all cancers, with a higher incidence in adults after the age of 60, with a slight predominance in men, with higher mortality in men than in women. About 5% of CNS tumors are hereditary (e.g., Li-Fraumeni syndrome, neurofibromatosis type I, II). The causes of most brain and spinal cord tumors are unclear, the effect of radiation has been definitely demonstrated, there is an increased risk in transplant patients and AIDS (Acquired Immune Deficiency Syndrome) patients, and the potentiating effects of some chemicals and viruses on the development of CNS neoplasms are uncertain. The effectiveness of treatment of brain and spinal cord tumors is influenced by the existence of the so-called hematoencephalic barrier, which protects the brain from the penetration of toxic substances, but at the same time prevents the penetration of most cytostatics to the tumor target. Another obstacle may be the localization of the tumor in areas difficult to access for histological verification (brain stem, optical chiasma) due to the high risk of complications even after stereotactic biopsy. In some cases, in an effort not to cause an irreversible neurological deficit by inconsiderate tissue collection, the sample of histological material can then become inconclusive to tumor cells, i.e., tumor cells are not captured. Last but not least, the radiosensitivity of some brain structures is also limiting, which makes it impossible to apply a higher dose of ionizing radiation to a tumor affecting sensitive tissues or located near of these sensitive tissues. The rapid development of immunohistochemical (IHC) and molecular genetic analysis methods has significantly refined diagnostics and thus theoretically facilitates the choice of the optimal treatment procedure for the individual patient. While advances in modern conformal photon and particle (currently the most frequently proton) radiotherapy, stereotactic radiosurgery has enabled accurately targeted irradiation of the CNS tumor site and at the same time spare the high-risk brain structures, thereby significantly reduc

Duodenum is currently the most popular site to obtain samples of intestinal mucosa for recognition of a disorder leading to malabsorption. Although there are significant overlaps between histological findings described in various non-neoplastic diseases of the duodenum, recognition of one of the six basic morphologic patterns, namely coeliac disease-like pattern, active chronic duodenitis, acute GvHD-like pattern, enteritis with predominant eosinophilic infiltration, enteritis with predominant infiltration by macrophages, and non-inflammatory enteropathy, usually allows diagnostic separation, especially if subtle histological details, clinical setting and serological investigation are taken into account.

The current progress and increasing knowledge about the genetic causes of cancer opens up new possibilities for its treatment. However, it is necessary to combine the results obtained using classical pathological methods with sensitive, multiplex molecular pathological methods. The method that meets the required criteria is MLPA based on multiplex PCR reaction. This method detects both changes in gene copy number and DNA methylation and, last but not least, point mutations. The MLPA reaction is applicable to even highly fragmented DNA. At the same time, it is a robust method that can be performed on standard thermocyclers, the fluorescent tip label requires automatic sequencers. Up to 50 genetic markers can be tested in one reaction, a number that allows a diagnostic and prognostic conclusion. All these features lead to the routine use of MLPA analysis not only in diagnosis but also in cancer research. The present article aims to summarize the different types of MLPA reactions, its benefits, but also the potential pitfalls.

Gastrointestinal (GIT) diseases represent an important part of pediatric health disorders. The recent years have brought not only significant improvement of digestive endoscopy technologies and a new equipment suitable for pediatric age but also progress in management of diagnostic approach and treatment of the pediatric GIT diseases. In contrast to adult patients, endoscopic examination in pediatrics is in most cases performed for diagnostic, not therapeutical purposes. The histological assessment of biopsy specimens taken during endoscopy therefore forms an integral part of the endoscopic examination and in most cases the diagnosis cannot be concluded without their evaluation. In particular, the clinical gastroenterologist expects from the pathologist a description that will help confirm or contradict the diagnosis considered after the macroscopic examination. In this review, we would like to highlight the most common endoscopic findings of the gastrointestinal tract in pediatric population and the role of histology in determining the correct diagnosis.

The 5th edition of WHO classification of the urinary tract tumors is only mildly edited version of the previous WHO classification (from year 2016). The most prominent changes are represented by modifications in the structure and concept of chapters and there are minor alterations in the nomenclature of some entities. Histological characteristics are still the gold standard for classification of urothelial tract neoplasms.

We present a case report of a 51-year-old patient who underwent totalization of thyroidectomy - resection of the right thyroid lobe for growth progression of the largest nodule from which a fine needle aspiration biopsy (FNAB) was performed and was cytologically suspected of malignancy. Nodule was a graywhite colored tumor with a solid structure, histologically with an unusual morphology and immunoprofile, called cribriform morular thyroid carcinoma (CMTC). Usually, the tumor behaves indolently with a good prognosis. CMTC can be familial or sporadic, predominantly as a solitary or a multifocal lesion, often associated with autosomal dominant adenomatous polyposis syndrome (FAP), so it is necessary to point this out in the report. The syndrome of familial adenomatous polyposis was ruled out, the APC gene mutation was somatic.

Similarly to testicular tumors, key changes on penile and scrotal neoplasia were incorporated into WHO classification 2016. Therein, penile squamous cell carcinomas were divided into two groups based on the pathogenesis, namely HPV-associated and HPV-independent. This remains unchanged in WHO classification 2022. For those carcinomas where HPV status can not be determined, a category of squamous cell carcinoma NOS was added. Variants of squamous cell carcinoma, namely basaloid, papillary-basaloid, warty, warty-basaloid, clear cell and lymphoepithelioma-like carcinomas are not recognized as distinctive variants of HPV-associated group anymore. Similarly, squamous cell carcinoma, usual type, pseudohyperplastic, pseudoglandular, verrucous carcinoma, carcinoma cunniculatum, papillary, adenosquamous, sarcomatoid and mixed carcinoma are no more not recognized as distinctive variants of HPV-independent carcinomas. Instead, these variants are now called subtypes. Some previously distinct subtypes now belong to the morphological spectrum of other subtypes. Basaloid-papillary subtype belongs to basaloid squamous cell carcinoma and carcinoma cunniculatum is currently recognized as morphological variation of verrucous carcinoma. Pseudohyperplastic and mixed subtypes were removed from the classification. Adenosquamous carcinoma is currently termed adenosquamous and mucoepidermoid carcinoma and represents distinct entity. Precursor lesions of squamous cell carcinoma underwent substantial modifications in the WHO classification 2016 as well, and remain unchanged in WHO classification 2022. Terminology for HPV - induced lesions have been unified to low grade squamous intraepithelial lesions (LSIL) and high grade squamous intraepithelial lesions (HSIL). This classification applies to the whole anogenital area, including penis, anus, perianal region, vulva, vagina and uterine cervix. LSIL is further divided to condyloma accuminatum and (penile) intraepithelial neoplasia grade 1 (PeIN1), HSIL is divided to PeIN2 and PeIN3. Penile HPV-independent precursor lesions are named differrentiated penile intraepitelial neoplasia (dPeIN) and are identical to analogous lesions on vulva.