Carcinosarcoma
The histologic classification of malignant tumors is important not only from an academic (histogenetic) standpoint, but also from that of prognosis and treatment. Thus the application and dosage of irradiation are primarily and principally dependent upon histologic detail, as is also the grading of malignant tumors. While ordinarily it is fairly well within the power of the pathologist to classify a malignant tumor, occasional growths are encountered which, despite obvious malignant features, cannot, because of their peculiar histologic detail, easily be classed as the descendants of one particular cell type. These tumors present features which may lead to the belief that they are the result of atypical growth of more than one cell type.
Interest in these tumors is as old as histopathology itself. All early pathologists considered their origin to be of dual nature. Thus, Virchow labeled them carcinosarcoma. He believed that within the primary carcinomatous or sarcomatous elements, the stromal or epithelial portions respectively were subsequently or simultaneously stimulated to malignant growth. Herxheimer and others believed this occurrence to be more frequent in primary carcinomas. They held that a carcinoma could stimulate an excessive growth of the stroma; that when the stroma-proliferation reached the stage of malignancy, the resulting tumor would be a carcinosarcoma. Perhaps, also, the secondary malignancy might supersede the primary one. This opinion was corroborated by Ehrlich and Apolant, and others, who observed that transplanted mouse carcinomas changed their histologic appearance, first to carcinosarcoma and eventually to sarcoma.[1]
Uterine Carcinosarcoma
Carcinosarcoma is a rare but highly aggressive uterine malignancy. Pathologically, carcinosarcoma is a biphasic neoplasm composed of a mixture of malignant epithelial and mesenchymal components. A comprehensive approach for management is recommended with complete surgical staging to assess tumor dissemination followed by multimodal therapy with combinations of external beam irradiation or vaginal brachytherapy and systematic chemotherapy in patients with both early and advanced stage disease.[2]
Integrated Molecular Characterization of Uterine Carcinosarcoma
We performed genomic, epigenomic, transcriptomic, and proteomic characterizations of uterine carcinosarcomas (UCSs). Cohort samples had extensive copy-number alterations and highly recurrent somatic mutations. Frequent mutations were found in TP53, PTEN, PIK3CA, PPP2R1A, FBXW7, and KRAS, similar to endometrioid and serous uterine carcinomas. Transcriptome sequencing identified a strong epithelial-to-mesenchymal transition (EMT) gene signature in a subset of cases that was attributable to epigenetic alterations at microRNA promoters. The range of EMT scores in UCS was the largest among all tumor types studied via The Cancer Genome Atlas. UCSs shared proteomic features with gynecologic carcinomas and sarcomas with intermediate EMT features. Multiple somatic mutations and copy-number alterations in genes that are therapeutic targets were identified.[3]
Carcinosarcoma of Ovary, it’s Histopathological, Management and Prognostic Analysis with Review of Literature
Carcinosarcoma is a mixed malignant biphasic tumour representing a rare entity and comprises of both epithelial and mesenchymal components. Primary ovarian carcinosarcoma is a rare neoplasm with a number of cases reported in the literature in the hundreds. It accounts for less than 1% of all ovarian tumours. These tumours are usually diagnosed at older age and advanced stage. It has aggressive clinical behaviour and survival depends on stage at presentation. Radiological imagings cannot differentiate carcinosarcomas from other ovarian cancers. Diagnosis is based upon histological findings. Cytoreductive debulking surgery is a crucial part in the treatment of carcinosarcoma of ovary. The role of adjuvant chemotherapy regimen is still controversial. Combination chemotherapy with taxane and platinum based regimen or ifosfamide and platinum based regimen are considered as adjuvant treatment. Despite aggressive treatment modalities such as surgery and chemotherapy, the outcome is poor. Response to therapy and overall survival for carcinosarcoma are poor in comparison to that of epithelial ovarian malignancies. Due to rarity of the disease, such poor prognosis needs collaboration of studies with molecular analysis to obtain new therapeutic guidelines to improve survival of the patients.[4]
Sarcomatoid Carcinoma (Carcinosarcoma) of the Prostate Gland: A Review of the Literature
Background: Adenocarcinomas of the prostate gland are commonly encountered globally but other uncommon variants of carcinoma of the prostate are sporadically encountered including primary sarcomatoid carcinoma of the prostate (PSCP).
Aims: To review the literature of PSCP.
Methods: Various internet search engines were searched for literature on PSCP.
Literature Review: About 100 cases of PSCP have so far been reported. PSCP may develop de novo or may emanate following hormonal treatment or radiotherapy for adenocarcinoma of prostate; PSCP may present with LUTS, haematuria, perineal/back pain. Histology of prostate biopsy tends to show a biphasic tumour which has an adenocarcinoma component as well as a second component which is a clearly recognizable type of sarcoma component which could be angiosarcoma, chondrosarcoma, leiomyosarcoma, osteosarcoma or rhabdomyosarcoma. With regard to immunohistochemistry Immunohistochemistry, the epithelial component of sarcomatoid carcinoma of prostate stains positively for cytokeratin and PAP, and negatively for PSA; the sarcoma component stains negatively for PSA, EMA and keratin. There is no consensus opinion on treatment. TURP has been performed for lower urinary tract obstruction symptoms and urinary retention, radical prostatectomy, pelvic exenteration, and chemotherapy are some of the treatments employed. A number of cases of PSCP had presented at advanced stages of the disease. PCSP is aggressive with poor prognosis; however, early aggressive surgery in some cases had resulted in survival.
Conclusions: A multi-centre trial is required to determine the best treatment option for PSCP. Perhaps patients with progressing prostate cancer following radiotherapy of castrate resistant prostate cancer should have repeat prostate biopsies to determine if they have developed dedifferentiation into PSCP or other variants of prostate cancer and to try cases of PSCP on chemotherapy as a trial.[5]
Reference
[1] Saphir, O. and Vass, A., 1938. Carcinosarcoma. The American Journal of Cancer, 33(3), pp.331-361.
[2] El-Nashar, S.A. and Mariani, A., 2011. Uterine carcinosarcoma. Clinical obstetrics and gynecology, 54(2), pp.292-304.
[3] Cherniack, A.D., Shen, H., Walter, V., Stewart, C., Murray, B.A., Bowlby, R., Hu, X., Ling, S., Soslow, R.A., Broaddus, R.R. and Zuna, R.E., 2017. Integrated molecular characterization of uterine carcinosarcoma. Cancer cell, 31(3), pp.411-423.
[4] Nayak, R. and Sahoo, T.K., 2016. Carcinosarcoma of Ovary, it’s Histopathological, Management and Prognostic Analysis with Review of Literature. Journal of Cancer and Tumor International, pp.1-10.
[5] Venyo, A.K.G., 2015. Sarcomatoid Carcinoma (Carcinosarcoma) of the Prostate Gland: A Review of the Literature. Journal of Cancer and Tumor International, pp.128-143.