The World Health Organization (WHO) classification of the lymphoid neoplasms updated in 2008 represents a worldwide consensus on lymphoma diagnosis and is based in two major principles: the stratification of neoplasms according to their cell lineage and their derivation of precursor or mature cells and the definition of non-overlapping distinct diseases that are clinically relevant. The identification of these diseases is based on a combination of morphology, immunophenotype, genetic, molecular, and clinical features. In addition to well-defined entities, the classification addresses open issues, such as provisional entities that correspond to categories for which there were insufficient evidence to support its recognition as distinct diseases at the time of publication and borderline categories with overlapping features between large B-cell lymphomas and Burkitt or Hodgkin lymphoma.

The World Health Organization Classification of Lymphoid Neoplasms

This group of ovarian neoplasms is composed of a number of histologically different tumor types and embraces all the neoplasms considered to be ultimately derived from the primitive germ cells of the embryonic gonad. The concept of germ cell tumors as a specific group of gonadal neoplasms has evolved in the last three decades. It is based on (1) the common histogenesis of these neoplasms, (2) the relatively frequent presence of histologically different neoplastic elements within the same tumor mass, and (3) the presence of histologically similar neoplasms in extragonadal locations along the line of migration of the primitive germ cells from the wall of the yolk sac to the gonadal ridge,332 as well as on the remarkable homology between the various tumors in the male and the female.

Germ Cell Tumors of the Ovary

Human germ cell tumours (GCTs) are derived from stem cells of the early embryo and the germ line. They occur in the gonads (ovaries and testes) and also in extragonadal sites, where migrating primordial germ cells are located during embryogenesis. This group of heterogeneous neoplasms is unique in that their developmental potential is in effect determined by the latent potency state of their cells of origin, which are reprogrammed to omnipotent, totipotent or pluripotent stem cells. Seven GCT types, defined according to their developmental potential, have been identified, each with distinct epidemiological and (epi)genomic features. Heritable predisposition factors affecting the cells of origin and their niches likely explain bilateral, multiple and familial occurrences of the different types of GCTs. Unlike most other tumour types, GCTs are rarely caused by somatic driver mutations, but arise through failure to control the latent developmental potential of their cells of origin, resulting in their reprogramming. Consistent with their non-mutational origin, even the malignant tumours of the group are characterized by wild-type TP53 and high sensitivity for DNA damage. However, tumour progression and the rare occurrence of treatment resistance are driven by embryonic epigenetic state, specific (sub)chromosomal imbalances and somatic mutations. Thus, recent progress in understanding GCT biology supports a comprehensive developmental pathogenetic model for the origin of all GCTs, and provides new biomarkers, as well as potential targets for treatment of resistant disease. Human germ cell tumours are a heterogeneous group of neoplasms that occur in the gonads and extragonadal sites along the midline of the body. This Review outlines a developmental pathogenetic model for the origin of all germ cell tumours, which is based on the unscheduled reprogramming of cells of the early embryo and germ line.

Human germ cell tumours from a developmental perspective.

Background. Severe disease attributable to Plasmodium vivax infection is already well described worldwide; however, autopsies in these patients are scarce. Methods. From 1996 to 2010, 19 patient deaths with a clinical diagnosis of P. vivax infection occurred in a tertiary care center in the Brazilian Amazon. Seventeen of these 19 deaths were fully autopsied. Clinical charts, macroscopic autopsy reports, and stored paraffinized tissue blocks were retrieved. Nested polymerase chain reaction was performed in paraffinized samples of spleen and lung to confirm P. vivax monoinfection. Immunohistofluorescence was used to detect P. vivax parasitized red blood cells (RBCs). Results. Of 17 autopsies, 13 revealed that death could be attributed to P. vivax infection; in the remaining 4, acute diseases other than malaria were found to be the cause of death. The primary complication in patients in which malaria contributed to death was acute respiratory distress syndrome (ARDS) and pulmonary edema associated with the accumulation of neutrophils in the interalveolar space (6 cases). Spleen rupture (3 cases) and multiorgan dysfunction syndrome (3 cases) were the second most common complications. One child evolving with coma was also characterized, but no parasite was detected in the brain tissue. In one patient who developed ARDS and presented negative peripheral parasitemia by the time of death, scattered parasitized red blood cells were seen inside pulmonary capillaries, suggesting some sequestration in the lung. Conclusions. In 13 of 17 deceased patients, P. vivax infection was the plausible cause of death. However, more studies are needed to understand pathogenesis related to severe disease.

Postmortem Characterization of Patients With Clinical Diagnosis of Plasmodium vivax Malaria: To What Extent Does This Parasite Kill?

Lymphomatoid papulosis (LyP) belongs to the spectrum of primary cutaneous CD30-positive lymphoproliferative disorders. Clinically, LyP is characterized by a variable number of self-healing papulo-nodular lesions, with the typical waxing and waning course. Histologically, 4 types (A, B, C, and D) have been delineated. Angioinvasive growth and large ulcers are rare findings in LyP and simulate aggressive lymphoma. We retrospectively analyzed the clinicopathologic and molecular features of angioinvasive LyP in a series of 16 patients. This new form of LyP is characterized by oligolesional papules that rapidly ulcerate and evolve into large necrotic eschar-like lesions with a diameter of 1 to 4 cm and an angiocentric and angiodestructive infiltrate of small-sized to medium-sized atypical lymphocytes expressing CD30 and frequently CD8. As in other forms of LyP, the lesions underwent spontaneous regression after a few weeks. Recurrences were common, but the prognosis was excellent with no extracutaneous spread or disease-related deaths. Complete remission occurred in 9 of 16 patients (56%). This LyP variant should be distinguished from aggressive forms of angiocentric and angiodestructive and cytotoxic T-cell lymphomas. We propose the term LyP type E for this clinically and histologically unusual variant.

/pdf/angioinvasive-lymphomatoid-papulosis-a-new-variant-2n22i5fxf2.pdf

Angioinvasive lymphomatoid papulosis: a new variant simulating aggressive lymphomas.

The clinical, morphological, and immunohistochemical findings in six cases of ovarian endometrioid tumors (five endometrioid carcinomas and one carcinosarcoma) with a yolk sac tumor (YST) component are described. The age of the patients ranged from 31 to 73 years (average, 53), and only two patients were premenopausal. Two cases were stage Ia tumors, three stage III, and one stage IV. A substantial postoperative elevation of alpha-fetoprotein (AFP) was seen in two patients and a mild increase in another two. All six patients had surgery and postoperative cisplatin-based chemotherapy regimens, four of whom died of tumor 3 to 14 months after surgery without response to treatment. Only a stage Ia patient is alive and well 1 year after surgery. The tumors were large (average, 17 cm). Benign endometrioid lesions were found in the homolateral ovary in two cases and in the contralateral ovary in another two. All cases had endometrioid ovarian carcinomas (EOC) of various types admixed with typical YST components. Immunohistochemically, EOC areas differed from YST in their positivity for OC 125, CA 19.9, and nuclear estrogen and progesterone receptors and in their negativity for AFP, which was conspicuously positive in the YST areas. The clinicopathological profile of ovarian endometrioid tumors with YST also differs from that of YST in that it occurs in the same age range as EOC, it shows coexistence of benign endometrioid lesions, and it has a poor response to chemotherapy. The histological pattern in transitional areas may be difficult to differentiate from "endometrioid-like" (enteroblastic) YST and clear cell tumors. Ovarian endometrioid tumors with YST component should be considered a variant of endometrial carcinoma. Its recognition is necessary in view of its unusually aggressive behavior and poor prognosis.

Ovarian endometrioid tumors with yolk sac tumor component, an unusual form of ovarian neoplasm. Analysis of six cases.

γδ T cells represent a minor T-cell subset that is mainly distributed in mucosal surfaces. Two distinct lymphomas derived from these cells have been recognized: hepatosplenic γδ T-cell lymphoma (HSTL) and primary cutaneous γδ T-cell lymphoma (PCGD-TCL). However, whether other anatomic sites may also be involved and whether they represent a spectrum of the same disease are not well studied. The lack of T-cell receptor (TCR)β expression has been used to infer a γδ origin when other methods are not available. We studied 35 T-cell tumors suspected to be γδ TCL using monoclonal antibodies reactive with TCR δ or γ in paraffin sections. We were able to confirm γδ chain expression in 22 of 35 cases. We identified 8 PCGD-TCLs, 6 HSTLs, and 8 γδ TCLs without hepatosplenic or cutaneous involvement involving mainly extranodal sites. Two such cases were classified as enteropathy-associated T-cell lymphoma, type II. The other γδ TCL presented in the intestine, lung, tongue, orbit, and lymph node. In addition, we observed 13 cases with mainly extranodal involvement that lacked any TCR expression ("TCR silent"). In all cases, a natural killer cell origin was excluded. In conclusion, the lack of TCRβ expression does not always predict γδ-T-cell derivation, as TCR silent cases may be found. The recognition of γδ TCL presenting in extranodal sites other than skin and liver/spleen expands the clinical spectrum of these tumors. However, non-HSTL γδ TCL do not seem to represent a single entity. The relationship of these tumors with either HSTL or PCGD-TCL requires further study.

/pdf/nonhepatosplenic-gd-t-cell-lymphomas-represent-a-spectrum-of-4fyacbrn5f.pdf

Nonhepatosplenic γδ T-cell lymphomas represent a spectrum of aggressive cytotoxic T-cell lymphomas with a mainly extranodal presentation.

Alfa-fetoprotein-positive globules in involuting human yolk sac.

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Ovarian endometrioid tumors with yolk sac tumor component, an unusual form of ovarian neoplasm. Analysis of six cases.

Nonhepatosplenic γδ T-cell lymphomas represent a spectrum of aggressive cytotoxic T-cell lymphomas with a mainly extranodal presentation.

Alfa-fetoprotein-positive globules in involuting human yolk sac.