CD1a, Thymocytes Antibody
- Known as:
- CD1a, Thymocytes Antibody
- Catalog number:
- MAB418P
- Product Quantity:
- 5 ml
- Category:
- -
- Supplier:
- INNOVEX
- Gene target:
- CD1a Thymocytes Antibody
Ask about this productRelated genes to: CD1a, Thymocytes Antibody
- Gene:
- CD1A NIH gene
- Name:
- CD1a molecule
- Previous symbol:
- CD1
- Synonyms:
- -
- Chromosome:
- 1q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2017-07-07
Related products to: CD1a, Thymocytes Antibody
Related articles to: CD1a, Thymocytes Antibody
- Rosai-Dorfman disease (RDD), a rare non-Langerhans cell histiocytic disorder that primarily involves lymph nodes, rarely manifests as isolated posterior mediastinal extranodal lesions. We report a woman in her 30s with incidentally detected paravertebral masses in the posterior mediastinum on routine screening. Contrast-enhanced CT showed progressive homogeneous enhancement of the lesions; MRI revealed T1 isointensity, mild T2 hyperintensity, and marked fat-suppressed T2 hyperintensity relative to muscle. A neurogenic tumor was initially suspected. Video-assisted thoracoscopic excision established RDD: large pale histiocytes with emperipolesis, S100 and CD68 positive, CD1a negative. The patient had an uncomplicated postoperative course, with no clinical or radiologic recurrence over 2 years of follow-up. This case underscores extranodal soft-tissue RDD as a rare mimic of posterior mediastinal neurogenic tumors, highlighting the need for mandatory radiologic-pathologic correlation to prevent misdiagnosis and guide surgical management and long-term surveillance. - Source: PubMed
Publication date: 2026/08/21
He YinLi XinyuHuang JingfengXiao Zeyu - A 92-year-old man with a history of diffuse large B-cell lymphoma treated with chemoradiotherapy, and later with radiotherapy for an isolated cutaneous relapse with complete response, presented with a 1-month history of multiple asymptomatic erythematous-to-violaceous papules and nodules on the face, trunk, and upper limbs. Given his oncological history and previous skin involvement, lymphoma relapse was the leading diagnostic concern, with cutaneous metastases and sarcoidosis also considered. However, skin biopsies showed a non-Langerhans cell histiocytic infiltrate expressing CD45, CD68, and CD163, without CD1a, CD20, PAX5, S100, or Langerin expression. Skin and blood flow cytometry identified no abnormal cell populations, and a PET-CT scan showed no abnormal metabolic activity. Clinicopathological correlation narrowed the differential to group C (cutaneous) histiocytosis, and subsequent spontaneous regression of the lesions over 3 months without treatment supported the diagnosis of generalised eruptive histiocytosis. At 15 months of follow-up, there was no recurrence or evidence of active disease. This case illustrates that cutaneous histiocytoses can mimic several inflammatory and neoplastic conditions, including lymphoma relapse, reinforcing the need to actively resist cognitive bias in people who have had cancer through reflective reassessment, broad differential diagnosis, and biopsy confirmation. - Source: PubMed
Publication date: 2026/08/27
Martins FranciscoCaetano DavidCalvão JoanaCardoso José Carlos - Cerebral venous sinus thrombosis (CVST) is an uncommon cerebrovascular disorder with heterogeneous manifestations and may occasionally precede the diagnosis of an underlying malignancy. We report the case of a 24-year-old man who presented with recurrent fever, headache, pharyngodynia, and systemic inflammation initially attributed to a sinonasal or odontogenic infectious process. He subsequently developed binocular horizontal diplopia, left abducens nerve palsy, papilledema, severe headache, and nausea. Neuroimaging demonstrated extensive CVST involving the left internal jugular vein, bilateral transverse sinuses, and superior sagittal sinus, without ischemic, hemorrhagic, or tumoral brain parenchymal lesions. Thrombophilia testing identified heterozygous prothrombin G20210A as the only established inherited thrombophilic factor. Despite initial neurological stabilization, the patient developed a rapidly recurrent frontal calvarial, epicranial, and cranio-dural lesion extending toward the superior sagittal sinus, without brain parenchymal involvement or imaging evidence of leptomeningeal disease. Initial morphological assessment suggested Langerhans cell histiocytosis. However, comprehensive histopathological and immunohistochemical reassessment demonstrated diffuse strong CD30 expression, nuclear and cytoplasmic ALK positivity, CD43 expression, and focal epithelial membrane antigen and granzyme B positivity, while CD1a and S100 were negative. These findings established the diagnosis of systemic ALK-positive anaplastic large cell lymphoma with secondary extra-axial cranio-dural involvement. Systemic staging demonstrated disseminated nodal disease and a noncontiguous cranio-dural extranodal lesion, consistent with stage IV disease. Treatment with anticoagulation and six cycles of brentuximab vedotin combined with cyclophosphamide, doxorubicin, and prednisone resulted in a favorable neurological and oncological outcome, with no metabolically active or residual enhancing disease on follow-up imaging. This case emphasizes the importance of continued etiological investigation in young patients with extensive CVST and an atypical clinical course, even when plausible infectious and inherited thrombotic risk factors coexist. - Source: PubMed
Publication date: 2026/08/13
Dan Traian FlaviusPis Alexandra TimeeaUlucean Ana-Maria-SmarandaCopil AlexandraBertici RazvanMiron AdelinaBorz Andreea MihaelaMunteanu GeorgianaIacob NicoletaIonita IoanaJianu Silviana NinaJianu Dragos Catalin - : Erdheim-Chester disease (ECD) is a rare non-Langerhans cell histiocytosis characterized by multisystem infiltration of foamy histiocytes, leading to chronic inflammation, fibrosis, and organ dysfunction. Breast involvement in ECD is extremely uncommon, and the sonographic features of ECD involving the breast remain poorly described. : We report the case of a 59-year-old woman with chronic bone pain and multisystem disease who experienced an extended diagnostic course despite undergoing renal biopsy, biopsy of a right elbow lesion, bone marrow examination, and multidisciplinary evaluation. Breast ultrasound revealed bilateral infiltrative hypoechoic lesions involving the breasts and axillae. These were classified as BI-RADS 4C and were highly suspicious for breast malignancy. Subsequently, an ultrasound-guided core needle biopsy was performed on the breast and axillary lesions. : Histopathology showed fibroadipose tissue infiltrated by numerous foamy histiocytes, scattered epithelioid cells, and occasional Touton giant cells. Immunohistochemistry showed positivity for CD68, CD163, CD4, and Cyclin D1, partial positivity for OCT2 and CD30, and negativity for S100, CD1a, Langerin, ALK, CK (Pan), and GATA3. The Ki-67 index was approximately 3%. Molecular testing detected the BRAF V600E mutation, supporting the diagnosis of ECD. A review of reported cases showed that breast involvement in ECD lacks specific ultrasound findings and may closely mimic primary breast malignancy. : Breast involvement in ECD is rare and may present as bilateral infiltrative hypoechoic lesions with axillary involvement on ultrasound. In patients with chronic bone pain, symmetric osteosclerosis, or multisystem disease, ECD should be considered in the differential diagnosis. Ultrasound-detected superficial lesions may provide accessible biopsy targets, helping to establish a timely diagnosis and reduce diagnostic delay. - Source: PubMed
Publication date: 2026/08/16
Chen JuanmeiRuxian AyibotaLi DanyingJiang YongMa Buyun - Myeloid/lymphoid neoplasms with FGFR1 rearrangement (MLN-FGFR1), also known as 8p11 myeloproliferative syndrome, are rare and aggressive hematologic malignancies arising from pluripotent stem cells. The FGFR1::ZMYM2 fusion resulting from t(8;13)(p11.2;q12) characteristically co presents as T-lymphoblastic lymphoma in lymph nodes alongside a myeloproliferative neoplasm in the bone marrow. The disease is resistant to tyrosine kinase inhibitors and conventional chemotherapy, and carries a median survival of less than 12 months without allogeneic hematopoietic stem cell transplantation (allo-HSCT). : We report a 23-year-old female who presented with progressive cervical lymphadenopathy and hyperleukocytosis (WBC 186.6 K/μL). Excisional lymph node biopsy demonstrated T-cell acute lymphoblastic lymphoma (T-ALL) with eosinophilic infiltration; immunohistochemistry confirmed lymphoblasts positive for CD1a, CD2, CD3, CD4, CD5, CD7, CD8, and TdT. Concurrent bone marrow biopsy showed a myeloproliferative neoplasm without excess blasts. Chromosomal analysis confirmed t(8;13)(p11.2;q12) with FGFR1::ZMYM2 rearrangement, and NGS identified a concurrent CSF3R variant (Q741*). She received induction chemotherapy per the PEDS AALL1231 protocol (Arm A) followed by consolidation, with a course complicated by hyperleukocytosis, venous thromboembolism, bacteremia, and severe mucositis requiring PICU admission. Despite initial response, the disease progressed to acute myeloid leukemia (AML) with acquisition of a PTEN variant; the patient was offered but did not complete allo-HSCT and died of refractory AML approximately 10 months after diagnosis. : This case highlights the aggressive clinical course and diagnostic challenges of MLN-FGFR1, a rare stem cell-derived myeloid/lymphoid neoplasm. To our knowledge, this appears to be the first reported case documenting sequential CSF3R and PTEN variant acquisition with complete follow-up through fatal AML transformation, and the first to describe treatment with a pediatric ALL induction protocol (PEDS AALL1231) in this setting. The characteristic histomorphologic pattern of eosinophil-rich T-ALL in lymph nodes with concurrent myeloproliferative neoplasm in bone marrow should prompt immediate molecular workup. Allo-HSCT must be pursued urgently at diagnosis, as complications rapidly narrow the transplant window and the disease is uniformly fatal without it. - Source: PubMed
Publication date: 2026/08/06
Krishnareddigari MehaPatel GopalBokhari AqibaGraff John PaulDwyre Denis MPanigrahi Arun