Academic literature on the topic 'INDOLENT PRECURSOR'

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Journal articles on the topic "INDOLENT PRECURSOR"

1

Pinto-Lopes, Pedro, Francisco Adao Fonseca, Roberto Silva, Pedro von Hafe, and Elsa Fonseca. "Indolent systemic mastocytosis limited to the bone: a case report and review of the literature." Sao Paulo Medical Journal 131, no. 3 (2013): 198–204. http://dx.doi.org/10.1590/1516-3180.2013.1313460.

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CONTEXT Systemic mastocytosis is defined as a clonal disorder of mast cells and their precursor cells and is currently classified as a myeloproliferative neoplasm. Its clinical course has a wide spectrum, ranging from indolent disease, with normal life expectancy, to highly aggressive disease, associated with multisystemic involvement and poor overall survival. The aim of this study was to report a case of indolent systemic mastocytosis, focusing on the diagnostic challenges, with a review of the literature. CASE REPORT A 79-year-old Caucasian woman with osteoporosis was evaluated at the Emergency Department because of complaints of low back pain. Before this, she had consulted an orthopedist and had undergone some imaging examinations, namely a bone scan that revealed a “superscan” pattern. Due to her pain complaints and these test results, the patient was admitted to the Department of Internal Medicine. After undergoing several analytical tests and some additional imaging examinations to rule out some important differential diagnoses, she then underwent bone marrow biopsy, which made it possible to identify indolent systemic mastocytosis. CONCLUSION Systemic mastocytosis is a rare entity that is difficult to diagnose. Its symptoms are often unspecific and frequently ignored. Skeletal changes may be the first and only manifestation of the disease and in some cases, like this one, the diagnosis is made only after histological examination. The key point for the diagnosis is to contemplate the possibility of systemic mastocytosis.
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2

Canberk, Sule. "Precursor and borderline lesions of the thyroid (indolent lesions of epithelial origin): from theory to practice." Gland Surgery 9, no. 5 (2020): 1724–34. http://dx.doi.org/10.21037/gs-20-429.

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3

Lussier, Tyler, Natalie Schoebe, and Sabine Mai. "Risk Stratification and Treatment in Smoldering Multiple Myeloma." Cells 11, no. 1 (2021): 130. http://dx.doi.org/10.3390/cells11010130.

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Smoldering multiple myeloma is a heterogeneous asymptomatic precursor to multiple myeloma. Since its identification in 1980, risk stratification models have been developed using two main stratification methods: clinical measurement-based and genetics-based. Clinical measurement models can be subdivided in three types: baseline measurements (performed at diagnosis), evolving measurements (performed over time during follow-up appointments), and imaging (for example, magnetic resonance imaging). Genetic approaches include gene expression profiling, DNA/RNA sequencing, and cytogenetics. It is important to accurately distinguish patients with indolent disease from those with aggressive disease, as clinical trials have shown that patients designated as “high-risk of progression” have improved outcomes when treated early. The risk stratification models, and clinical trials are discussed in this review.
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Marchegiani, Giovanni, Stefano Andrianello, Tommaso Pollini, et al. "Natural History of Intraductal Papillary Mucinous Neoplasm of the Pancreas Reappraisal of the Indolent Precursor of Pancreatic Cancer." Journal of the American College of Surgeons 227, no. 4 (2018): e37-e38. http://dx.doi.org/10.1016/j.jamcollsurg.2018.08.099.

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5

Purdy, Adam, Firas Ido, and Deborah Stahlnecker. "Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH): A Case of Indolent Pulmonary Nodules Diagnosed with Robotic-Assisted Navigational Bronchoscopy." Case Reports in Pulmonology 2021 (December 10, 2021): 1–4. http://dx.doi.org/10.1155/2021/6312296.

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Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) is an atypical pulmonary disorder with limited understanding. Given the rare nature of this disease, it is essential to obtain adequate tissue pathology to confirm the diagnosis. This disease is mainly diagnosed in middle-aged, nonsmoking females, and it is now accepted as a precursor lesion to pulmonary carcinoid tumors. DIPNECH presents with characteristic radiographic and histologic findings, but its diagnosis, management, and prognosis are often underrecognized and poorly understood. Those with symptoms may present with shortness of breath, wheezing, and persistent cough and are often misdiagnosed with reactive airway disease. Pulmonary function testing may reveal airflow obstruction and air trapping. Imaging is characterized by multiple lung nodules, typically less than 5 mm in size, with a background mosaic attenuation on computed tomography imaging. Histologically, DIPNECH can be suspected based on the presence of hyperplastic neuroendocrine cells. DIPNECH is considered a precursor to invasive neuroendocrine tumor, and up to 50% of patients may have a well-differentiated neuroendocrine tumor at the time of presentation. Here, we present the case of a 46-year-old female with a history of ulcerative colitis on mesalamine who presented with a 6-month history of ongoing shortness of breath, chest tightness, wheezing, and cough. She was initially diagnosed with asthma before imaging later revealed as multiple pulmonary nodules with a diffuse mosaic pattern. Using robotic-assisted navigational bronchoscopy, she underwent sampling of a dominant 1.8 cm right middle lobe pulmonary nodule and pathology was consistent with low-grade neuroendocrine tumor.
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6

Garcia-Montero, Andres C., Maria Jara-Acevedo, Ivan Alvarez-Twose, et al. "KIT D816V Mutation Positive Bone Marrow Mesenchymal Stem Cells in Indolent Systemic Mastocytosis Are Associated with Disease Progression." Blood 126, no. 23 (2015): 4058. http://dx.doi.org/10.1182/blood.v126.23.4058.4058.

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Abstract PURPOSE: Multilineageinvolvement of bone marrow (BM) hematopoiesis by the somatic KIT D816V mutation is present in a subset of adult indolent systemic mastocytosis (ISM) patients in association with a poorer prognosis. Here we investigated the potential involvement of BM mesenchymal stem cells (MSC) from ISM patients by the KIT D816V mutation and its potential impact on disease progression and outcome. METHODS: The KIT D816V mutation was investigated in highly-purified BM MSC and other BM cell populations from 83 ISM patients followed for a median of 116 months. MC clonality was further evaluated in female patients by the pattern of inactivation of the X chromosome (XCIP). RESULTS: KIT D816V-mutated MSC were detected in 22/83 (27%) ISM patients. All MSC-mutated patients had multilineage KIT mutation (100% vs. 30%, p=0.0001) and they more frequently showed involvement of lymphoid plus myeloid BM cells (59% vs 22%; P =.03) and a polyclonal XCIP of the KIT- mutated BM MC (64% vs 0%; P =0.01) vs other multilineage ISM cases. Moreover, presence of KIT D816V-mutated MSC was associated with more advanced disease features of ISM, a greater rate of disease progression (50% vs 17%; P =.04) and a shorter progression-free survival at 10, 20 and 30 years (P ≤.003). CONCLUSION: Overall, these results support the notion that ISM patients with mutated MSC may have acquired the KIT mutation in a common pluripotent progenitor cell, prior to differentiation into MSC and hematopoietic precursor cells, before the X-chromosome inactivation process occurs. From a clinical point of view, acquisition of the KIT mutation in an earlier BM precursor cell confers a significantly greater risk for disease progression and a poorer outcome. Disclosures No relevant conflicts of interest to declare.
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7

Marchegiani, Giovanni, Stefano Andrianello, Tommaso Pollini, et al. "The natural history of intraductal papillary mucinous neoplasms of the pancreas: Reappraisal of the indolent precursor of pancreatic cancer." Pancreatology 18, no. 4 (2018): S2—S3. http://dx.doi.org/10.1016/j.pan.2018.05.011.

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8

Marchegiani, G., S. Andrianello, T. Pollini, et al. "The natural history of intraductal papillary mucinous neoplasm of the pancreas: Reappraisal of the indolent precursor of pancreatic cancer." HPB 20 (September 2018): S195. http://dx.doi.org/10.1016/j.hpb.2018.06.051.

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9

López, Cristina, Pablo Mozas, Armando López-Guillermo, and Sílvia Beà. "Molecular Pathogenesis of Follicular Lymphoma: From Genetics to Clinical Practice." Hemato 3, no. 4 (2022): 595–614. http://dx.doi.org/10.3390/hemato3040041.

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Follicular lymphoma (FL), a generally indolent disease that derives from germinal center (GC) B cells, represents around 20–25% of all new lymphomas diagnosed in Western countries. The characteristic t(14;18)(q32;q21) translocation that places the BCL2 oncogene under control of the immunoglobulin heavy-chain enhancer occurs in pro- or pre-B cells. However, additional secondary alterations are required for the development of overt FL, which mainly affects genes involved in epigenetic and transcriptional regulation, signaling and B cell differentiation, the BCR/NF-κB pathway, and proliferation/apoptosis. On the other hand, new insights into the FL pathogenesis suggest that FL lacking the BCL2 translocation might be a distinct biological entity with genomic features different from the classical FL. Although FL is considered an indolent disease, around 10–20% of cases eventually transform to an aggressive lymphoma, usually a diffuse large B cell lymphoma, generally by a divergent evolution process from a common altered precursor cell acquiring genomic alterations involved in the cell cycle and DNA damage responses. Importantly, FL tumor cells require interaction with the microenvironment, which sustains cell survival and proliferation. Although the use of rituximab has improved the outlook of most FL patients, further genomic studies are needed to identify those of high risk who can benefit from innovative therapies. This review provides an updated synopsis of FL, including the molecular and cellular pathogenesis, key events of transformation, and targeted treatments.
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10

Khanlari, Mahsa, and Jennifer R. Chapman. "Follicular lymphoma: updates for pathologists." Journal of Pathology and Translational Medicine 56, no. 1 (2022): 1–15. http://dx.doi.org/10.4132/jptm.2021.09.29.

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Follicular lymphoma (FL) is the most common indolent B-cell lymphoma and originates from germinal center B-cells (centrocytes and centroblasts) of the lymphoid follicle. Tumorigenesis is believed to initiate early in precursor B-cells in the bone marrow (BM) that acquire the t(14;18)(q32;q21). These cells later migrate to lymph nodes to continue their maturation through the germinal center reaction, at which time they acquire additional genetic and epigeneticabnormalities that promote lymphomagenesis. FLs are heterogeneous in terms of their clinicopathologic features. Most FLs are indolent and clinically characterized by peripheral lymphadenopathy with involvement of the spleen, BM, and peripheral blood in a substantial subset of patients, sometimes accompanied by constitutional symptoms and laboratory abnormalities. Diagnosis is established by the histopathologic identification of a B-cell proliferation usually distributed in an at least partially follicular pattern, typically, but not always, in a lymph node biopsy. The B-cell proliferation is biologically of germinal center cell origin, thus shows an expression of germinal center-associated antigens as detected by immunophenotyping. Although many cases of FLs are typical and histopathologic features are straightforward, the biologic and histopathologic variability of FL is wide, and an accurate diagnosis of FL over this disease spectrum requires knowledge of morphologic variants that can mimic other lymphomas, and rarely non-hematologic malignancies, clinically unique variants, and pitfalls in the interpretation of ancillary studies. The overall survival for most patients is prolonged, but relapses are frequent. The treatment landscape in FL now includes the application of immunotherapy and targeted therapy in addition to chemotherapy.
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