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Volumetric Approach to the Lips
Published in Neil S. Sadick, Illustrated Manual of Injectable Fillers, 2020
Necrosis is a rare but real complication of any dermal filler, including HA fillers. There are two main etiologies of necrosis: first, compression of the vessel either by the product itself or by intradermal bleeding, and second by intra-arterial injection and occlusion of the artery (33). Knowing the signs and symptoms of necrosis is vitally important, as much tissue can be saved if the vascular compromise is caught prior to the death of the cutaneous tissue. Typical signs and symptoms of impending necrosis are a blanching or grey discoloration of the skin, a reticulate or lacy erythema, increasing pain or unusual sensation, or loss of sensation (33). If a patient describes any strange or unusual symptom, it is wise of the physician to insist the patient return to clinic for further evaluation. If impending necrosis is suspected or if necrosis has started, the treatment is with vigorous massage, nitroglycerin ointment, aspirin, warm compresses, and flooding the area of necrosis with two vials of hyaluronidase (33). There are numerous strategies one can employ while injecting to decrease the risk of necrosis; these include refluxing prior to each injection, monitoring the skin’s response with each injection—immediate blanching is a sign of intra-arterial injection, injecting in a retrograde fashion, injecting small amounts with each stroke of the needle, and injecting slowly. Additionally, knowing your vascular anatomy and staying away from danger zones is highly recommended with any facial rejuvenation.
Renal Cell Cancer
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Macroscopically clear-cell RCCs have a characteristic appearance with solid areas often interspersed with areas of cystic degeneration. These tumors are richly vascular with numerous vessels throughout the supporting stroma. Microscopically, tumor cells have a clear cytoplasm with a low nuclear to cytoplasmic ratio. The Fuhrman and WHO/ISUP grading systems can aid in the prediction of clinical tumor behavior. Both consist of four grades (I–IV) on the basis of morphologic tumor appearance. Sarcomatoid change may be seen, and represents a poor prognostic feature occurring in approximately 5% of tumors. The presence of tumor necrosis is also of prognostic significance and is associated with a worse survival.6 For the vast majority of patients with clear-cell RCC, the key molecular driver underlying development and progression of both sporadic and hereditary disease is loss of function of the Von Hippel–Lindau (VHL) gene through a process of deletion, mutation, or methylation.7,8 Increasingly evident with the progress in genetic sequencing is that multiple other genes are also responsible for malignant cell proliferation. Located on chromosome 3p in addition to VHL are PBRM1, SETD2, and BAP1 epigenetic/chromatin regulators. Loss of function of these tumor suppressor genes is thought to play a key role in cancer progression. PBRM-1 is mutated in around 40% ccRCC, and subclonal mutations in BAP-1 and SETD2 identified in 10–15% of tumor samples.8,9
Pyrexia Two Weeks after an Attack of Alcohol-Induced Acute Pancreatitis
Published in Savio George Barreto, Shailesh V. Shrikhande, Dilemmas in Abdominal Surgery, 2020
The gross pathology of acute pancreatitis is remarkably similar across the different aetiologies. It is customary to distinguish interstitial edematous acute pancreatitis (which is usually associated with milder acute pancreatitis), from necrotizing pancreatitis. The latter is also associated with edema and is a hallmark of more severe disease. The necrosis can be patchy and minimal, confluent, and extensive and/or involving the peripancreatic tissue in the retroperitoneum. The extent of necrosis appears to be related to disease severity [1,2].
Metformin induces myeloma cells necrosis and apoptosis and it is considered for therapeutic use
Published in Journal of Chemotherapy, 2023
Zhentian Wu, Lianghua Wu, Liangliang Zou, Muqing Wang, Xin Liu
In our study, cellular and molecular mechanisms responsible for the actions of metformin differed from cell line to cell line. For U266 cells, it induced necrosis. For H929, RPMI8226, and MM.1s cells, it induced apoptosis. Cell cycle analysis showed that the cycle arrest also varied from cell to cell following metformin treatment. We found no change in U266 cells, in H929 and MM.1s cells, it induced at the G0/G1 phase, and in RPMI8226, it induced at the G2/M phase. Cell cycle arrest is controlled by some cyclin-dependent kinases (CDKs), such as cyclin-D1 in the G1/S transition and cyclin-B1 in the G2/M transition. We hypothesize that metformin acts powerfully on the cell cycle via different pathways in different MM cells. For H929 and MM.1s cells, the down-regulation of CyclinD1 leads to G1/G0 arrest and suppresses the cell proliferation. Cyclin-B1 is a key regulator of the cell cycle, it is involved in regulating the events of mitosis. It increased in the early G2 phase, and it is necessary for transition from G2 to M. Here we show that RPMI8226 cells arrested in G2/M with down-regulation of cyclin-B1 while metformin treated. It suggests that this reduction leads to accumulation of MM cells in the G2 phase and inhibits transition to the M phase. Necrosis is an unordered and accidental form of cellular dying, and usually with no changes in cell cycle arrest. For U266, we found necrosis related protein iNOS increasingly expressed and no apoptosis-associated protein was detected. It further confirmed that metformin might induce U266 necrosis.
Hot topics in renal cancer pathology: implications for clinical management
Published in Expert Review of Anticancer Therapy, 2022
Alessia Cimadamore, Anna Caliò, Laura Marandino, Stefano Marletta, Carmine Franzese, Luigi Schips, Daniele Amparore, Riccardo Bertolo, Stijn Muselaers, Selcuk Erdem, Alexandre Ingels, Nicola Pavan, Angela Pecoraro, Önder Kara, Eduard Roussel, Umberto Carbonara, Riccardo Campi, Michele Marchioni
Tumor necrosis is a pathological feature included in several prognostic scores. Presence of necrosis has been correlated to tumor size, grade, presence of distant metastasis and CSS both in univariate and multivariate analysis. However, contradictory reports showed no correlation with OS. These studies have included in their series different subtypes of RCC, tumor with focal microscopic necrosis and tumor with extensive necrosis, features that may have altered their results [44–47]. In the assessment of necrosis, attention should be paid to excluding area of hyalinization, hemorrhage, and fibrosis. Also, a distinction should be made between microscopic coagulative necrosis and extensive necrosis, due in most cases to infarction, secondary to large vessels obstruction. Some authors have proposed the term ‘granular necrosis’ to specifically describe the tumor-associated necrosis characterized by the presence of well-defined necrotic foci being sharply demarcated from the adjacent viable tumor [48]. Compared to other forms of necrosis, granular necrosis shows loss of architecture, granular nuclear with extensive karyorrhexis and cytoplasmic debris, without an associated neutrophilic infiltrate [48].(Figure 6)
Gastrointestinal stromal tumor metastatic to the orbit
Published in Orbit, 2022
Wesley L. Brundridge, Hans B. Heymann, Adam Spengler, Christopher M. DeBacker, David E. E. Holck
Gastrointestinal stromal tumors (GISTs) are a rare mesenchymal tumor that represent 0.1–3% of all the GI malignancies. The annual incidence of GIST is roughly 10–20 per million. GISTs can arise from any portion of the GI tract originating from gut pacemaker cells known as interstitial cells of Cajal (ICC) or their stem cell precursors that are distributed along the GI tract from the esophagus to the anus.1–3 It occurs predominantly in adults with a median age of 60 years and has roughly equal gender representation.1–3 The major cause of a GIST is the presence of an abnormal form of tyrosine protein kinase (KIT) protein also known as CD117, which causes uncontrollable growth of the GI cells.1 Prognosis depends on the primary site of occurrence, size of the tumor, mitotic activity, staining of proliferating cells, and tumor necrosis.1 While local recurrence and metastasis to intra-abdominal and liver sites are common and well described in the literature, orbital metastasis is exceedingly rare.4–9 The authors report a case of a patient with biopsy-proven GIST with orbital metastasis. To our knowledge, this is only the fifth case of biopsy-proven GIST metastasis to the orbit, only the second case with predominantly epithelioid morphology, and only the second case of bilateral orbital metastasis. The collection and evaluation of protected patient health information was HIPAA-compliant and adhered to the ethical principles outlined in the Declaration of Helsinki as amended in 2013.