Ana Maria Medina

Dr. Ana Maria Medina

orcid

Research Focus & Metrics

Academic Career Length

7Years (2020-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 May 2021 in Cardiovascular Pathology
Verified
Journal Article
Closed access
KOKei Shing Oh
Kei Shing Oh
CFChristopher A. Febres-Aldana
Christopher A. Febres-Aldana
NKNicholas Kuritzky
Nicholas Kuritzky
FUFrancisco Ujueta
Francisco Ujueta
IAIvan A. Arenas
Ivan A. Arenas
RPRobert Poppiti
Robert Poppiti

17 January 2023 in Current Oncology
Verified
Journal Article
Open access
PDF file
JMJuan Carlos Alvarez Moreno
Juan Carlos Alvarez Moreno
Hisham BahmadHisham Bahmad
Hisham Bahmad
Abed AljamalAbed Aljamal
Abed Aljamal
RDRuben Delgado
Ruben Delgado
ASAli SALAMI
Ali SALAMI
VSVathany Sriganeshan
Vathany Sriganeshan
Diffuse large B-cell lymphoma (DLBCL) is the most common lymphoma in adults. We evaluated the immunohistochemical (IHC) expression of p63 and p53 in DLBCL and their significance on overall survival (OS) and progression-free survival (PFS). We conducted a retrospective cohort study of 177 patients with DLBCL who presented to Mount Sinai Medical Center of Florida (Miami Beach, Florida) between 2010 and 2020. IHC staining for p63 and p53 protein expression was performed. A significant correlation was found between p63 positivity and p53 expression, p53/p63 co-positivity, Ki-67 proliferation index, MYC expression, and MYC/BCL2 double expression. Regardless of the germinal center B-cell like (GCB) subgrouping, there was a trend among p53+ patients to have MYC/BCL2 double expression, positive MYC expression, and lower OS and PFS. A tendency of poor OS was seen in p53+ patients in the non-GCB, GCB, and double expressors subgroups and poor PFS in p53+ patients regardless of the subgrouping. In conclusion, our results suggest that p63 and p53 may represent potential additional prognostic biomarkers in DLBCL and may be included in the initial diagnostic work up of patients with DLBCL.

1 November 2024 in Diseases
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Journal Article
Open access
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ADArunima Deb
Arunima Deb
VFVielka Fernandez
Vielka Fernandez
EKEkim Kilinc
Ekim Kilinc
Hisham BahmadHisham Bahmad
Hisham Bahmad
NCNicholas S. Camps
Nicholas S. Camps
AMAna Maria Medina
Ana Maria Medina
Kikuchi–Fujimoto disease (KFD), also known as histiocytic necrotizing lymphadenitis, is a rare, self-limiting disorder characterized by fever typically lasting for 1 week up to 1 month and painful necrotizing lymphadenopathy, primarily affecting young adults of Asian ancestry. Although the exact cause remains unclear, infectious and autoimmune mechanisms have been implicated in the pathogenesis of the disease. In this case series, we aim to describe the histopathological features of KFD over a ten-year period at Mount Sinai Medical Center of Florida, and review the current understanding of its pathogenesis, clinical presentation, diagnosis, and management. A retrospective review of our pathology database between January 2013 and May 2024 was performed to identify patients diagnosed with KFD at our institution. Eight cases of KFD were identified, with a mean age of 35 years (range 24–49) and slight male predilection (5:3). Three patients exhibited leukopenia, and two had concurrent HIV infection. One patient developed systemic lupus erythematosus (SLE), and another developed IgA nephropathy during follow-up. Histopathological examination revealed the characteristic features of KFD, including lymph node architectural effacement, histiocytic infiltration, and necrosis. In conclusion, KFD remains a diagnostic challenge due to its overlapping clinical features with other infectious and autoimmune diseases, particularly SLE. While most cases resolve spontaneously, long-term follow-up is warranted due to the potential for recurrence and autoimmune associations.

7 August 2020 in Laboratory Medicine
Verified
Journal Article
Closed access
KKKritika Krishnamurthy
Kritika Krishnamurthy
AMAna Maria Medina
Ana Maria Medina
LHLydia Howard
Lydia Howard
Objective: Because of its wide tissue distribution, elevation of serum lactate dehydrogenase (LD) is a nonspecific finding. Although serum LD is still included in the prognosis and staging of metastatic melanoma and germ cell tumors, its nonspecificity has led to decreased usefulness. Methods: In this study, we analyzed the serum LD assays performed in a 726-bed hospital during a 1-year period and reviewed charts of patients with serum LD of >3 standard deviations (SD). Results: Of 312 patients with elevated serum LD, only 9 were patients with melanoma and germ cell tumors. The other 303 patients had other malignancies, chronic conditions, and sepsis. Conclusion: Elevated serum LD (even >3 SD) is an extremely nonspecific finding that does not contribute to clinical management in a majority of patients. As such, serum LD testing should be retired from routine clinical order sets and restricted in use.

1 January 2021 in Autopsy Case Reports
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Journal Article
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Hisham BahmadHisham Bahmad
Hisham Bahmad
LALuis E. Rosario Alvarado
Luis E. Rosario Alvarado
KMKiranmayi P. Muddasani
Kiranmayi P. Muddasani
AMAna Maria Medina
Ana Maria Medina
Autops Case Rep, vol.11, e2021260, 2021

1 December 2022 in Diseases
Verified
Journal Article
Open access
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Abed AljamalAbed Aljamal
Abed Aljamal
MEMohamad K. Elajami
Mohamad K. Elajami
EMEphraim H. Mansour
Ephraim H. Mansour
Hisham BahmadHisham Bahmad
Hisham Bahmad
AMAna Maria Medina
Ana Maria Medina
MCMike Cusnir
Mike Cusnir
Ataxia-telangiectasia is an autosomal recessive disorder that usually manifests in childhood due to mutations in the Ataxia-Telangiectasia Mutated (ATM) gene. It is believed that there is an association between this gene mutation/polymorphism and cancer risk, including breast, lung, and pancreatic cancers. We report a rare case of a 69-year-old woman who developed three different primary cancers, including non-small cell lung cancer (NSCLC) in both lungs and pancreatic adenocarcinoma, and was later found to have a rarely reported variant mutation in the ATM gene, namely Exon 39, c.5644 C > T. We hypothesize that the ATM gene, c.5644 C > T mutation could be a plausible contributor in the pathogenesis of these three cancers. This hypothesis has yet to be validated by larger studies that focus on a mechanistic approach involving DNA repair genes such as the ATM. More importantly, this paves the way to developing new patient-specific targeted therapies and inaugurating precision medicine as a cornerstone in cancer therapeutics.