Tulane Univ.Sch. Of Med. (Sl79), 1430 Tulane Ave.
New Orleans LA 70112
Medical School: Other - 1984
Accepts Medicare: Yes
Participates In eRX: No
Participates In PQRS: Yes
Participates In EHR: No
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Awards & Recognitions
Dr. Krzysztof Moroz is associated with these group practices
|HCPCS Code||Description||Average Price||Average Price
Allowed By Medicare
|HCPCS Code:88305||Description:Tissue exam by pathologist||Average Price:$153.04||Average Price Allowed
|HCPCS Code:88307||Description:Tissue exam by pathologist||Average Price:$183.00||Average Price Allowed
|HCPCS Code:88173||Description:Cytopath eval fna report||Average Price:$145.68||Average Price Allowed
|HCPCS Code:88342||Description:Immunohistochemistry||Average Price:$120.68||Average Price Allowed
|HCPCS Code:88162||Description:Cytopath smear other source||Average Price:$89.00||Average Price Allowed
|HCPCS Code:88108||Description:Cytopath concentrate tech||Average Price:$62.99||Average Price Allowed
|HCPCS Code:88172||Description:Cytp dx eval fna 1st ea site||Average Price:$70.82||Average Price Allowed
|HCPCS Code:88141||Description:Cytopath c/v interpret||Average Price:$62.00||Average Price Allowed
|HCPCS Code:88312||Description:Special stains group 1||Average Price:$58.21||Average Price Allowed
|HCPCS Code:88304||Description:Tissue exam by pathologist||Average Price:$34.00||Average Price Allowed
|HCPCS Code:88313||Description:Special stains group 2||Average Price:$26.59||Average Price Allowed
HCPCS Code Definitions
- Cytopathology, evaluation of fine needle aspirate; immediate cytohistologic study to determine adequacy for diagnosis, first evaluation episode, each site
- Cytopathology, smears, any other source; extended study involving over 5 slides and/or multiple stains
- Cytopathology, cervical or vaginal (any reporting system), requiring interpretation by physician
- Cytopathology, concentration technique, smears and interpretation (eg, Saccomanno technique)
- Special stain including interpretation and report; Group I for microorganisms (eg, acid fast, methenamine silver)
- Level III - Surgical pathology, gross and microscopic examination Abortion, induced Abscess Aneurysm - arterial/ventricular Anus, tag Appendix, other than incidental Artery, atheromatous plaque Bartholin's gland cyst Bone fragment(s), other than pathologic fracture Bursa/synovial cyst Carpal tunnel tissue Cartilage, shavings Cholesteatoma Colon, colostomy stoma Conjunctiva - biopsy/pterygium Cornea Diverticulum - esophagus/small intestine Dupuytren's contracture tissue Femoral head, other than fracture Fissure/fistula Foreskin, other than newborn Gallbladder Ganglion cyst Hematoma Hemorrhoids Hydatid of Morgagni Intervertebral disc Joint, loose body Meniscus Mucocele, salivary Neuroma - Morton's/traumatic Pilonidal cyst/sinus Polyps, inflammatory - nasal/sinusoidal Skin - cyst/tag/debridement Soft tissue, debridement Soft tissue, lipoma Spermatocele Tendon/tendon sheath Testicular appendage Thrombus or embolus Tonsil and/or adenoids Varicocele Vas deferens, other than sterilization Vein, varicosity
- Level V - Surgical pathology, gross and microscopic examination Adrenal, resection Bone - biopsy/curettings Bone fragment(s), pathologic fracture Brain, biopsy Brain/meninges, tumor resection Breast, excision of lesion, requiring microscopic evaluation of surgical margins Breast, mastectomy - partial/simple Cervix, conization Colon, segmental resection, other than for tumor Extremity, amputation, non-traumatic Eye, enucleation Kidney, partial/total nephrectomy Larynx, partial/total resection Liver, biopsy - needle/wedge Liver, partial resection Lung, wedge biopsy Lymph nodes, regional resection Mediastinum, mass Myocardium, biopsy Odontogenic tumor Ovary with or without tube, neoplastic Pancreas, biopsy Placenta, third trimester Prostate, except radical resection Salivary gland Sentinel lymph node Small intestine, resection, other than for tumor Soft tissue mass (except lipoma) - biopsy/simple excision Stomach - subtotal/total resection, other than for tumor Testis, biopsy Thymus, tumor Thyroid, total/lobe Ureter, resection Urinary bladder, TUR Uterus, with or without tubes and ovaries, other than neoplastic/prolapse
- Cytopathology, evaluation of fine needle aspirate; interpretation and report
- Level IV - Surgical pathology, gross and microscopic examination Abortion - spontaneous/missed Artery, biopsy Bone marrow, biopsy Bone exostosis Brain/meninges, other than for tumor resection Breast, biopsy, not requiring microscopic evaluation of surgical margins Breast, reduction mammoplasty Bronchus, biopsy Cell block, any source Cervix, biopsy Colon, biopsy Duodenum, biopsy Endocervix, curettings/biopsy Endometrium, curettings/biopsy Esophagus, biopsy Extremity, amputation, traumatic Fallopian tube, biopsy Fallopian tube, ectopic pregnancy Femoral head, fracture Fingers/toes, amputation, non-traumatic Gingiva/oral mucosa, biopsy Heart valve Joint, resection Kidney, biopsy Larynx, biopsy Leiomyoma(s), uterine myomectomy - without uterus Lip, biopsy/wedge resection Lung, transbronchial biopsy Lymph node, biopsy Muscle, biopsy Nasal mucosa, biopsy Nasopharynx/oropharynx, biopsy Nerve, biopsy Odontogenic/dental cyst Omentum, biopsy Ovary with or without tube, non-neoplastic Ovary, biopsy/wedge resection Parathyroid gland Peritoneum, biopsy Pituitary tumor Placenta, other than third trimester Pleura/pericardium - biopsy/tissue Polyp, cervical/endometrial Polyp, colorectal Polyp, stomach/small intestine Prostate, needle biopsy Prostate, TUR Salivary gland, biopsy Sinus, paranasal biopsy Skin, other than cyst/tag/debridement/plastic repair Small intestine, biopsy Soft tissue, other than tumor/mass/lipoma/debridement Spleen Stomach, biopsy Synovium Testis, other than tumor/biopsy/castration Thyroglossal duct/brachial cleft cyst Tongue, biopsy Tonsil, biopsy Trachea, biopsy Ureter, biopsy Urethra, biopsy Urinary bladder, biopsy Uterus, with or without tubes and ovaries, for prolapse Vagina, biopsy Vulva/labia, biopsy
- Immunohistochemistry or immunocytochemistry, each separately identifiable antibody per block, cytologic preparation, or hematologic smear; first separately identifiable antibody per slide
- Special stain including interpretation and report; Group II, all other (eg, iron, trichrome), except stain for microorganisms, stains for enzyme constituents, or immunocytochemistry and immunohistochemistry
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Cardiovascular Disease (Cardiology)
*These referrals represent the top 10 that Dr. Moroz has made to other doctors
Examining the Bethesda criteria risk stratification of thyroid nodules. - Pathology, research and practice
The Bethesda criteria are proposed for appropriate stratification of malignancy risk in thyroid nodules, but controversy exists regarding their accuracy and reliability in decision making. Additionally, previous studies have suggested higher rates of both malignancy and false negative fine needle aspiration biopsy (FNA) associated with increasing nodule size. This study aims to determine the accuracy of ultrasound (US)-guided FNA using the current Bethesda criteria in surgical practice. We also aimed to investigate the relationship between nodule size and malignancy.A retrospective analysis of US-guided FNAs by a single surgeon during a 4.5 year period. FNA results using Bethesda criteria were compared to final surgical pathology.611 patients with thyroid nodules underwent US-guided FNA. FNA results in 375 subsequently excised thyroid nodules were recorded according to the Bethesda criteria: 192 (51%) benign, 65 (17%) atypia of unknown significance/follicular lesion of undetermined significance (AUS/FLUS), 42 (11%), suspicious for follicular neoplasm (SFN), 17 (5%) suspicious for malignancy (SM), 28 (8%) malignancy, and 31 (8%) non-diagnostic. Malignancy was confirmed by surgical pathology in 15%, 34%, 50%, 88%, 100%, and 39% of the above groups respectively. Sensitivity, specificity, and false-negative rate were 61%, 99%, and 15% respectively. No correlation existed between the size of nodules with indeterminate FNA results and malignancy rate (p=0.89), or size of nodules with non-diagnostic FNA and malignancy rate (p=0.50).The current Bethesda risk stratification system underestimated malignancy rates in benign, indeterminate and non-diagnostic cytopathologic categories in our experience. There was no positive linear correlation between nodule size and malignancy rate in these cytopathologic categories.Copyright Â© 2015 Elsevier GmbH. All rights reserved.
The impact of thyroid nodule size on the risk of malignancy in follicular neoplasms. - Anticancer research
Studies have shown that the risk of malignancy in follicular neoplasms is as high as 30%. Often, surgery is recommended for such lesions, not for therapeutic purposes but as a diagnostic method, leading to increased hospital costs and related morbidities. Recent studies have suggested that tumor size predicts malignant potential of these follicular neoplasms. Our aim was to identify the impact of nodule size on the risk of malignancy for such lesions.A retrospective medical chart review was undertaken for patients who underwent thyroid surgery at a single academic North American Institution. A total of 120 follicular lesions, follicular neoplasms (Bethesda category IV) or follicular lesions of undetermined significance (Bethesda category III) in 110 patients undergoing thyroid surgery were evaluated. Nodule size as measured by ultrasound, fine-needle aspiration cytological results, and final histopathology reports were reviewed. Analysis was performed by classification according to nodule size: <3 cm, â‰¥3 cm, <4 cm and â‰¥4 cm.Out of the 120 nodules, 48 (40%) were reported to be malignant on final pathological examination. The malignancy rate in nodules<3 cm and â‰¥ 3cm was 41% and 37.8%, respectively (p=0.84). When 4 cm was used as the cut-off, the rate in nodules<4 cm and â‰¥4 cm was 40.6% and 37.5%, respectively (p=0.82).Increased thyroid nodule size does not increase the malignancy rate for follicular neoplasms. Hence, we recommend against routine total thyroidectomy for patients with follicular neoplasms based on the size criteria.CopyrightÂ© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.
EWS-WT1 oncoprotein activates neuronal reprogramming factor ASCL1 and promotes neural differentiation. - Cancer research
The oncogenic fusion gene EWS-WT1 is the defining chromosomal translocation in desmoplastic small round-cell tumors (DSRCT), a rare but aggressive soft tissue sarcoma with a high rate of mortality. EWS-WT1 functions as an aberrant transcription factor that drives tumorigenesis, but the mechanistic basis for its pathogenic activity is not well understood. To address this question, we created a transgenic mouse strain that permits physiologic expression of EWS-WT1 under the native murine Ews promoter. EWS-WT1 expression led to a dramatic induction of many neuronal genes in embryonic fibroblasts and primary DSRCT, most notably the neural reprogramming factor ASCL1. Mechanistic analyses demonstrated that EWS-WT1 directly bound the proximal promoter of ASCL1, activating its transcription through multiple WT1-responsive elements. Conversely, EWS-WT1 silencing in DSRCT cells reduced ASCL1 expression and cell viability. Notably, exposure of DSRCT cells to neuronal induction media increased neural gene expression and induced neurite-like projections, both of which were abrogated by silencing EWS-WT1. Taken together, our findings reveal that EWS-WT1 can activate neural gene expression and direct partial neural differentiation via ASCL1, suggesting agents that promote neural differentiation might offer a novel therapeutic approach to treat DSRCT.Â©2014 American Association for Cancer Research.
In vivo anticancer synergy mechanism of doxorubicin and verapamil combination treatment is impaired in BALB/c mice with metastatic breast cancer. - Experimental and molecular pathology
The development of resistance to anticancer drugs is a major unsolved problem in the chemotherapy treatment of metastatic breast cancer. We have shown that increased expression of P-glycoprotein (P-gp) prevented nuclear entry of the doxorubicin molecules into murine breast cancer cells (4T1-R) leading to doxorubicin chemoresistance. This study was performed to test whether inhibition of P-gp using verapamil could overcome doxorubicin chemoresistance and eliminate multiorgan metastasis 4T1-R cells in BALB/c mouse. The 4T1-R cells were treated with doxorubicin alone, verapamil alone, and a combination of both. Multiorgan metastasis of 4T1-R cells in the presence and in the absence of combination treatment was determined in the BALB/c mouse model. Verapamil induced nuclear translocation of doxorubicin, G2-phase growth arrest and synergistically induced 100% cytotoxicity in 4T1-R cells in culture. However, the combination treatment using verapamil and doxorubicin did not improve the overall survival of BALB/c mice with metastatic breast cancer. Our results indicate that the combination treatment of verapamil and doxorubicin did not inhibit tumor growth in the lungs and liver indicating that the anticancer synergy mechanism of verapamil and doxorubicin is impaired in vivo in BALB/c mouse model with metastatic breast cancer. We propose that understanding the mechanisms as to why the combination of doxorubicin and verapamil treatment was impaired in the mouse model should allow novel approaches to improve chemotherapy response of metastatic breast cancer.Copyright Â© 2014 Elsevier Inc. All rights reserved.
Neoplastic reprogramming of patient-derived adipose stem cells by prostate cancer cell-associated exosomes. - Stem cells (Dayton, Ohio)
Emerging evidence suggests that mesenchymal stem cells (MSCs) are often recruited to tumor sites but their functional significance in tumor growth and disease progression remains elusive. Herein we report that prostate cancer (PC) cell microenvironment subverts PC patient adipose-derived stem cells (pASCs) to undergo neoplastic transformation. Unlike normal ASCs, the pASCs primed with PC cell conditioned media (CM) formed prostate-like neoplastic lesions in vivo and reproduced aggressive tumors in secondary recipients. The pASC tumors acquired cytogenetic aberrations and mesenchymal-to-epithelial transition and expressed epithelial, neoplastic, and vasculogenic markers reminiscent of molecular features of PC tumor xenografts. Our mechanistic studies revealed that PC cell-derived exosomes are sufficient to recapitulate formation of prostate tumorigenic mimicry generated by CM-primed pASCs in vivo. In addition to downregulation of the large tumor suppressor homolog2 and the programmed cell death protein 4, a neoplastic transformation inhibitor, the tumorigenic reprogramming of pASCs was associated with trafficking by PC cell-derived exosomes of oncogenic factors, including H-ras and K-ras transcripts, oncomiRNAs miR-125b, miR-130b, and miR-155 as well as the Ras superfamily of GTPases Rab1a, Rab1b, and Rab11a. Our findings implicate a new role for PC cell-derived exosomes in clonal expansion of tumors through neoplastic reprogramming of tumor tropic ASCs in cancer patients.Â© 2013 AlphaMed Press.
Impaired autophagy response in human hepatocellular carcinoma. - Experimental and molecular pathology
Autophagy is a cellular lysosomal degradation mechanism that has been implicated in chronic liver diseases and hepatocellular carcinoma (HCC). Association of autophagy defect with the development of human HCC has been shown in transgenic mouse model.We performed this study to verify whether a defect in autophagy would play a role in human hepatocellular carcinoma (HCC).Archival tissue sections of 20 patients with HCC with or without hepatitis C virus (HCV) infection were studied. All slides were immunostained using monoclonal antibodies to p62 and glypican-3 with appropriate positive and negative controls. The expression of p62 and glycican-3 in the HCC and the surrounding non-tumor was semiquantitated. The cytoplasmic staining was graded as negative, weak or strong.Positive p62 staining was found in 20 out of 20 (100%) HCCs and negative staining was observed in 20 out of 20 non-tumor areas and cirrhotic nodules. Positive glypican-3 staining was found in 70% of HCCs and negative staining was seen in all non-tumor areas. An autophagy defect leading to increased expression of p62 and glypican-3 was also seen in the HCC cell line (Huh-7.5), but not in the primary human hepatocytes. Activation of cellular autophagy in Huh-7.5 cells efficiently cleared p62 and glypican-3 expression and inhibition of autophagy induced the expression of p62 and glypican-3.This study shows that p62 is increased in HCC compared to the surrounding non-tumorous liver tissue suggesting that human HCCs are autophagy defective. We provide further evidence that glypican-3 expression in HCC may also be related to defective autophagy. Our study indicates that p62 immunostain may represent a novel marker for HCC.Copyright Â© 2013 Elsevier Inc. All rights reserved.
Clinical significance of CD146 and latexin during different stages of thyroid cancer. - Molecular and cellular biochemistry
Molecular mechanisms underlying thyroid tumorigenesis and identifying new therapeutic targets are still under investigation. We aim to investigate the role of CD146 and latexin (Lxn) and examine whether they have any clinical significance in thyroid cancer. Human thyroid papillary (PTC), follicular (FTC), anaplastic (ATC) cancer cells, and other control cells were used in this study. Western blot, cell proliferation, invasion assay, and shRNA were applied to study the expression levels and functional significances of CD146 and Lxn in thyroid cells. The protein expression was evaluated by immunohistochemistry using human tissue microarray (TMA) slides. Multivariate analysis was used to examine whether these proteins have any clinical significance in patients with thyroid cancer. The protein expressions of CD146 and Lxn were detected in most thyroid cancer cell lines when compared with normal cells. Notably, knockdown of CD146 reduced the migration and invasion in K1 (PTC) and OCUT-1 (ATC) cells. TMAs showed more immunoreactivity against CD146 and Lxn in PTC cores compared with FTC, ATC, and normal tissues. A positive correlation was established between CD146 and both Lxn (r = 0.421, p = 0.045) and age (r = 0.566, p = 0.012); however, it showed a negative correlation with tumor stage (r = -0.231, p = 0.010). In conclusion, CD146 and Lxn increased tumor migration and invasion in vitro and showed a high expression in PTC compared to those in ATC and normal human tissues demonstrating their role in early stage of thyroid tumorigenesis. CD146 was positively correlated with age, but negatively correlated with tumor stage.
High circulating estrogens and selective expression of ERÎ² in prostate tumors of Americans: implications for racial disparity of prostate cancer. - Carcinogenesis
Although estrogen receptor beta (ERÎ²) has been implicated in prostate cancer (PCa) progression, its potential role in health disparity of PCa remains elusive. The objective of this study was to examine serum estrogens and prostate tumor ERÎ² expression and examine their correlation with clinical and pathological parameters in African American (AA) versus Caucasian American (CA) men. The circulating 17Î²-estradiol (E2) was measured by enzyme immunoassay in blood procured from racially stratified normal subjects and PCa patients. Differential expression profile analysis of ERÎ² was analyzed by quantitative immunohistochemistry using ethnicity-based tissue microarray encompassing 300 PCa tissue cores. In situ ERÎ² expression was validated by quantitative reverse transcription-PCR in matched microdissected normal prostate epithelium and tumor cells and datasets extracted from independent cohorts. In comparison with normal age-matched subjects, circulating E2 levels were significantly elevated in all PCa patients. Further analysis demonstrates an increase in blood E2 levels in AA men in both normal and PCa in comparison with age- and stage-matched counterparts of CA decent. Histochemical score analysis reveals intense nuclear immunoreactivity for ERÎ² in tumor cores of AA men than in CA men. Gene expression analysis in microdissected tumors corroborated the biracial differences in ERÎ² expression. Gene expression analysis from independent cohort datasets revealed correlation between ERÎ² expression and PCa progression. However, unlike in CA men, adjusted multivariate analysis showed that ERÎ² expression correlates with age at diagnosis and low prostate-specific antigen recurrence-free survival in AA men. Taken together, our results suggest that E2-ERÎ² axis may have potential clinical utility in PCa diagnosis and clinical outcome among AA men.
The diagnostic value of parathyroid hormone washout after fine-needle aspiration of suspicious cervical lesions in patients with hyperparathyroidism. - The Laryngoscope
We aimed to study the diagnostic value of parathyroid hormone (PTH) concentration in the needle washout of fine-needle aspiration (FNA) compared to cytology of suspicious lesions suggestive of culprit parathyroid glands in patients with recurrent or persistent primary hyperparathyroidism (PHPT).Retrospective review.Patients with recurrent or persistent PHPT, who were referred to one surgeon and underwent FNA of the culprit parathyroid lesion preoperatively, were included in this study. All patients underwent comprehensive neck ultrasound, and suspicious lesions underwent ultrasound-guided FNA by the same surgeon. The aspiration cytology was read by a single dedicated cytopathologist blinded to the PTH washout results. A positive cutoff value for PTH washout concentration was defined as superior to serum PTH level obtained at the same time. The final diagnosis after reoperative surgery was confirmed by the same cytopathologist.Twenty-four consecutive patients were included. The mean serum PTH and calcium were 111.5 Â± 106.25 pg/mL (normal: 15-65 pg/mL) and 10.8 Â± 0.5 mg/dL (normal: 8.6-10.2 pg/mL), respectively. Twenty-two patients (91.6%) had elevated PTH washout concentrations with a positive predictive value (PPV) of 100%. Cytopathology was successful in confirming parathyroid tissue only in seven patients (29%). An adenoma was identified in 19 patients (79.1%); however, five patients (20.8%) were found to have multiglandular disease.An elevated PTH washout concentration can help identify culprit parathyroid gland lesions with a high PPV in patients requiring reoperative parathyroid surgery. This diagnostic technique allows for targeted surgical approach in reoperative settings, especially in patients with negative preoperative sestamibi scans.4.Copyright Â© 2013 The American Laryngological, Rhinological and Otological Society, Inc.
Genetic and epigenetic alterations of steroidogenic factorâ€‘1 in ovarian tumors. - International journal of oncology
Steroidogenic factor-1 (SFâ€‘1), the product of the NR5A1 gene, is an essential transcription factor that is known to regulate steroidogenesis in ovarian epithelia, including the synthesis of progesterone, a suppressor of ovarian cancer. Expression of the SFâ€‘1 protein, a potential ovarian tumor suppressor, has been demonstrated in normal OSE cells, but is lost in most ovarian tumors and ovarian tumor cell lines. We examined loss of heterozygosity (LOH) and promoter methylation as potential mechanisms that may explain the loss of SFâ€‘1 protein in ovarian tumor tissues. Genotyping of three NR5A1 SNPs in matched tumor/normal tissues identified LOH in 16/36 (44%) of the ovarian tumors successfully analyzed, and somatic mutations (gain of allele) in 10% of the tumors. Furthermore, a methylation-sensitive restriction enzyme method was used to demonstrate statistically significant (p<0.0001) increase in the frequency of NR5A1 gene methylation in ovarian tumors (36/46; 78%) versus normal ovaries (1/11; 9%). These data suggest that the SFâ€‘1 encoding gene exhibits frequent genetic (LOH/base substitution) and epigenetic (methylation) somatic alterations in ovarian tumors. These data also present novel molecular mechanisms that may explain the loss of SFâ€‘1 protein in ovarian tumors, and its potential role in ovarian carcinogenesis.
Map & Directions
Tulane Univ.Sch. Of Med. (Sl79), 1430 Tulane Ave. New Orleans, LA 70112
1542 Tulane Ave Box T4m-2
1601 Perdido St
1430 Tulane Ave Sl-42, Rm 3518
2020 Gravier St 7Th Floor
1430 Tulane Ave # Sl11