https://www.facebook.com/2138177899565869/

Dr. Raghwa Sharma, Prague (2026)

16/07/2026

AI in pathology diagnostics is a rapidly advancing field transforming how pathologists analyze slides, integrate data, and support clinical decisions. Current Applications and Capabilities
• Whole Slide Imaging (WSI) + AI Analysis: AI algorithms excel at tumor detection, grading (e.g., prostate, breast), quantification (e.g., Ki-67, PD-L1 scoring), and biomarker assessment. Tools can pre-screen slides, flag regions of interest, and reduce review time.
• Diagnostic Assistance:
• Cancer subtyping and molecular prediction (e.g., inferring mutations or MSI status from H&E images).
• Detection of rare events like micrometastases or infectious agents.
• Quality control (e.g., identifying artifacts or poor staining).
• Workflow Integration: Digital pathology platforms with AI triage improve efficiency in high-volume labs, aiding prioritization of complex cases.
Key Benefits
• Efficiency Gains: Studies and real-world use show 20-50%+ reduction in time for routine tasks, helping address pathologist shortages.
• Consistency and Objectivity: Reduces inter-observer variability in grading/staging.
• Augmented Intelligence (not replacement): Pathologists at USCAP 2026 events consistently view AI as a supportive tool for productivity, not a replacement. Human oversight remains essential for complex cases, integration with clinical context, and liability.
• Precision Medicine Support: AI helps predict treatment response or prognosis by combining image features with genomics (multimodal AI).

03/07/2026

ISGYP 170.6: 56 year old female with right ovarian mass.
Diagnosis: Mixed germ cell tumour: yolk sac tumour, choriocarcinoma and teratoma. Metastatic deposit of ETT and Choriocarcinoma in lung.
Comment: Germ cell tumours are ovarian tumours formed by cells derived from primordial germ cells. Those that differentiate in an extraembryonic (placental or trophoblastic) direction result in yolk sac tumours or choriocarcinomas. Mixed subtypes of germ cell tumours also occur frequently. Choriocarcinomas are germ cell tumours formed by placental elements (namely, villous type trophoblastic cellular elements). Choriocarcinomas in the o***y occur as gestational and non-gestational types. Non-gestational choriocarcinomas spread mainly via lymphatics and gestational choriocarcinomas spread primarily via the bloodstream . Non-gestational choriocarcinomas have no paternal chromosomes . It is important to distinguish between these types, as the prognosis and chemotherapeutic response may differ . Sustained remission is achieved in most patients, but it is less common in those with non-gestational choriocarcinomas. Gestational choriocarcinomas may follow decades after an antecedent pregnancy.
Association between ovarian carcinoma and choriocarcinoma could be because of a true collision tumour between a carcinoma and a choriocarcinoma. The second hypothesis is that of a divergent differentiation of carcinoma called as “neometaplastic” process or as “retrodifferentiation” or “dedifferentiation”.

03/07/2026

ISGYP 170.5: 49 year old. 3cm haemorrhagic mass mainly involving LUS. Section of cervix.
Diagnosis: Epithelial trophoblastic tumour with colonisation of cervix mucosa.
Comment: Epithelioid Trophoblastic Tumour Malignant. Derived from chorionic-type intermediate trophoblasts. Mass-forming. Well-circumscribed but destructive nodular proliferation of medium-sized trophoblastic cells. Unform cells with moderate amounts of granular to clear eosinophilic cytoplasm and round nuclei. Distinct cell membranes. Hyaline-like material Frequently extensive necrosis. IHC: (+)p63, inhibin, GATA-3. Ki67 >10%
Placental Site Trophoblastic Tumour : Malignant. Derived from implantation site intermediate trophoblasts. Mass-forming. Infiltrative aggregates of large, polyhedral to round, predominantly mononucleated cells. Scattered multinucleated cells. Abundant amphophilic to eosinophilic cytoplasm. Pronounced nuclear atypia. Infiltrate myometrium and vessels. IHC: (+) hPL, MUC4. Ki67 >10%
Gestational Choriocarcinoma: Malignant cytotrophoblasts, trophoblasts, (mononuclear) and syncytiotrophoblasts (multinucleated) Abundant Hemorrhage, necrosis, and LVI. Marked Pleomorphism/atypia Numerous mitoticfigures. Infiltrative, destructive, solid growth. Very elevated Serum hCG Can get after molar pregnancy (most common), normal pregnancy (intraplacental), or abortion Most common gestational trophoblastic neoplasm. Can be mixed with other tumors. IHC: (+) hCG, hPL, inhibin, SALL4, MUC4, p63. Ki67 >90% Excellent response to chemotherapy.

03/07/2026

ISGYP 170.4: 43 year old. 8cm haemorrhagic mass replacing endometrial cavity.
Diagnosis: Choriocarcinoma.
Choriocarcinoma is a rare and aggressive form of cancer that arises from trophoblastic cells, which normally form the placenta during pregnancy.
It most commonly occurs as gestational choriocarcinoma, a type of gestational trophoblastic disease (GTD), developing in the uterus after a molar pregnancy (especially complete hydatidiform mole), miscarriage, ectopic pregnancy, abortion, or even a normal term delivery. Less commonly, non-gestational forms can arise in the ovaries or te**es as germ cell tumors and more rarely from differentiated somatic cancers.

03/07/2026

ISGYP 170.3: 33 year old. 13cm focally necrotic and haemorrhagic uterine mass with increasing BHCG. Last pregnancy 10 years ago.
Diagnosis: Mixed GTT with PSTT, ETT and choriocarcinoma.
Comment: The commonest mixed tumour is of choriocarcinoma and ETT. It is also possible for admixed PSTT and ETT without choriocarcinoma, and rarest of all, three malignant tumours together. A common precursor to mixed tumours is chemotherapy, and there may be extensive necrosis.
Immunocytochemical staining will show different combinations of expression depending on the cells in the part of tumour in question. Aside from the usual cell typing markers, the proliferation index can be especially helpful in determining areas of choriocarcinoma vs PSTT vs ETT in mixed tumours . Prognosis depends on the mix of tumours and the stage. The choriocarcinoma component is most likely to metastasize, though given its chemosensitivity this still has good prognosis.

03/07/2026

ISGYP 170.2: 36 year old. POC.
Diagnosis: EBV associated B cell lymphoma confined to fetal tissue, mother well.
Comment: The entire specimen was submitted, showing decidualised endometrium, chorionic villi and trophoblastic cells. No significant active inflammation or chorioamnionitis is present. There is no abnormal trophoblastic proliferation. Most chorionic villi show within loose stroma an atypical population of lymphocytes and plasmacytoid cells, moderate in number and of mixed morphology, intermediate to large in size with coarse chromatin, the large forms having irregular nuclear membranes and voluminous cytoplasm with variably prominent nucleoli. There are mitotic figures and apoptotic debris is noted. Immunohistochemical staining shows this population is entirely B cell phenotype, without any CD3+ T cell component within chorionic villi (seen only in maternal decidual tissue). The atypical lymphocytes are highlighted by CD20, PAX5, MUM1 and the plasmacytoid forms by CD138. There is diffuse positivity in these cells with EBER, LMP1 and EBNA2, in keeping with EBV-association latency stage III. There is kappa light chain restriction, aberrant overexpression of EBER and proliferation rate is high (70%) by MIB1 staining. Staining for BCL2 is moderate (30%) and C-MYC highlights 60% of atypical cells. Some large forms show CD30 expression. No expression of CD56 is seen (highlighting only rare NK cells in decidua), no expression of CD10 or BCL6 is seen, ALK1 is negative and CD45 shows patchy expression. Background histiocytes are highlighted by CD68-KP1. No myeloid marker (CD117, CD35 or myeloperoxidase) expression is seen. Immunohistochemistry for HSV1 and 2 as well as CMV are negative. T. pallidum immunohistochemistry is also negative. The decidualised material tissue appears uninvolved by the EBV-associated lymphoid proliferation, where present showing moderate numbers of CD3+ T cells without significant or atypical B lymphocytes.
Concurrent pregnancy loss microarray analysis has been performed at the Cytogenetics Unit, Diagnostic Genomics: Reported: Inconclusive result most likely consistent with significant maternal cell contamination. Y chromosome material noted. Unable to assess for clinically significant copy number variants. Gene rearrangement studies (IGH and IGK) was performed using BIOMED-2 primers. These studies show monoclonal rearrangements of the IgH and IgK genes detected.
Within most chorionic villi is an atypical EBV-associated B cell population, showing polymorphous morphology, with high proliferation rate (70%) and EBV latency stage III. In this clinical context precise classification is difficult; with clonality confirmed the immunomorphology is of an EBV+ B CELL LYMPHOMA with polymorphous large cell morphology, the atypical B lymphocytes appearing to only involved fetal tissue while maternal tissue appears uninvolved. Clinical correlation with maternal EBV serology and viral load would be of value.

03/07/2026

ISGYP 170.1: 53 year old female with right ovarian mass.
Diagnosis: Grade 3 endometrioid adenocarcinoma with choriocarcinoma.
Comment: Gestational choriocarcinoma and non-gestational choriocarcinoma are distinct entities, with significant differences in their etiology, pathogenesis, clinical presentation, management, and prognosis. A clinical history of pregnancy, amenorrhea, or antecedent gestational trophoblastic disease helps to establish the gestational or non-gestational nature of choriocarcinoma. In difficult cases, tissue genotyping should be employed to confirm the diagnosis and to tailor apt management strategies, since both gestational and non-gestational choriocarcinoma exhibit identical clinical and radiological features, serum biochemical markers, histology, and immunohistochemical characteristics.
Histomorphologically, both gestational choriocarcinoma and non-gestational choriocarcinoma are composed of mono-nucleate and multi-nucleate trophoblastic cells in varying proportions. The cytotrophoblasts and intermediate trophoblasts display centrally placed small, round hyperchromatic nuclei, with clear-to-eosinophilic cytoplasm and distinct cell borders. The multi-nucleated cells are larger with irregular outlines, and correspond to syncytiotrophoblasts. These tumors often show extensive areas of hemorrhage and necrosis. The degree of trophoblastic differentiation may vary from well differentiated to poorly differentiated, and villous structure is absent. If choriocarcinoma is found in combination with other germ cell tumors in a pre-menarchal girl, then it can be ascertained to be of the non-gestational type. Non-gestational choriocarcinoma arising in association with somatic carcinoma will display adjacent areas of squamous-, transitional-, or adeno-carcinoma like above case.
The intermediate trophoblastic cells exhibit strong and diffuse cytoplasmic positivity for MUC-4, HLA-G, Mel-CAM, hPL (human placental lactogen), p63, and inhibin. In contrast, the cytotrophoblasts are immune-negative for the above markers, and show nuclear positivity for beta-catenin. Syncytiotrophoblasts cells are strongly reactive to beta-hCG, hPL. These immunohistochemical markers or cytokeratin 18 are usually used to confirm trophoblastic differentiation in poorly differentiated adenocarcinomas (ie, non-gestational choriocarcinoma arising in association with somatic malignancies) or mixed germ cell tumors. All types of trophoblastic cells show membranous positivity for cytokeratin 18 and AE1/AE3.
SALL4 (spalt-like transcription factor 4 and sal-like protein 4) has shown up to 100% specificity and sensitivity in detecting seminoma, dysgerminoma, embryonal carcinoma, and yolk sac tumor. In contrast, SALL4 is only focally or weakly expressed in choriocarcinoma. However, according to some experts, if SALL4 positivity is present, it almost certainly rules out gestational choriocarcinoma, and confirms the diagnosis of non-gestational choriocarcinoma in tumors exhibiting trophoblastic differentiation.

27/05/2026

Inaugural Scientific Meeting of the Australasian Molecular Pathology Society in Brisbane. Updates into the rapidly evolving world of molecular diagnostics and its transformative role in precision personalised medicine. With expert talks spanning molecular testing in cancer, circulating tumour DNA, variant interpretation standards, and automated frameworks for precision oncology, the program beautifully illustrates how advances in molecular pathology are enabling clinicians to move beyond one-size-fits-all treatments toward therapies tailored to each patient’s unique genomic profile 🧬

08/03/2026

It’s good to get into Ai training folks.. it’s right here..

Learning Claude (Anthropic's AI family, especially the latest 2026 models like Claude Opus 4.6 and Sonnet 4.6)ASAP isn't just about keeping up with hype — it's about gaining real leverage in productivity, skills, career, and even income potential right now.

Here's why many people (developers, knowledge workers, students, entrepreneurs) are saying "learn it yesterday":

1. It's Becoming the Go-To for Deep, Agentic Work (Not Just Chat)
Claude has evolved far beyond a simple chatbot. In 2026:
- Claude Code— runs in your terminal/editor, refactors entire codebases, debugs autonomously, writes tests, and handles long-running tasks better than most rivals (leads on benchmarks like SWE-bench Verified, Terminal-Bench).

- Claude Cowork— desktop agent that automates workflows across tools (files, Gmail, Drive, Docs, etc.), organizes your computer, creates reports.
Skills + MCP (Model Context Protocol)** — turn repetitive tasks into one-command automations (e.g., auto-generate PRDs from meetings, deploy apps, run cross-tool workflows). Connect GitHub, Notion, Slack, Vercel → Claude executes, not just suggests.

This shifts it from "ask questions" → "AI teammate that does real ex*****on." Mastering these layers (chat → code → skills → agents) gives massive leverage in vibe coding, automation, and building fast.

2. Frontier-Level Performance in Reasoning, Coding, and Knowledge Work
Recent releases (Opus 4.6 / Sonnet 4.6) show:
- 1M token context windows (handle huge documents/codebases without losing track).
- Superior long-horizon agentic tasks (sustains hours-long focused effort, plans carefully, self-corrects).
- Top scores on hard evals: agentic coding, complex multidisciplinary reasoning, security vulnerability finding (e.g., found 22 Firefox bugs in 2 weeks, many high-severity).
- Better natural writing, structured reasoning, fewer hallucinations via Constitutional AI updates.

For coding, research, analysis, design, finance/legal tasks — it's frequently preferred over alternatives for depth and reliability.

3. Productivity & Skill Multiplier (But With a Catch)
- Speeds up experienced tasks dramatically (up to 80% time savings in studies).
- Anthropic pushes "AI fluency" via free courses (Claude 101, developer tools, API integration) — they even launched a full free learning platform in 2026.
- Helps non-coders automate/monetize (build apps, reports, content workflows).
- Caveat from Anthropic's own research: heavy reliance while learning new skills can hinder deep understanding/debugging ability. Use it thoughtfully (e.g., explanatory modes, iterate/refine) to build skills faster, not offload thinking.

4. Career & Economic Edge
- Enterprise adoption exploding (Anthropic dominates coding/AI-for-work market share in many reports; massive revenue growth projected).
- Companies mastering Claude/agents move faster, build better, automate more → individuals who fluently use it gain "superpowers."
- Free tier now powerful (Sonnet 4.6 default, includes files, connectors, skills).
- Early adopters automate jobs, freelance faster, or prototype startups in days.

5. It's Still Early — But Closing Fast
Many still treat it like "another ChatGPT." Those who learn the full system (prompt layering, projects for persistent context, tools/skills) pull way ahead. Anthropic keeps iterating rapidly (new models every few months), so the gap between casual users and power users widens quickly.

Bottom line: If you're in tech, content, business, education, research, or anything involving thinking/creating/automating — Claude in 2026 is one of the highest-leverage tools available. Start with the free claude.ai (try Sonnet 4.6), do Anthropic's Claude 101 course, play with Projects/Skills/Code, and build one small automation workflow this week.

The people saying "learn it ASAP" aren't exaggerating — the compound advantage from fluency here is already showing up in real output, income, and career speed. 🚀

25/02/2026

ISGYP 169.7: 67-year-old female. Uterine mass.

Diagnosis: Grade 3 Pilomatrix-like endometroid carcinoma.

Comment
Pilomatrix-like high-grade endometrioid carcinoma (PiMHEC) of the endometrium is an extremely rare, aggressive endometrial cancer characterized by features resembling cutaneous pilomatrix carcinoma, such as ghost cell keratinization and, frequently, widespread metastasis at diagnosis. It is a variant of endometrioid carcinoma with poor prognosis. The tumour shows high-grade, solid basaloid cells, extensive geographic necrosis, and distinct "ghost" (shadow) cells. It is associated CTNNB1 exon 3 mutations, often showing diffuse nuclear b-catenin expression. Immunohistochemistry shows nuclear β-catenin and CDX2 expression and loss of estrogen and progesterone receptors and PAX8. Other frequent features were geographic necrosis and a low-grade endometrioid component. CK7, neuroendocrine, and basal/squamous markers. All cases with available follow-up showed poor prognosis. PiMHEC should be distinguished from mimickers, such as high-grade endometrioid carcinoma with geographic necrosis, low-grade endometrioid carcinoma with ghost cell keratinization, and undifferentiated/dedifferentiated carcinoma. PiMHEC is characterized by solid nests of high-grade basaloid cells exhibiting ghost cell keratinization, similar to that observed in hair matrix tumour. Geographic necrosis is commonly found. The solid component of PiMHEC often coexists with a separate endometrioid component, which supports the endometrioid lineage of the tumour. Immunohistochemically, the basaloid cells show diffuse nuclear accumulation of β-catenin which reflects the presence of an underlying CTNNB1 mutation and is typically accompanied by CDX2 (caudal-type homeobox transcription factor 2) positivity. Interestingly, the tumour is negative for PAX8 and estrogen and progesterone receptors, suggesting a loss of Müllerian differentiation; these markers are positive in the endometrioid component, if present. The expression of CK7 (cytokeratin 7), as well as of basal/squamous cell markers p63 and p40, is variable. A multifocal expression of neuroendocrine markers chromogranin and synaptophysin is frequently observed. PiMHEC is typically p53-wild-type; MMR-deficiency has been described in a subset of cases
PiMHEC is highly aggressive, frequently presenting with advanced disease.
Reported treatments include a combination of surgical resection, chemotherapy, radiation, and immune checkpoint inhibitors.

Dr. Raghwa Sharma

16/07/2026

03/07/2026

03/07/2026

03/07/2026

03/07/2026

03/07/2026

03/07/2026

27/05/2026

08/03/2026

25/02/2026

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